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Kuramoto, Eriko. "Two types of thalamocortical projections from the motor thalamic nuclei of the rat: a single neuron tracing study using viral vectors." Kyoto University, 2009. http://hdl.handle.net/2433/124305.
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Nakamura, Hisashi. "Different cortical projections from three subdivisions of the rat lateral posterior thalamic nucleus: a single neuron tracing study with viral vectors." Kyoto University, 2016. http://hdl.handle.net/2433/216156.
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Final publication is available at http://dx.doi.org/10.1111/ejn.12882Kyoto University (京都大学)
0048
新制・論文博士
博士(医学)
乙第13040号
論医博第2115号
新制||医||1017(附属図書館)
33032
京都大学大学院医学研究科医学専攻
(主査)教授 渡邉 大, 教授 影山 龍一郎, 教授 髙橋 良輔
学位規則第4条第2項該当
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SERRA, LINDA. "Role of the Sox2 and COUP-TF1 transcription factors in the development of the visual system by conditional knock-out in mouse." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/261939.
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Il fattore di trascrizione Sox2 è espresso nel sistema nervoso dall’inizio del suo sviluppo dove è richiesto per il mantenimento delle cellule staminali. Nell'uomo, le mutazioni eterozigoti di Sox2 sono collegate a vari difetti del sistema nervoso centrale, inclusi i difetti visivi. Il sistema visivo è composto dall'occhio, dal nucleo talamico genicolato dorsolaterale (dLGN) e dalla corteccia visiva, che sono altamente interconnessi. L'occhio, infatti, invia le afferenze retiniche ad uno specifico nucleo talamico dorsale, il dLGN, i cui neuroni a loro volta proiettano verso l'area corticale visiva. La corteccia visiva elabora input visivi e proietta al dLGN in un circuito complesso. Numerosi geni sono importanti per il corretto sviluppo del sistema visivo e Sox2 è uno di questi. Sox2 è espresso in tutti e tre i componenti del sistema visivo nel topo; mentre il suo ruolo nello sviluppo della retina è ben descritto si sa poco riguardo al suo ruolo nel talamo. Per studiare l’importanza di Sox2 nel talamo per il corretto sviluppo dell'asse visivo, abbiamo generato un knockout condizionale talamico di Sox2 nei neuroni post-mitotici. Abbiamo osservato che la perdita di Sox2 nel dLGN porta a una forte riduzione delle dimensioni del dLGN, all’alterazione delle proiezioni neuronali retino-talamiche, talamo-corticali e cortico-talamiche e, di conseguenza, a una difettiva definizione dell'area visiva corticale. Abbiamo scoperto che nei mutanti talamici di Sox2 il gene Efna5, importante nel guidare gli assoni retinici verso il dLGN, e i geni SERT e vMAT2 che codificano per trasportatori di serotonina, importanti per la corretta formazione di proiezioni talamo-corticali, sono fortemente sottoregolati nel dLGN mutante. Per identificare tutti i potenziali geni che potrebbero mediare la funzione di Sox2 nel talamo, abbiamo eseguito il sequenziamento dell'RNA (RNA-seq) su dLGN di controlli e mutanti di Sox2. Abbiamo scoperto che i geni deregolati sono arricchiti in geni che codificano per molecole importanti per la guida degli assoni e per molecole coinvolte nella neurotrasmissione e nelle sinapsi. È interessante notare che l'ablazione talamica di un altro fattore di trascrizione, COUP-TF1, porta a difetti del sistema visivo simili a quelli descritti per Sox2. Inoltre, le mutazioni eterozigoti nel gene COUP-TF1 nell'uomo portano all'atrofia ottica e a disabilità intellettive. Abbiamo scoperto che Sox2 e COUP-TF1 sono co-espressi negli stessi neuroni post-mitotici del dLGN. Sorprendentemente, l'espressione di COUP-TF1 non varia nei mutanti talamici di Sox2, facendo nascere la possibilità che Sox2 e COUP-TF abbiano target comuni nel talamo. Pertanto, abbiamo esaminato l'espressione, nei mutanti COUP-TF1, di geni sottoregolati nei mutanti talamici di Sox2 e sorprendentemente abbiamo scoperto che sembrano sovraregolati, suggerendo che i due fattori di trascrizione potrebbero agire sugli stessi geni ma in modo opposto. Per capire meglio se i due fattori di trascrizione regolano geni comuni, stiamo eseguendo l'analisi dell'espressione genica mediante RNA-seq anche sui mutanti talamici COUP-TF1. Inoltre, stiamo generando topi doppi mutanti per Sox2 e COUP-TF1 per scoprire come questi geni regolano espressione genica; è plausibile che regolino geni comuni per bilanciare la loro espressione nei neuroni talamici.The transcription factor Sox2 is expressed in the nervous system from the beginning of its development where it is required for stem cells maintenance. In humans, Sox2 heterozygous mutations are linked to various central nervous system defects, including visual defects. The visual system is composed of the eye, the dorsolateral geniculate thalamic nucleus (dLGN) and the visual cortex, which are highly interconnected. The eye, in fact, sends retinal afferent to a specific dorsal thalamic nucleus, the dLGN, whose neurons in turn project to the visual cortical area. The visual cortex elaborates visual inputs and projects back to the dLGN in a complex circuit. Several genes are important for the correct development of the visual system and Sox2 is one of them. Sox2 is expressed in all the three components of the visual system in mouse; while its role in the development of the retina is well characterized little is known about its role in the thalamus. To investigate Sox2 requirement in the thalamus for the correct establishment of the visual axis, we generated a thalamic Sox2 conditional knock-out in post-mitotic neurons. We observed that Sox2 loss in the dLGN leads to a strong reduction in size of the dLGN, aberrant retino-geniculate, thalamo-cortical and cortico-thalamic neural projections and, consequently, to a defective patterning of the cortical visual area. We found that in Sox2 thalamic mutants the Efna5 gene, important in guiding retinal axons towards the dLGN, and the serotonin transporters encoding genes SERT and vMAT2, involved in the establishment of thalamo-cortical projections, are strongly downregulated in the mutant dLGN. To identify all the potential genes that could mediate Sox2 function in the thalamus, we performed RNA sequencing (RNA-seq) on control and Sox2 mutant dLGNs. We noticed that misregulated genes are enriched in genes encoding axon guidance molecules and molecules involved in neurotransmission and synapses. Interestingly, thalamic ablation of another transcription factor, COUP-TF1, leads to defects of the visual system similar to the ones described for Sox2. In addition, heterozygous mutations in the COUP-TF1 gene in human lead to optic atrophy and intellectual disabilities. Interestingly, we found that Sox2 and COUP-TF1 are co-expressed in the same post-mitotic neurons of the dLGN. Surprisingly, COUP-TF1 expression does not vary in Sox2 thalamic mutants, arising the possibility that Sox2 and COUP-TF have common target in the thalamus. Therefore, we looked at the expression, in COUP-TF1 mutants, of genes downregulated in Sox2 thalamic mutants and we surprisingly found that they appear upregulated, suggesting that the two transcription factors could act on the same genes but in an opposite way. To better understand if the two transcription factors regulate common genes, we are performing gene expression analyses by RNA-seq also on COUP-TF1 thalamic mutants, with the aim to identify an overlap with Sox2 regulated genes. Moreover, we are generating Sox2 and COUP-TF1 double mutant mice to unveil how these genes regulate gene expression; it is plausible that they regulate common genes to balance their expression in thalamic neurons.
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Dacre, Joshua Rupert Heaton. "Thalamic control of motor behaviour." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/29530.
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The primary motor cortex (M1) is a key brain area for the generation and control of motor behaviour. Output from M1 can be driven in part by long-range inputs from a collection of thalamic nuclei termed the motor thalamus (MTh), but how MTh input shapes activity in M1 and forelimb motor behaviour remains largely unresolved. To address this issue, we first defined the 3D anatomical coordinates of mouse forelimb motor thalamus (MThFL) by employing conventional retrograde and virus-based tracing methods targeted to the forelimb region of M1 (M1FL). These complimentary approaches defined MThFL as a ~0.8 mm wide cluster of neurons with anatomical coordinates 1.1 mm caudal, 0.9 mm lateral to bregma and 3.2 mm below the pial surface. Thus, MThFL incorporates defined areas of the ventrolateral, ventral anterior and anteromedial thalamic nuclei. To investigate the importance of M1FL and MThFL during skilled motor behaviour, we developed and optimised a quantitative behavioural paradigm in which head-restrained mice execute forelimb lever pushes in response to an auditory cue to receive a water reward. Forelimb movement trajectories were mapped using high-speed digital imaging and multi-point kinematic analysis. We inactivated both M1FL and MThFL of mice performing this motor behaviour using a pharmacological strategy, which in both cases resulted in a significant reduction in task performance. Inactivating M1FL significantly affected forelimb coordination and dexterity, resulting in erratic motion and posture. In contrast, mice with MThFL inactivated displayed a reduction in total motor output, although correct posture was maintained. We performed extracellular recordings in MThFL of expert-level mice, demonstrating that motor thalamic output during execution of task was dominated by a robust response to the onset of the auditory cue. Cue-evoked responses were also observed in motor thalamic neurons of naive mice. We have developed a novel solution to the stability problem encountered when performing whole-cell patch-clamp recordings from the motor cortex of head-restrained mice performing forelimb motor behaviour, and present preliminary recordings maintained through the execution of forelimb behaviour.
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Wu, Huiying. "Modeling thalamic activity and neural bursting." Thesis, The University of Sydney, 2009. https://hdl.handle.net/2123/28236.
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The human brain is the most complicated organ in the central nervous system.
Although an enormous number of studies have been conducted to attempt to
understand the brain and its activity, most of the functions of the brain and the
mechanisms of its large scale activities are still not clear. In this thesis, a mean—
field approach is used to study the thalamus, which is the sensory gateway of
the brain and a key component of the thalamocortical system, and also neural
bursting, which is an important type of neural activity.
Chapter 1 provides an overview of the thesis, as well as brief a background
on the thalamus and neural bursting, including their neurophysiology and re—
lated modeling studies. In Chapter 2, a physiologically based mean-field model
is used to study the role of the thalamus and its substructures in genesis of
electroencephalograms (EEGS), particularly spindle oscillations. An existing
corticothalamic mean-field model is modified to represent an isolated thala—
mus. In addition to the populations of neurons previously considered in the
context of this model, an additional population of thalamic neurons, the 10—
cal interneurons (Lls), is added. Interconnections between thalamic nuclei are
then studied and substructures of the thalamus are analyzed. It is found that
the isolated reticular (RE) nucleus cannot generate spindle oscillations on its
own, but is nonetheless essential to their genesis. This finding is consistent
with experiments in vitro. The MS can generate spindle oscillations in con—
junction with the other relay cells and are shown to have similar effects to the
RE nucleus, except that they are purely inhibitory, whereas the latter nucleus
has both direct inhibitory and indirect excitatory effects on the relay cells.
Chapters 3 and 4 study neural bursting based on a method of obtaining a
neural rate equation from a conductance—based model, which is in Appendix
A. In Chapter 3, to study neural bursting, or bursting neurons, a conductance-based
model is incorporated into a mean—field model to obtain a prototype
mean—field bursting model. Properties of the model are explored via study of
its frequency responses under various inputs, which include sinusoidal signals
and white noise perturbations. The main finding of this study is that neurons
with various initial states are capable of phase-locked or intermittent firing,
depending on their baseline voltage. Moreover, depending on this voltage, the
bursting frequency of the neurons either slaves to the original unperturbed
bursting frequency or approaches a steady value as the external driving fre—
quency increases. White noise peturbations produce a bursting frequency
similar to the one seen in the unperturbed case, which indicates that the dy—
namics of the system are robust and a more general external stimulus only
alters the firing pattern slightly.
Chapter 4 contains a study of a simplified version of the thalamocortical—
corticothalamic (TC-CT) loop structure, whose activity is modeled by the
mean—field bursting model developed in Chapter 3. To explore the effects of the
feedback loop, the frequency response of the system is studied as a function of
the loop coupling strength and time delay. At a fixed time delay, variation of
coupling strength causes the dominant response frequency to switch from the
unperturbed bursting frequency and its harmonics to the response frequency
of the loop and its harmonics. Furthermore, there are many fine structures in
spectral density plots that are shown to be affected by dendritic parameters.
However, the full mechanism behind these fine structures is not clear. Depending
on the magnitude of the coupling strength, frequency response patterns
are different as the time delay is varied. Although the response frequency al—
ternates between the frequencies induced by the bursting neurons and those
induced by the loop structure for both small and large coupling strengths, the
patterns of alternation are different. None of these frequency responses, except
the bursting dynamics at very weak coupling strengths, are seen in Chapter 3.
This indicates that the loop structure produces rich and complicated dynamics.
Chapter 5 briefly reviews the main outcomes of this thesis and outlining
possible future investigations. Overall, the present work provides improved
understanding of brain rhythm genesis in the thalamus and a prototype mean—
field bursting model that can be used in future studies of the thalamocortical
system.
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Lee, Stephanie G. "Medial lemniscal evoked responses in thalamic ethmoid neurons." Thesis, University of British Columbia, 2006. http://hdl.handle.net/2429/31658.
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This thesis describes electrophysiological and pharmacological properties of neurons in
the ethmoid nucleus of the rat thalamus. According to the atlas by Paxinos and Watson,
the ethmoid nucleus is located dorsal to the medial lemniscus, the major somatosensory
input to the thalamus. The ethmoid also lies ventral to the parafascicular nucleus, caudal
to the ventrobasal thalamus and rostral to the scaphoid nucleus. The ethmoid is
considered a higher order nucleus, which implies that it serves as a link in corticothalamo-
cortical pathways that process sensory information. The literature on this
nucleus is scarce and this thesis represents the first known attempt to study these neurons.
Hence, a major objective of this thesis was to determine the passive and active properties
of ethmoid neurons.
Recent evidence from this laboratory has shown that stimulation of the medial lemniscus
produced glycinergic and GABAergic inhibition in ventrobasal neurons. This inhibition
was not sensitive to ionotropic glutamate receptor antagonism by kynurenate. A
prediction from these studies was that the ethmoid was an intermediate nucleus in a
circuit between the medial lemniscus and neurons of the ventrobasal thalamus. Thus, a
key aim of this thesis was to examine the possible involvement of ethmoid neurons in this
novel circuit.
This thesis provides evidence that ethmoid neurons have passive and active properties
similar to other neurons of the dorsal thalamus. Ethmoid neurons have a mean resting membrane potential of ~ -53 mV, a mean input resistance of ~670 MΩ and a mean
membrane time constant of ~64 ms. Ethmoid neurons also have the ability to generate
spikes in the tonic and burst firing modes. The active properties were sensitive to
blockade by internal application of QX-314, a quaternary blocker of Na⁺ channels and by
extracellular application of Ni2 ⁺ , a Ca2 ⁺ channel antagonist. These observations are
consistent with Na⁺ dependent action potentials when a neuron is in the tonic firing mode
and low threshold Ca2 ⁺ spikes when in the burst firing mode.
We showed that stimulation of the medial lemniscus evoked depolarizations in all
recorded ethmoid neurons. We categorized the depolarization responses into two groups.
Group I were monophasic depolarizations and group II were biphasic depolarizations.
The medial lemniscal evoked depolarization of ethmoid neurons persisted in the presence
of kynurenate. These observations are consistent with the participation of ethmoid
neurons in a circuit that results in glycinergic inhibition in ventrobasal neurons.
This thesis marks the first known attempt to study neurons of the ethmoid nucleus. The
observations provide evidence for functional similarities of ethmoid neurons to other
thalamic neurons, as well as evidence for novel inputs activated by stimulation of the
medial lemniscus.Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Pudenz, Christiane [Verfasser]. "Thalamo-cortical circuits for the processing of tactile information : thalamic inputs onto excitatory neurons in layer IV of the mouse barrel cortex." Freiburg : Universität, 2010. http://d-nb.info/1115490478/34.
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Shiraishi, Atsushi. "Generation of thalamic neurons from mouse embryonic stem cells." Kyoto University, 2018. http://hdl.handle.net/2433/230993.
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Meuth, Patrick [Verfasser], and Martin [Akademischer Betreuer] Burger. "Thalamic neurons in silico / Patrick Meuth. Betreuer: Martin Burger." Münster : Universitäts- und Landesbibliothek der Westfälischen Wilhelms-Universität, 2011. http://d-nb.info/1027017827/34.
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Ruffo, Mark. "The role of the corticothalamic projection in the primate motor thalamus /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/10626.
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Lozsadi, Dora A. "The neural circuits of the thalamic reticular nucleus." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260159.
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Tennigkeit, Frank. "Intrinsic membrane properties affecting signal transformation in auditory thalamic neurons." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ34633.pdf.
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Lau, Yau-pok. "Postnatal development of thalamic neurons in response to vertical movement /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B3834810X.
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劉友璞 and Yau-pok Lau. "Postnatal development of thalamic neurons in response to vertical movement." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011369.
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Jalics, Jozsi Z. "EXISTENCE OF SLOW WAVES IN MUTUALLY INHIBITORY THALAMIC NEURONAL NETWORKS." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1023324103.
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Patra, Sanjay. "Response properties of human thalamic neurons to high frequency micro-stimulation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ63200.pdf.
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Asseri, Khalid. "Effects of AMBD and isovaline on GABAergic transmission in thalamic neurons." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/35078.
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In central neurons, the endogenous amino acid γ-aminobutyric acid (GABA) exerts synaptic inhibition mediated through ionotropic GABAA-, or metabotropic GABAB-receptors. These receptors exist on both pre- and postsynaptic membranes. The synthetic structural analogues of GABA, 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide (AMBD) and R-isovaline have received little study on synaptic inhibition in the mammalian thalamus. AMBD was originally proposed as a taurine antagonist whereas R-isovaline is a non-biogenic amino acid that increases postsynaptic K⁺ conductance of thalamocortical neurons. The aim of this work was to assess the prediction that AMBD and R-isovaline would affect presynaptic release of GABA onto neurons of ventrobasal nuclei.
AMBD and R-isovaline were applied by perfusion of thalamic slices obtained from juvenile Sprague-Dawley rats (P10 -13). During whole-cell patch clamp recording from thalamocortical neurons, we voltage-clamped neurons at a holding potential of -70 mV. Miniature inhibitory postsynaptic currents (mIPSCs) were recorded in the presence of tetrodotoxin (TTX). Kynurenic acid and internal Cs⁺ were used to block postsynaptic glutamate receptors and K⁺ conductances. We used the GABAA antagonist bicuculline to identify GABAergic mIPSCs, without affecting a possible presynaptic GABAB-component.
Applied alone at 250 μM, AMBD had no effect on the passive and active membrane properties of neurons. In the range of 10 µM to 1 mM, AMBD had no effect on amplitude or decay time constant of GABAergic mIPSCs. Acting with an IC₅₀ of 232 μM, AMBD reversibly reduced the frequency of GABAergic mIPSCs. The above observations implied that AMBD reduced presynaptic release of GABA. In a range of 25 to 200 µM, R-isovaline had no effect on the holding current or frequency, amplitude and decay time constant of GABAergic mIPSCs. Hence, R-isovaline did not affect release of GABA and did not affect receptors on nerve terminals.
In summary, AMBD reversibly decreased the presynaptic release of GABA, likely by an action on nerve terminals while having no effects on postsynaptic membrane properties that could account for the reduced frequency of GABAergic mIPSCs. The exact mechanism whereby AMBD decreased GABA release remains unclear. R-isovaline had no effect on GABA release in ventrobasal nuclei.
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Hirai, Daichi. "Shaping somatosensory responses in awake rats: cortical modulation of thalamic neurons." Kyoto University, 2018. http://hdl.handle.net/2433/232070.
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Fuentealba, Durand Pablo José. "Intrinsic and Synaptic Membrane Properties of Neurons in the Thalamic Reticular Nucleus." Thesis, Université Laval, 2004. http://www.theses.ulaval.ca/2004/22126/22126.pdf.
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Le noyau réticulaire thalamique (RE) est une structure qui engendre des fuseaux, une oscillation bioélectrique de marque pendant les stades précoces du sommeil. De multiples propriétés neuronales, intrinsèques et synaptiques, sont impliquées dans la génération, la propagation, le maintien et la terminaison des ondes en fuseaux. D’un autre côté, ce rythme constitue un état spécial de l’activité du réseau qui est généré par le réseau lui-même et affecte les propriétés cellulaires du noyau RE. Cette étude se concentre sur ces sujets: comment les propriétés cellulaires et les propriétés du réseau sont inter-reliées et interagissent pour engendrer les ondes fuseaux dans les neurones du RE et leurs cibles, les neurones thalamocorticaux.
La présente thèse fournit de nouvelles évidences montrant le rôle fondamental joué par les neurones du noyau RE dans la genèse des ondes en fuseaux, dû aux synapses chimiques établies par ces neurones. La propagation et la synchronisation de l’activité sont modulées par les synapses électriques entre les neurones réticulaires thalamiques, mais aussi par les composantes dépolarisantes secondaires des réponses synaptiques évoquées par le cortex. De plus, la forme générale et la terminaison des oscillations thalamiques sont probablement contrôlées en grande partie par les neurones du RE, lesquels expriment une conductance intrinsèque leurs procurant une membrane avec un comportement bistable. Finalement, les oscillations thalamiques en fuseaux sont aussi capables de moduler les propriétés membranaires et l’activité des neurones individuels du RE.The thalamic reticular nucleus (RE) is a key structure related to spindles, a hallmark bioelectrical oscillation during early stages of sleep. Multiple neuronal properties, both intrinsic and synaptic, are implicated in the generation, propagation, maintenance and termination of spindle waves. On the other hand, this rhythm constitutes a special state of network activity, which is generated within, and affects single-cell properties of the RE nucleus. This study is focused on these topics: how cellular and network properties are interrelated and interact to generate spindle waves in the pacemaking RE neurons and their targets, thalamocortical neurons. The present thesis provides new evidence showing the fundamental role played by the RE nucleus in the generation of spindle waves, due to chemical synapses established by its neurons. The propagation and synchronization of activity is modulated by electrical synapses between thalamic reticular neurons, but also by the secondary depolarizing component of cortically-evoked synaptic responses. Additionally, the general shaping and probably the termination of thalamic oscillations could be controlled to a great extent by RE neurons, which express an intrinsic conductance endowing them with membrane bistable behaviour. Finally, thalamic spindle oscillations are also able to modulate the membrane properties and activities of individual RE neurons.
Inscrit au Tableau d'honneur de la Faculté des études supérieures
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Pirttimäki, T. M. "Astrocyte-neuron signalling by synaptic stimulation in the ventrobasal thalamus." Thesis, Aston University, 2009. http://publications.aston.ac.uk/15371/.
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In the Ventrobasal (VB) thalamus, astrocytes are known to elicit NMDA-receptor mediated slow inward currents (SICs) spontaneously in neurons. Fluorescence imaging of astrocytes and patch clamp recordings from the thalamocortical (TC) neurons in the VB of 6-23 day old Wistar rats were performed. TC neurons exhibit spontaneous SICs at low frequencies (~0.0015Hz) that were inhibited by NMDA-receptor antagonists D-AP5 (50µM), and were insensitive to TTX (1µM) suggesting a non-neuronal origin. The effect of corticothalamic (CT) and sensory (Sen) afferent stimulation on astrocyte signalling was assessed by varying stimulus parameters. Moderate synaptic stimulation elicited astrocytic Ca2+ increases, but did not affect the incidence of spontaneous SICs. Prolonged synaptic stimulation induced a 265% increase in SIC frequency. This increase lasted over one hour after the cessation of synaptic stimulation, so revealing a Long Term Enhancement (LTE) of astrocyte-neuron signalling. LTE induction required group I mGluR activation. LTE SICs targeted NMDA-receptors located at extrasynaptic sites. LTE showed a developmental profile: from weeks 1-3, the SIC frequency was increased by an average 50%, 240% and 750% respectively. Prolonged exposure to glutamate (200µM) increased spontaneous SIC frequency by 1800%. This “chemical” form of LTE was prevented by the broad-spectrum excitatory amino acid transporter (EAAT) inhibitor TBOA (300µM) suggesting that glutamate uptake was a critical factor. My results therefore show complex glutamatergic signalling interactions between astrocytes and neurons. Furthermore, two previously unrecognised mechanisms of enhancing SIC frequency are described. The synaptically induced LTE represents a form of non-synaptic plasticity and a glial “memory” of previous synaptic activity whilst enhancement after prolonged glutamate exposure may represent a pathological glial signalling mechanism.
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Diadori, Paola. "An intracellular study of callosal and thalamic influences on neurons of cat somatosensory cortex /." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=65396.
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翁德心 and Tak-sum Yung. "Expression of GABAA receptor alpha-1 subunit in thalamic neurons responsive to vertical linear acceleration." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42610059.
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Yung, Tak-sum. "Expression of GABAA receptor alpha-1 subunit in thalamic neurons responsive to vertical linear acceleration." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42610059.
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Elijah, Daniel. "Neural encoding by bursts of spikes." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/neural-encoding-by-bursts-of-spikes(56f4cf97-3887-4e89-bc0d-8db183ce9ce1).html.
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Neurons can respond to input by firing isolated action potentials or spikes. Sequences of spikes have been linked to the encoding of neuron input. However, many neurons also fire bursts; mechanistically distinct responses consisting of brief high-frequency spike firing. Bursts form separate response symbols but historically have not been thought to encode input. However, recent experimental evidence suggests that bursts can encode input in parallel with tonic spikes. The recognition of bursts as distinct encoding symbols raises important questions; these form the basic aims of this thesis: (1) What inputs do bursts encode? (2) Does burst structure provide extra information about different inputs. (3) Is burst coding robust against the presence of noise; an inherent property of all neural systems? (4) What mechanisms are responsible for burst input encoding? (5) How does burst coding manifest in in-vivo neurons. To answer these questions, bursting is studied using a combination of neuron models and in-vivo hippocampal neuron recordings. Models ranged from neuron-specific cell models to models belonging to three fundamentally different burst dynamic classes (unspecific to any neural region). These classes are defined using concepts from non-linear system theory. Together, analysing these model types with in-vivo recordings provides a specific and general analysis of burst encoding. For neuron-specific and unspecific models, a number of model types expressing different levels of biological realism are analysed. For the study of thalamic encoding, two models containing either a single simplified burst-generating current or multiple currents are used. For models simulating three burst dynamic classes, three further models of different biological complexity are used. The bursts generated by models and real neurons were analysed by assessing the input they encode using methods such as information theory, and reverse correlation. Modelled bursts were also analysed for their resilience to simulated neural noise. In all cases, inputs evoking bursts and tonic spikes were distinct. The structure of burst-evoking input depended on burst dynamic class rather than the biological complexity of models. Different n-spike bursts encoded different inputs that, if read by downstream cells, could discriminate complex input structure. In the thalamus, this n-spike burst code explains informative responses that were not due to tonic spikes. In-vivo hippocampal neurons and a pyramidal cell model both use the n-spike code to mark different LFP features. This n-spike burst may therefore be a general feature of bursting relevant to both model and in-vivo neurons. Bursts can also encode input corrupted by neural noise, often outperforming the encoding of single spikes. Both burst timing and internal structure are informative even when driven by strongly noise-corrupted input. Also, bursts induce input-dependent spike correlations that remain informative despite strong added noise. As a result, bursts endow their constituent spikes with extra information that would be lost if tonic spikes were considered the only informative responses.
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Contreras, Diego. "Oscillatory properties of cortical and thalamic neurons and the generation of synchronized rhythmicity in the corticothalamic network." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1996. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq25228.pdf.
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Vigren, Patrick, Anders Tisell, Maria Engström, Thomas Karlsson, Leinhard Olof Dahlqvist, Peter Lundberg, and Anne-Marie Landtblom. "Low Thalamic NAA-Concentration Corresponds to Strong Neural Activation in Working Memory in Kleine-Levin Syndrome." Linköpings universitet, Neurologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-85927.
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Background Kleine Levin Syndrome (KLS) is a rare disorder of periodic hypersomnia and behavioural disturbances in young individuals. It has previously been shown to be associated with disturbances of working memory (WM), which, in turn, was associated with higher activation of the thalamus with increasing WM load, demonstrated with functional magnetic resonance imaging (fMRI). In this study we aimed to further elucidate how these findings are related to the metabolism of the thalamus. Methods fMRI and magnetic resonance spectroscopy were applied while performing a WM task. Standard metabolites were examined: n-acetylaspartate (NAA), myo-inositol, choline, creatine and glutamate-glutamine. Fourteen KLS-patients and 15 healthy controls participated in the study. The patients with active disease were examined in asymptomatic periods. Results There was a statistically significant negative correlation between thalamic fMRI-activation and thalamic NAA, i.e., high fMRI-activation corresponded to low NAA-levels. This correlation was not seen in healthy controls. Thalamic levels of NAA in patients and controls showed no significant differences between the groups. None of the other metabolites showed any co-variation with fMRI-activiation. Conclusion This study shows negative correlation between NAA-levels and fMRI-activity in the left thalamus of KLS-patients while performing a WM task. This correlation could not be found in healthy control subjects, primarily interpreted as an effect of increased effort in the patient group upon performing the task. It might indicate a disturbance in the neuronal networks responsible for WM in KLS patients, resulting in higher effort at lower WM load, compared with healthy subjects. The general relationship between NAA and BOLD-signal is also discussed in the article.
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Lacey, Carolyn Jane. "The neural networks interconnecting the basal ganglia and the thalamus." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437355.
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Chan, Lai-yung, and 陳麗蓉. "Early blockade of glutamate receptors within the vestibular nucleus deters the maturation of thalamic neurons in the system for detectionof linear acceleration." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44658825.
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Sottile, Sarah Yvonne. "Neuronal Nicotinic Receptor Dynamics in Medial Geniculate Body Neurons of Young and Aged Fischer Brown Norway Rats." OpenSIUC, 2017. https://opensiuc.lib.siu.edu/dissertations/1433.
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The medial geniculate body (MGB) is the thalamic nucleus situated between the inferior colliculus (IC) and auditory cortex (AC) in the ascending auditory pathway. It has classically been thought of as a relay station for auditory stimuli; however, we now know that is capable of significantly influencing incoming auditory information. As aging occurs, there is a loss of auditory signal fidelity as well as a disruption in the accurate coding of acoustic information. In order to compensate for the age-related loss of auditory signal quality, additional cortical resources play a role in knowledge-based optimization of input. This top-down processing is mediated in part by cholinergic systems, which direct attention to relevant incoming sensory information. The primary cholinergic input to the MGB is a large cholinergic projection from the pontomesencephalic tegmentum. The PMT is a brainstem structure composed of the pedunculopontine nucleus and laterodorsal tegmental nuclei. These structures provide acetylcholine (ACh) to the auditory thalamus and midbrain thereby playing a role in sustaining attention, sensory gating, and arousal. Acetylcholine may then act at pre- and postsynaptic receptors at the level of MGB and function to assign salience to auditory stimuli. The central goal of these studies is to examine the location of nAChRs in the local MGB circuitry, their subunit composition, physiology, and how these properties are impacted with age. We have found that ACh produces significant excitatory postsynaptic actions on young MGB neurons, likely mediated by β2-containing heteromeric nAChRs. Use of the β2-selective nAChR antagonist, dihydro-β-erythroidine, suggests that loss of cholinergic efficacy may also be due to an age-related subunit switch from high affinity β2-containing nAChRs to low affinity β4-containing nAChRs, in addition to a loss of total nAChR number. This age-related nAChR dysfunction may partially underpin the attentional deficits which contribute to the loss of speech understanding in the elderly. Activation of presynaptic nAChRs potentiated responses evoked by stimulation of excitatory corticothalamic terminals and inhibitory tectothalamic terminals. Conversely, application of ACh appeared to have no consistent effects on paired-pulse responses evoked from stimulation of excitatory tectothalamic terminals and inhibitory projections from the thalamic reticular nucleus. Responses to nAChR activation at excitatory corticothalamic and inhibitory tectothalamic inputs were attenuated by aging. The present findings suggest that the increased output from the cholinergic pedunculopontine neurons onto MGB neurons following presentation of difficult to identify stimuli or arousal increases the strength of tectothalamic inhibitory projections likely improving signal-to-noise ratio and enhancing signal detection, while increasing gain on corticothalamic excitatory signals facilitating top-down identification of the unknown stimulus. Thus, cholinergic inputs to MGB are positioned to maximize sensory processing by dynamically adjusting both top-down and bottom-up mechanisms in conditions of attention/arousal.
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Chaisuksunt, Vipavadee. "Differential expression of regeneration relevant molecules in neurons of adult rat brain after injury and the implantation of peripheral nerve grafts." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322006.
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Unzai, Tomo. "Quantitative Analyses of the Projection of Individual Neurons from the Midline Thalamic Nuclei to the Striosome and Matrix Compartments of the Rat Striatum." Kyoto University, 2018. http://hdl.handle.net/2433/230977.
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Delaunay, Delphine. "Etude de la neurogénèse et de la gliogénèse dans le diencephale de souris." Paris 6, 2006. http://www.theses.fr/2006PA066462.
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Depuis de nombreuses années, il existe un débat sur le mode de formation des neurones et des cellules gliales, précocement, à partir de la zone ventriculaire. Ces deux types cellulaires sont-ils issus d’une même cellule ventriculaire où bien existe-t-il deux progeniteurs chacun dédié à la mise en place d’un seul lignage ? Pour répondre à cette question, nous avons cherché un marqueur exprimé dans un domaine restreint de la zone ventriculaire au cours des périodes de neurogénèse et de gliogénèse et notre choix s’est porté sur le transcrit plp. L’étude des cellules plp+ ventriculaires à deux stades de développement, E9,5 et E13,5 nous a permis de démontrer par des cultures clonales in vitro et grâce a un marquage génétique permanent, in vivo, l’existence de deux progeniteurs plp+ indépendants : un progeniteur neuronal précoce et un progeniteur glial plus tardif. Ces résultats sont donc en faveur de l’existence de deux progeniteurs distincts, chacun dédié a un lignage neural, dans la zone ventriculaire. Par la suite, l’analyse du lignage plp par utilisation d’une souris transgénique plp-Cre a confirmé que ces cellules étaient capables de donner naissance à des cellules gliales et à des neurones et nous a permis d’établir un cartographie diencéphalique des dérivés neuronaux. Ceux-ci se repartissent dans différents noyaux prethalamiques et hypothalamiques, à l’intérieur desquels ils représentent une sous-population. Nous avons également cherché à mettre en évidence des facteurs impliqués dans la transition neurone/glie. Pour cela, nous avons comparé, par la technique des puces à ADN, le transcriptome des progeniteurs neuronaux plp+ avec celui des progeniteurs gliaux. Cette technique nous a permis de sélectionner trois gènes candidats potentiellement impliqués dans la gliogenèse.
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Richardson, Ben David. "Unique Response Properties and GABAA Receptor Function in Medial Geniculate Body Neurons of Young and Aged Fischer Brown Norway Rats." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/575.
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The auditory thalamus or medial geniculate body (MGB) is the final brain structure for acoustic information processing prior to, and functioning in reciprocity with, auditory cortex. MGB neurons process and gate aspects of acoustic stimuli, functions which depend partly on GABAergic inhibition. To characterize these properties, the inhibitory neurotransmitters involved and how they may be altered in the aged MGB, specific aims sought to: 1) determine the presence of functional high affinity GABAA receptors (GABAARs) in the MGB, 2) determine whether GABAAR function is altered with age and 3) determine to what degree MGB neurons of awake young and aged rats display stimulus-specific adaptation (SSA). Inhibitory neurotransmission is essential for accurate coding of acoustic information in the central auditory system, but appears disrupted in the aged. The present study required the development of a slice preparation that permitted whole cell recordings from juvenile, young adult and aged rat MGB neurons. The presence of high affinity GABAARs and the impact of aging on synaptic and high affinity GABAAR function were examined. Low concentrations of gaboxadol (GABAAR agonist) activated a gabazine-sensitive (GABAAR antagonist) tonic current, providing support for the expression of functional high affinity GABAARs in the MGB. Activation of high affinity GABAARs expressed by MGB neurons decreased input resistance, hyperpolarized resting membrane potential, reduced evoked firing rates and induced a transition from tonic to burst firing mode. In aged MGB neurons there was a significant 50.4% reduction in GABAAR-mediated tonic Cl- current. Synaptic GABAAR inhibition appeared differentially affected by age in lemniscal and non-lemniscal auditory thalamus although gramicidin perforated patch-clamp recordings indicated neuronal Cl- homeostasis was unaltered with age. Anesthetized rodent MGB single units show SSA, during which the firing rate in response to repetitive stimuli decreases/adapts over time but low probability stimuli (i.e. novel) continue to elicit robust responses. To examine the presence of SSA in the MGB of awake rats, a multichannel single unit recording preparation was implemented. This approach involved implanting young and aged rats with an array of four individually-advanceable tetrodes in order to evaluate SSA by recording responses to a frequency oddball paradigm and a random/non-random frequency range paradigm. Single units in the MGB of awake FBN rats were found to display SSA, which was stronger in the non-lemniscal than lemniscal regions of the MGB. SSA was most dramatic at lower intensities where 27 of 57 (47%) young adult single units and 28 of 54 (52%) aged single units displayed SSA. However, there were no significant age-related differences in average magnitude or time course of SSA of MGB single units studied. Data from aims 1 and 2 provide the initial description of functional high affinity GABAARs in the rodent MGB and the plasticity of these receptors with age. These data suggest that GABAAR subtype-selective agonists or modulators could be used to augment MGB inhibitory neurotransmission, possibly improving speech understanding for a subset of elderly individuals. Findings from aim 3 were the first to show that SSA by MGB neurons is not dependent on arousal level nor on the anesthetized state, but is a common response in the MGB of awake rats. SSA did not appear to be overtly altered in the aged auditory thalamus of awake rats.
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Mendes, Alexandre. "Homo- et hétérosynaptique spike-timing-dependent plasticity aux synapses cortico- et thalamo-striatales." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066432/document.
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D’après le postulat de Hebb, les circuits neuronaux ajustent et modifient durablement leurs poids synaptiques en fonction des patrons de décharges de part et d’autre de la synapse. La « spike-timing-dependent plasticity » (STDP) est une règle d’apprentissage synaptique hebbienne dépendante de la séquence temporelle précise (de l’ordre de la milliseconde) des activités appariées des neurones pré- et post-synaptiques. Le striatum, le principal noyau d’entrée des ganglions de la base, reçoit des afférences excitatrices provenant du cortex cérébral et du thalamus dont les activités peuvent être concomitantes ou décalées dans le temps. Ainsi, l’encodage temporal des informations corticales et thalamiques via la STDP pourrait être crucial pour l’implication du striatum dans l’apprentissage procédural. Nous avons exploré les plasticités synaptiques cortico- et thalamo-striatales puis leurs interactions à travers le paradigme de la STDP. Les principaux résultats sont :1. Les « spike-timing-dependent plasticity » opposées cortico-striatales et thalamo-striatales induisent des plasticités hétérosynaptiques. Si la très grande majorité des études sont consacrées à la plasticité synaptique cortico-striatale, peu ont exploré les règles de plasticité synaptique aux synapses thalamo-striatale et leurs interactions avec la plasticité cortico-striatale. Nous avons étudié la STDP thalamo-striatale et comment les plasticités synaptiques thalamo- et cortico-striatales interagissent…According to Hebbian postulate, neural circuits tune their synaptic weights depending on patterned firing of action potential on either side of the synapse. Spike-timing-dependent plasticity (STDP) is an experimental implementation of Hebbian plasticity that relies on the precise order and the millisecond timing of the paired activities in pre- and postsynaptic neurons. The striatum, the primary entrance to basal ganglia, integrates excitatory inputs from both cerebral cortex and thalamus whose activities can be concomitant or delayed. Thus, temporal coding of cortical and thalamic information via STDP paradigm may be crucial for the role of the striatum in procedural learning. Here, we explored cortico-striatal and thalamo-striatal synaptic plasticity and their interplay through STDP paradigm. The main results described here are:1. Opposing spike-timing dependent plasticity at cortical and thalamic inputs drive heterosynaptic plasticity in striatumIf the vast majority of the studies focused on cortico-striatal synaptic plasticity, much less is known about thalamo-striatal plasticity rules and their interplay with cortico-striatal plasticity. Here, we explored thalamo-striatal STDP and how thalamo-striatal and cortico-striatal synaptic plasticity interplay. a) While bidirectional and anti-Hebbian STDP was observed at cortico-striatal synapses, thalamo-striatal exhibited bidirectional and hebbian STDP
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Williams, Mark. "Dynamique de l’excitabilité corticale dans l’épilepsie-absence et intégration sensorielle Integrative properties and transfer function of cortical neurons initiating absence seizures in a rat genetic model Building Up Absence Seizures in the Somatosensory Cortex: From Network to Cellular Epileptogenic Processes." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS608.
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Une crise d’épilepsie résulte de la survenue soudaine d’une activité neuronale anormalement intense, rythmique et synchrone dans une région plus ou moins étendue du système nerveux central. Les conséquences cliniques sont extrêmement variées, selon les zones cérébrales affectées et la durée des crises, allant de brèves secousses musculaires très focalisées à une perte de conscience complète, éventuellement associée à des convulsions. Dans le cas de l’épilepsie-absence, une épilepsie généralisée d’origine génétique survenant fréquemment chez les enfants, les crises s’expriment essentiellement par une suspension des processus conscients dans toutes leurs dimensions, y compris une interruption des perceptions conscientes. Ces symptômes sont corrélés à des décharges de pointes-ondes (DPO) dans les électroencéphalogrammes (EEG) bilatéraux. Les mécanismes physiopathologiques des altérations de conscience au cours des crises d’épilepsie-absence restent l’objet de débats intenses, opposant des altérations fonctionnelles à grande échelle à un filtrage des informations exogènes par les oscillations épileptiques. Au cours de mes recherches, j’ai exploré l’hypothèse alternative, mais non exclusive, d’un dysfonctionnement dynamique dans les processus d’intégration sensorielle au sein des circuits thalamo-corticaux primaires. Des explorations électrophysiologiques fines n’étant pas réalisables chez les enfants épileptiques, j’ai utilisé un modèle génétique présentant une forte homologie avec la pathologie humaine : le Genetic Absence Epilepsy Rat from Strasbourg (GAERS). En combinant in vivo des enregistrements électrocorticographiques (ECoG) et intracellulaires dans le cortex somatosensoriel primaire (S1), précédemment identifié comme le site de déclenchement des crises, j’ai d’abord analysé les propriétés intégratives et d’excitabilité des neurones pyramidaux du cortex S1, durant et en dehors des crises, et je les ai comparées à celles des neurones homologues chez des rats non épileptiques. J’ai montré que ces neurones présentent lors des périodes inter-ictales une excitabilité accrue, s‘exprimant par une augmentation de la décharge des neurones en réponse à des stimulations excitatrices d’intensité croissante ainsi qu’une tendance exacerbée à se re-polariser suite à une hyperpolarisation de grande amplitude, suggérant un accroissement du courant cationique h. Au cours des crises, les mêmes neurones montraient des changements différentiels dans leur excitabilité membranaire selon la composante pointe ou onde dans l‘ECoG correspondant. La pointe était associée à une augmentation de décharge évoquée par un courant dépolarisant et à une diminution de résistance membranaire. Symétriquement, l’onde était corrélée avec une augmentation de résistance membranaire et une diminution d’excitabilité. Ces changements dynamiques des propriétés intégratives neuronales suggèrent une instabilité des réponses corticales lors du cycle pointe-onde pouvant « brouiller » les signaux sensoriels lors des crises. J’ai testé cette hypothèse en analysant les réponses des neurones corticaux, et des neurones thalamo-corticaux correspondants, à des stimulations appliquées sur les vibrisses controlatérales. Bien que les réponses synaptiques induites dans les neurones du cortex S1 par les stimulations sensorielles n’étaient pas globalement altérées lors des crises, elles étaient plus amples et plus efficaces pour déclencher des potentiels d’action pendant l’onde comparé à la composante pointe. Cet accroissement relatif de la réponse neuronale lors de l’onde ECoG résulte probablement de l’accroissement de résistance membranaire précédemment décrit, d’une augmentation de la force électromotrice des courants synaptiques glutamatergiques et de la forte probabilité de décharge des neurones thalamiques correspondants lors de cette composanteAn epileptic seizure results from the sudden occurrence of abnormally intense, rhythmic and synchronous neuronal activity, in a more or less broad region of the central nervous system. The clinical consequences are extremely varied, depending on the affected brain areas and the duration of the seizures, ranging from brief localized muscular twitches to a complete loss of consciousness, potentially associated with convulsions. Absence epilepsy is a generalised epilepsy of genetic origin, mostly affecting children of school age. During absence attacks, children experience a suspension of conscious processes in all their dimensions, including an interruption of conscious perceptions. These symptoms are correlated with bilateral spike-wave discharges (SWD) in the electroencephalograms (EEGs). The pathophysiological mechanisms underlying the alteration of consciousness during absences remain the subject of an intense debate, opposing functional dysfunctions on large scale neural networks to a filtering of sensory information by epileptic oscillations. During my PhD research, I explored the alternative, but not exclusive, hypothesis of a dynamic dysfunction in sensory integration processes within primary thalamo-cortical circuits. Given that multi-scale electrophysiological investigations cannot be conducted in epileptic children, I used a genetic model prsenting a strong homology with the human pathology: the Genetic Absence Epilepsy Rat from Strasbourg (GAERS).By combining in vivo electrocorticographic (ECoG) and intracellular recordings in the primary somatosensory cortex (S1), previously identified as the site of seizure initiation, I first analysed the integrative properties and excitability of S1 pyramidal neurons, during and in between seizures, and compared them to those measured in homologous neurons from non-epileptic rats. I showed that these neurons exhibit a higher excitability during inter-ictal periods, expressed as an increased firing response to excitatory stimuli of increasing intensity, as well as an exacerbated tendency to depolarize following a hyperpolarization of large amplitude, suggesting an augmented cationic current h. During seizures, the same neurons showed specific changes in their membrane excitability, according to the spike or wave component in the corresponding ECoG. The spike component was associated with increased current-evoked firing and a decreased membrane resistance. Conversely, the wave was correlated with an increase in membrane resistance and a decrease in excitability. These dynamic changes in neuronal integrative properties suggest an instability of cortical responses during the spike-wave epileptic cycle that could "scramble" sensory signals during seizures. I tested this hypothesis by analysing the sensory responses of cortical neurons, and corresponding thalamo-cortical neurons, to stimulations applied to contralateral whiskers. Although synaptic responses induced in S1 neurons by sensory stimuli were not globally impaired during seizures, they were larger and more likely to trigger action potentials during wave compared to the spike component. This relative increase in neuronal responsiveness during the ECoG wave probably results from the previously described increase in membrane resistance, an augmented driving force of glutamatergic synaptic currents and a higher probability of action potentials discharge in the corresponding thalamic neurons during this component. My doctoral research indicates that sensory inputs processing persists in the thalamo-cortical circuits during SWDs, but that the alternation of the spike and wave components introduces a strong instability of the neuronal responses during seizures. This new pathophysiological mechanism could contribute to the inability to generate a conscious, stable and effective, perception during generalised epileptic seizures
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Gervasi, Nicolas. "Dynamique spatio-temporelle et régulation de l'activité de laprotéine kinase activée par l'adénosine monophosphate cycliquedans des préparations de neurones en trancheetLes mécanismes cellulaires d'action du GHB dans le thalamusventrobasal." Phd thesis, Université Pierre et Marie Curie - Paris VI, 2006. http://tel.archives-ouvertes.fr/tel-00069635.
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Dans le système nerveux central, le principal effecteur de la voie de transduction de l'AMPcest la protéine kinase activée par l'AMPc (PKA). L'activation de la PKA est impliquée dans de
nombreux processus comme la modulation de l'excitabilité neuronale par phosphorylation de
canaux ioniques, de l'homéostasie cellulaire par phosphorylation de cibles cytosoliques et de la
régulation génique par phosphorylation de facteurs de transcription. La régulation de l'activité de la
PKA ainsi que son activation spatiale et temporelle sont des paramètres indispensables à la
compréhension des mécanismes cellulaires à l'origine des effets de cette voie de seconds messagers.
Faute d'approches méthodologiques adaptées, très peu d'études se sont intéressées à la dynamique
spatiale et temporelle, à la spécificité et à la régulation de l'activité de la PKA dans les neurones.
Grâce aux sondes fluorescentes codées génétiquement, il est possible maintenant d'avoir
accès à ces paramètres. A l'aide d'un vecteur viral, nous avons fait exprimer une sonde sensible à
l'activité PKA (sonde AKAR pour A-kinase activity reporter) dans des préparations de neurones en
tranches. Cette sonde utilise le principe du transfert d'énergie par résonance (FRET) et permet de
mesurer par imagerie ratiométrique l'activité kinase de la PKA. Nous avons montré que la sonde
AKAR2, exprimée dans les neurones, modifie son spectre d'émission en réponse à une stimulation
de la voie AMPc. L'utilisation d'une sonde mutante, dont le site de phosphorylation a été modifié,
démontre que les changements observés dans le spectre d'émission de la sonde AKAR2 sont bien
attribuables à une phosphorylation.
Dans une première partie, nous avons étudié la phosphorylation de protéines cibles de la
PKA dans différents compartiments subcellulaires en réponse à différentes stimulations
extracellulaires. La phosphorylation de la sonde AKAR2, nous a permis de suivre en temps réel
l'activité de la PKA dans le cytosol. Afin de mesurer l'activité de la PKA dans le noyau, nous avons
adressé la sonde AKAR2 en utilisant un signal de localisation nucléaire (NLS). Enfin, la mesure de
l'activité de la PKA à la membrane a été réalisée grâce à l'étude de la phosphorylation des canaux
responsables du courant de l'AHP lente (IsAHP). Nous avons montré que la phosphorylation des
canaux ioniques est plus rapide que la phosphorylation des cibles cytosoliques, elles-mêmes plus
rapide que la phosphorylation des protéines nucléaires. De plus, nous avons montré que l'activité de
la PKA stimulée par l'activation de récepteurs couplés aux protéines G (RCPG) est différente de
l'activation directe des adénylyl cyclases (AC). En effet, l'activation de la PKA résultant de la
stimulation des RCPG produit des amplitudes de phosphorylation plus faible de la sonde AKAR2
dans le cytosol et le noyau.
Dans une deuxième partie, nous avons étudié le rôle des phosphodiestérases de type 4
(PDE4) dans la régulation des réponses β-adrénergiques. L'inhibition des PDE4 produit une
activation de la PKA dans les neurones traduisant ainsi une activité tonique des AC. Nous montrons
également que l'inhibition des PDE4 permet de potentialiser l'activité de la PKA en réponse à de
faibles concentrations d'agonistes β adrénergiques. Cette famille de PDEs, en dégradant l'AMPc,
participe donc à la régulation et la propagation des signaux PKA dans les neurones.
Enfin, au cours de ma thèse, je me suis également intéressé au γ-hydroxybutyrate (GHB)
composé qui est utilisé pour soigner certains troubles du sommeil et provoque chez le rat
l'apparition de signes comportementaux et de tracés encéphalographiques similaires à ceux observés
chez l'humain lors de crises d'épilepsie de type absence. L'ensemble de ces effets du GHB passe
probablement par une action sur la boucle thalamocorticale mais les mécanismes cellulaires à leurs
origines sont inconnus. Nous avons montré grâce à l'utilisation d'enregistrements
électrophysiologiques, que les courants post-synaptiques inhibiteurs sont beaucoup moins sensibles
au GHB que les courants post-synaptiques excitateurs et les courants potassiques à rectification
entrante (GIRK). Cette différence de sensibilité serait à l'origine d'un déséquilibre de la balance
excitation/inhibition reçue par les neurones thalamocorticaux ce qui participerait à la genèse d'une
activité oscillante du potentiel membranaire de ces neurones.
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Massaux, Aurélie. "Contribution des bursts du thalamus auditif au codage sensoriel et influence du noyau réticulaire thalamique." Paris 6, 2005. http://www.theses.fr/2005PA066330.
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Cañete, Carmenada L. "Distribution of FABP7 in Neural Tissue of Socially Defeated Adult Anolis Carolinensis." Digital Archive @ GSU, 2012. http://digitalarchive.gsu.edu/biology_theses/35.
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Due to its significance in many cellular functions, fatty acid binding protein 7 (FABP7) has become a rising topic of interest for many scientists. Immunocytochemistry was used to map the distribution of FABP7 and test whether the amount of FABP7 immunoreactivity (FABP7-IR) differed in animals that were defeated in a fight, as compared to control animals that did not engage in any social interaction. The male green anole was used as the subject because its natural tendency to establish social classes within its species provides an ideal model to observe for variation in FABP7-IR. The results showed FABP7-IR in cells and fibers of the cortex, hypothalamus, thalamus, medial preoptic area, dorsoventricular ridge, amygdala, suprachiasmatic nucleus, nucleus accumbens, nucleus rotundus, habenular area, tectum, dorsal noradrenergic and lateral forebrain bundles, and lining the third and lateral ventricles. Qualitative observation suggested higher FABP7 levels in socially defeated males than controls in all areas.
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Zavala, Arturo Rubin. "The effects of lesions to the superior colliculus and ventromedial thalamus on [kappa]-opioid-mediated locomotor activity in the preweanling rat." CSUSB ScholarWorks, 2003. https://scholarworks.lib.csusb.edu/etd-project/2404.
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The purpose of this thesis was to determine the neuronal circuitry mediating U50,488-induced locomotion in preweanling rats. To this end, preweanling rats received bilateral electrolytic lesions of the ventromedial thalamus or superior colliculus and, two days later, the same rats received a challenge injection of U50,488. It was predicted that bilateral lesions of the ventromedial thalamus or superior colliculus would attenuate the U50,488-induced locomotor activity of 18-day-old rats.
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Müller, Eli Justin. "Modeling Epilepsy and Parkinson’s Disease and the Impact of Electrical Brain Stimulation." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/19898.
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Parkinson's disease (PD) is neurological disorder characterized by degeneration of dopaminergic neurons in motor circuits of the brain. Pathologically synchronous activity within the corticothalamic-basal ganglia (CTBG) network has been identified to play an important role in the motor symptoms of the disease; however, the mechanisms underpinning this aberrant activity remain an open matter of debate. While the efficacy of deep brain stimulation (DBS) treatments is apparent in their clinical outcomes, it is not clear what impact stimulation has on large scale brain activity and how this leads to an effective therapy in PD. Additionally, it remains to be shown what DBS parameters are most therapeutically effective as these have traditionally been estimated via trial and error. Chapter 1 presents an overview of the relevant background material, including the pathophysiology of PD, DBS treatments, and large scale brain modeling, with a particular focus on the neural field theory used in this thesis. Chapter 2 unifies existing neural field models of generalized epilepsy in the corticothalamic (CT) system, and PD in the CTBG system, and explores parallels between the two disorders. Chapter 3 further develops the neural field model of the CTBG system and introduces a novel theory of DBS of the subthalamic nucleus (STN). The results show how pathologically synchronous CTBG activity in the beta frequency band (13-30 Hz) are produced via weakly damped resonances in key loops formed between the basal ganglia and cortex. Furthermore, it is demonstrated how DBS suppresses this enhanced beta activity by reducing aberrant gains in a frequency dependent manner. Chapter 4 expands upon the work in Ch. 3 using the DBS model to compare the suppressive effects of several stimulation protocols, including target nuclei, on pathological levels of beta activity within the basal ganglia, and coherence between the basal ganglia and cortical populations.
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Zhou, Shijia. "A deep learning approach to localisation tasks in medical images." Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/28595.
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Deep Learning (DL), enabled by convolutional neural network (CNN), is widely applied to automate image interpretation tasks in different imaging modalities. Localisation is an important aspect of medical imaging interpretations for specialists such as radiologists; when a radiologist reports an X-ray to be abnormal, the exact location and nature of the abnormality of the lesion must also be described in words. For example, radiologists may describe a fracture as "a complete, displaced fracture of the distal right femur". However, since radiologists do not directly label the location of the reported lesions on the X-rays, the literal description of lesions in X-rays cannot be directly used to build an imaging dataset labelled for lesion detection. As a result, researchers can only build classification algorithms, which do not show the exact locations of the lesions or abnormalities. In addition to reporting abnormalities, measuring organs' dimensions and structures' sizes is also an important part of interpreting acquired medical images. Measurement task is also a localisation problem since imaging specialists need to place measurement markers correctly. For example, during 2-dimensional (2D) ultrasound (US) scans, sonographers frequently place markers on US images to measure the thickness and sizes of organs and lesions. However, there is a lack of research on applying the DL approach to automate measuring tasks when interpreting 2D images such as 2D-US images.
Research in natural imaging has shown that a well-trained CNN could encode the spatial information of important high-level features relevant to its classification results. Therefore, the motivation of this thesis is to leverage the ability of CNN to solve the localisation problems in X-rays and 2D-US images interpretation. Chapter 3 presents a novel training method that leverages the similarities in humans' and animals' musculoskeletal (MSK) X-rays. In this novel
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method, the CNN is first sensitised to image features relevant to MSK X-ray lesions by learning to classify between tens of thousands of normal and abnormal human MSK X-rays before finetuned with a small animal MSK X-ray dataset. This novel training method overcomes data scarcity in animal X-rays by leveraging the similarity in MSK lesions in humans and animals. Compared to not using human MSK X-rays, this novel training method resulted in a threefold increase in localisation accuracies in the small animal dataset where the bounding boxes derived from heatmaps generated via gradient-weighted class activation mapping (grad-CAM) localise the underlying lesions. Chapter 4 presents a novel method to automatically detect measurement points on 2D-US images. This novel method enables the automatical measurement of organ structures that are not routinely measured by sonographers. The proposed method has a high level of accuracy and achieved a better intraclass correlation coefficient score than the two board-certificated sonographers who developed the ground truth labels.
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Tasserie, Jordy. "Functional Neuro-Imaging Study of Deep Brain Stimulation Mechanisms for the Restoration of Consciousness Using a Non-Human Primate Mode Pypreclin: An Automatic Pipeline for Macaque Functional MRI." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASL051.
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Les traumatismes crâniens les plus sévères peuvent altérer les communications entre des régions cérébrales distantes et conduire à des désordres chroniques de la conscience. Il a été rapporté que la Stimulation Cérébrale Profonde (SCP) du Thalamus module l'éveil et améliore le comportement des patients en état de conscience minimale. Cependant, il n'existe aucune démonstration évidente des mécanismes cérébraux pour la restauration spécifique et causale de l˅accès conscient, i.e. la prise de conscience, par la stimulation électrique. Dans cette étude, nous dressons l'hypothèse que la stimulation thalamique spécifique pourrait restaurer à la fois la vigilance et la prise de conscience à travers la restauration de l'activité thalamo-corticale et de la réorganisation des dynamiques corticales subséquentes.Nous avons créé une installation expérimentale qui combine la SCP et l'Imagerie par Résonance Magnétique fonctionnelle 'IRMf' chez le Primate Non-Humain (PNH) et appliqué une anesthésie finement contrôlée pour supprimer la conscience. Nous avons enregistré l'activité cérébrale du cerveau entier et développé un module de pré-traitement des images, Pypreclin, pour résoudre le problème d'artéfact lié à l'électrode. Sous sédation profonde, la stimulation électrique du noyau Centro-Median du Thalamus (CMT) a induit une forte vigilance de façon binaire. Lorsque la SCP du CMT a été déclenchée, le signal IRMf mesuré a augmenté dans les cortex préfrontal, pariétal et cingulaire, pour retourner progressivement à la valeur de référence quelques secondes après que le stimulateur a été éteint. De plus, la SCP du CMT a conduit à une reconfiguration des dynamiques corticales des états de repos en diminuant la similarité entre fonction et structure, précédemment décrite comme signature de la conscience. Enfin, la SCP du CMT a rétabli une vaste réponse hiérarchique à la régularité auditive globale qui était interrompuesous anesthésie générale. Ainsi, la SCP du CMT a restauré les deux dimensions principales de la conscience que sont l˅éveil et le contenu conscient, ouvrant la voie vers une application thérapeutique chez les patients atteint de désordres chroniques de la conscienceSevere brain injuries may lead to the disruption of long-range inter-region brain communications resulting in chronic Disorders of Consciousness (DoC). Electrical Deep Brain Stimulation (DBS) of the Thalamus has been reported to modulate arousal and ameliorate behavior in Minimally Conscious State (MCS) patients. However, there is no clear demonstration of the cerebral mechanisms for the specific and causal restoration of conscious access, i.e. awareness, with DBS. Here we hypothesized that specific thalamic DBS might restore both arousal and awareness through the restoration of thalamo-cortical activity and the subsequent reorganization of cortical dynamics. We first designed an experimental set-up combining DBS and functional Magnetic Resonance Imaging (fMRI) in Non-Human Primate (NHP) and applied finely tuned anesthesia to suppress consciousness. We recorded whole brain activity and developed a preprocessing pipeline, Pypreclin, to tackle the electrode-induced artifact. During deep sedation, Centro-Median Thalamic (CMT) DBS robustly induced arousal in an ON-OFF fashion. When CMT DBS was switched ON, fMRI signal increased in prefrontal, parietal and cingulate cortices, and gradually returned to baseline seconds after the stimulator was turned OFF. Moreover, CMT DBS led to a reconfiguration of Resting State cortical dynamics bydecreasing the function-structure similarity, previously described as a consciousness signature. Finally, CMT DBS restored a broad hierarchical response to global auditory regularities that was disrupted under general anesthesia. Thus, CMT DBS restored the two main dimensions of consciousness, i.e. arousal and awareness, paving the way to its therapeutical translation in patients with chronic DoC
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Hashemi, Meysam. "Modélisation mathématique et simulation numérique de populations neuronales thalamo-corticales dans le contexte de l'anesthésie générale." Thesis, Université de Lorraine, 2016. http://www.theses.fr/2016LORR0014/document.
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Bien que l’anesthésie générale soit un outil indispensable dans la chirurgie médicale d’aujourd’hui, ses mécanismes sous-jacents précis sont encore inconnus. Au cours de la sédation induite par le propofol les actions anesthésiques à l’échelle microscopique du neurone isolé conduisent à des changements spécifiques à l’échelle macroscopique qui sont observables comme les signaux électroencéphalogrammes (EEG). Pour une concentration faible en propofol, ces changements caractéristiques comprennent une augmentation de l’activité dans les bandes de fréquence delta (0.5-4 Hz) et alpha (8 13 Hz) dans la région frontal, une l’activité augmentée de delta et une l’activité diminuée de alpha dans la région occipitale. Dans cette thèse, nous utilisons des modèles de populations neuronales thalamo-corticales basés sur des données expérimentales. Les effets de propofol sur les synapses et sur les récepteurs extra-synaptiques GABAergiques situés dans le cortex et le thalamus sont modélisés afin de comprendre les mécanismes sous-jacents aux changements observés dans certaines puissances de l’EEG spectrale. Il est démontré que les modèles reproduisent bien les spectrales caractéristiques observées expérimentalement. Une des conclusions principales de ce travail est que l’origine des delta rythmes est fondamentalement différente de celle des alpha rythmes. Nos résultats indiquent qu’en fonction des valeurs moyennes des potentiels de l’état du système au repos, une augmentation ou une diminution des fonctions de gain thalamo-corticale résulte respectivement en une augmentation ou une diminution de alpha puissance. En revanche, l’évolution de la delta puissance est plutôt indépendant de l’état du système au repos; l'amélioration de la puissance spectrale de delta bande résulte de l’inhibition GABAergique synaptique ou extra-synaptique pour les fonctions de gain non linéaire à la fois croissante et décroissante. De plus, nous cherchons à identifier les paramètres d’un modèle de thalamo-corticale en ajustant le spectre de puissance de modèle pour les enregistrements EEG. Pour ce faire, nous considérons la tâche de l’estimation des paramètres dans les modèles qui sont décrits par un ensemble d’équations différentielles ordinaires ou bien stochastiques avec retard. Deux études de cas portant sur des données pseudo-expérimentales bruyantes sont d’abord effectuées pour comparer les performances des différentes méthodes d’optimisation. Les résultats de cette élaboration montrent que la méthode utilisée dans cette étude est capable d’estimer avec précision les paramètres indépendants du modèle et cela nous permet d’éviter les coûts de calcul des intégrations numériques. En considérant l’ensemble, les conclusions de cette thèse apportent de nouveaux éclairages sur les mécanismes responsables des changements spécifiques qui sont observées pendant la sédation propofol-induite dans les modèles de EEGAlthough general anaesthesia is an indispensable tool in today’s medical surgery, its precise underlying mechanisms are still unknown. During the propofol-induced sedation, the anaesthetic actions on the microscopic single neuron scale lead to specific changes in macroscopic-scale observables such as electroencephalogram (EEG) signals. For low concentration of propofol these characteristic changes comprised increased activity in the delta (0.5-4 Hz) and alpha (8-13 Hz) frequency bands over the frontal head region, but increased delta and decreased alpha power activity over the occipital region. In this thesis, we employ thalamo-cortical neural population models, and based on the experimental data, the propofol effects on the synaptic and extrasynaptic GABAergic receptors located in the cortex and thalamus are modelized to understand the mechanisms underlying the observed certain changes in EEG-spectral power. It is shown that the models reproduce well the characteristic spectral features observed experimentally. A key finding of this work is that the origin of delta rhythm is fundamentally different from the alpha rhythm. Our results indicate that dependent on the mean potential values of the system resting states, an increase or decrease in the thalamo-cortical gain functions results in an increase or decrease in the alpha power, respectively. In contrast, the evolution of the delta power is rather independent of the system resting states; the enhancement of spectral power in the delta band results from the increased synaptic or extra-synaptic GABAergic inhibition for both increasing and decreasing nonlinear gain functions. Furthermore, we aim to identify the parameters of a thalamo-cortical model by fitting the model power spectrum to the EEG recordings. To this end, we address the task of parameter estimation in the models that are described by a set of stochastic ordinary or delay differential equations. Two case studies dealing with noisy pseudo-experimental data are first carried out to compare the performance of different optimization methods. The results of this elaboration show that the method used in this study is able to accurately estimate the independent model parameters while it allows us to avoid the computational costs of the numerical integrations. Taken together, the findings of this thesis provide new insights into the mechanisms responsible for the specific changes in EEG patterns that are observed during propofol-induced sedation
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Wintermann, Gloria-Beatrice, Markus Donix, Peter Joraschky, Johannes Gerber, and Katja Petrowski. "Altered Olfactory Processing of Stress Related Body Odors and Artificial Odors in Patients with Panic Disorder." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-132093.
Full textAbstract:
Background: Patients with Panic Disorder (PD) direct their attention towards potential threat, followed by panic attacks, and increased sweat production. Onés own anxiety sweat odor influences the attentional focus, and discrimination of threat or non-threat. Since olfactory projection areas overlap with neuronal areas of a panic-specific fear network, the present study investigated the neuronal processing of odors in general and of stress-related sweat odors in particular in patients with PD.
Methods: A sample of 13 patients with PD with/ without agoraphobia and 13 age- and gender-matched healthy controls underwent an fMRI investigation during olfactory stimulation with their stress-related sweat odors (TSST, ergometry) as well as artificial odors (peach, artificial sweat) as non-fearful non-body odors.
Principal Findings: The two groups did not differ with respect to their olfactory identification ability. Independent of the kind of odor, the patients with PD showed activations in fronto-cortical areas in contrast to the healthy controls who showed activations in olfaction-related areas such as the amygdalae and the hippocampus. For artificial odors, the patients with PD showed a decreased neuronal activation of the thalamus, the posterior cingulate cortex and the anterior cingulate cortex. Under the presentation of sweat odor caused by ergometric exercise, the patients with PD showed an increased activation in the superior temporal gyrus, the supramarginal gyrus, and the cingulate cortex which was positively correlated with the severity of the psychopathology. For the sweat odor from the anxiety condition, the patients with PD showed an increased activation in the gyrus frontalis inferior, which was positively correlated with the severity of the psychopathology.
Conclusions: The results suggest altered neuronal processing of olfactory stimuli in PD. Both artificial odors and stress-related body odors activate specific parts of a fear-network which is associated with an increased severity of the psychopathology.
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Magrinelli, Elia. "Le récepteur nucléaire orphelin COUP-TFI contrôle l’identité sensorielle et l'activité neuronale dans les cellules post-mitotiques du néocortex chez la souris." Thesis, Nice, 2016. http://www.theses.fr/2016NICE4037/document.
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Le néocortex est une région du cerveau qui traite toutes les entrées sensorielles et créé des réponses comportementales. Il est subdivisé en zones fonctionnelles, chacune ayant une cytoarchitecture, un motif d’expression génique et un profil de connectivité spécifiques. L'organisation en zones est pré-modelée par des gènes organisateurs, et ensuite affinée par l’activité sensorielle. Dans cette étude, j'ai étudié d'abord si ce pré-modelage est établi dans les progéniteurs et/ou les cellules post-mitotiques, et si l'activité neuronale spontanée est nécessaire pour l’établissement de la connectivité correcte entre néocortex et thalamus, station relais principale des données sensorielles. Avec l'aide d'une série de souris transgéniques, j’ai montré que la fonction du gène organisateur COUP-TFI est suffisante et nécessaire pour organiser l'identité sensorielle dans les cellules post-mitotiques, et que COUP-TFI régule l'activité intrinsèque des neurones corticaux, influençant la bonne intégration des entrées thalamiques dans le cortex somatosensoriel. J’ai montré que COUP-TFI contrôle directement l'expression du gène Egr1, qui dépend fortement de l'activité neuronale. COUP-TFI et Egr1 agissent sur l'acquisition de la morphologie des cellules étoilées dans les neurones de la couche 4, cibles principales des axones thalamiques et trait typique des zones somatosensoriels primaires. En conclusion, ce travail montre que le pré-modelage cortical dépend primordialement d’un programme génétique établi dans les cellules post-mitotiques et que l'activité intrinsèque et les propriétés génétiques agissent ensemble pour façonner l'organisation des premiers circuits dans le néocortexThe neocortex is a region of the brain that processes all sensory inputs creating appropriate behavioral responses. It is subdivided into functional areas, each with a specific cytoarchitecture, gene expression pattern and connectivity profile. The organization into areas is pre-patterned by the action of areal patterning genes, and subsequently refined by sensory evoked activity. In this study, I have first investigated whether early areal patterning is committed in progenitor and/or post-mitotic cells, and then assessed whether spontaneous neuronal activity is required in establishing correct connectivity between the neocortex and the thalamus, the principal relay station of peripheral sensory inputs. With the help of a series of transgenic mice, my work showed that the function of the areal patterning gene COUP-TFI is sufficient and necessary to organize sensory identity in post-mitotic cells, and that COUP-TFI regulates intrinsic activity properties of cortical neurons, and thus proper integration of thalamic inputs into the somatosensory cortex. In particular, I found that COUP-TFI directly controls the expression of the immediate early gene Egr1, which expression levels strongly depend on neuronal activity. Both COUP-TFI and Egr1 act on the acquisition of the stellate cell morphology of layer 4 neurons, the main targets of thalamic axons and a typical trait of primary somatosensory areas. In conclusion, this work demonstrates that cortical area patterning primordially depends on a genetic program established in post-mitotic cells and that intrinsic genetic and activity properties act together to shape the organization of early circuits in the neocortex
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Wintermann, Gloria-Beatrice, Markus Donix, Peter Joraschky, Johannes Gerber, and Katja Petrowski. "Altered Olfactory Processing of Stress Related Body Odors and Artificial Odors in Patients with Panic Disorder." Public Library of Science, 2013. https://tud.qucosa.de/id/qucosa%3A27420.
Full textAbstract:
Background: Patients with Panic Disorder (PD) direct their attention towards potential threat, followed by panic attacks, and increased sweat production. Onés own anxiety sweat odor influences the attentional focus, and discrimination of threat or non-threat. Since olfactory projection areas overlap with neuronal areas of a panic-specific fear network, the present study investigated the neuronal processing of odors in general and of stress-related sweat odors in particular in patients with PD.
Methods: A sample of 13 patients with PD with/ without agoraphobia and 13 age- and gender-matched healthy controls underwent an fMRI investigation during olfactory stimulation with their stress-related sweat odors (TSST, ergometry) as well as artificial odors (peach, artificial sweat) as non-fearful non-body odors.
Principal Findings: The two groups did not differ with respect to their olfactory identification ability. Independent of the kind of odor, the patients with PD showed activations in fronto-cortical areas in contrast to the healthy controls who showed activations in olfaction-related areas such as the amygdalae and the hippocampus. For artificial odors, the patients with PD showed a decreased neuronal activation of the thalamus, the posterior cingulate cortex and the anterior cingulate cortex. Under the presentation of sweat odor caused by ergometric exercise, the patients with PD showed an increased activation in the superior temporal gyrus, the supramarginal gyrus, and the cingulate cortex which was positively correlated with the severity of the psychopathology. For the sweat odor from the anxiety condition, the patients with PD showed an increased activation in the gyrus frontalis inferior, which was positively correlated with the severity of the psychopathology.
Conclusions: The results suggest altered neuronal processing of olfactory stimuli in PD. Both artificial odors and stress-related body odors activate specific parts of a fear-network which is associated with an increased severity of the psychopathology.
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Fonoff, Erich Talamoni. "Efeitos da estimulação elétrica do córtex motor na modulação da dor: análise comportamental e eletrofisiológica em ratos." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-28012008-092511/.
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Introdução. Nos últimos a função motora vem sendo associada com a atenuação sensitiva e de dor, logo antes, durante e apos a contração muscular. No entanto as vias anatômicas e funcionais deste fenômeno não são conhecidas. O objetivo deste estudo é o de criar um modelo animal e investigar o efeito da estimulação subliminar do córtex motor (ECM) no limiar nociceptivo e na atividade neuronal subcortical. Método. O limiar nociceptivo foi avaliado por teste plantar e reflexo de retirada da cauda antes e após o implante dos eletródios epidurais sobre o córtex motor da pata posterior orientado por mapa funcional na mesma cepa de ratos. Os mesmos testes foram repetidos antes, durante e após a ECM. Antagonismo sistêmico do por naloxona foi incluído neste protocolo para investigar a relação com mediação opióide. O registro neuronal multiunitário do núcleo centro mediano (CM) e ventral posterolateral (VPL) do tálamo e da substância periaqüeductal (SPM) foi realizado antes, durante e após ECM ipso e contralateral. Resultados. O implante per se não causou alterações no limiar nociceptivo. ECM induziu significativa antinocicepção seletiva na pata contralateral mas não na ipsolateral. Este efeito não mais foi observado 15 minutos após o término da estimulação. Nenhuma alteração motora e comportamental foi observada nos testes de campo aberto. A mesma estimulação no córtex sensitivo e parietal posterior não causou quaisquer alterações de limiar nociceptivo. Administração sistêmica de naloxone reverteu completamente o efeito antes observado com a ECM. O registro neuronal multiunitário evidenciou diminuição na atividade do CM durante e após a ECM contra e ipsolateral. O ritmo de disparos neuronais no VPL também mostrou diminuição apenas com a ECM ipsolateral. No entanto os neurônios da SPM aumentaram significativamente a freqüência de disparos com ECM ipsolateral e não com a contralateral. Conclusão. A ECM subliminar está relacionada consistentemente com a atenuação sensitiva durante o comportamento, provavelmente mediado por inibição talâmica e ativação da SPM.Background. The motor function has been associated to sensory and pain attenuation, before during and shortly after the muscle activity. How ever the anatomical and functional basis of this phenomenon is not yet defined. The present study was designed to set an animal model and investigate the effect of subthreshold electrical stimulation of motor cortex (MCS) on pain threshold and neuron activity of thalamus and periaqüedutal gray. Method. Nociceptive thresholds of hind paws and the tail flick reflex were evaluated before and after surgical placement of epidural electrodes; before during and after electrical stimulation of motor cortex. Opioid antagonism was also included in this protocol in order to define neurotransmitter mediation of this process. Multiunit recording of thalamic median center (CM) and ventral posterolateral nuclei (VPL) and lateral periaqüedutal gray (SPM) were performed before and after electrical stimulation of ipso and contralateral motor cortex. Results. The procedure itself did not induce any threshold changes. MCS induced selective antinociception of contralateral paw, but no changes were detected in the nociceptive threshold of the ipsolateral side. This effect disappeared completely 15 minutes after the stimulation was ceased. No behavioral or motor impairment were observed during and after the stimulation session in the open field test. The same stimulation on sensory and posterior parietal cortex did not elicit any changes in behavioral and nociceptive tests. Systemic administration of naloxone completely reversed the previous observed antinociceptive effect. Multiunit recording evidenced decrease in spontaneous neuron firing in CM with short recovery time during ipso and contralateral MCS. Neuron activity in VPL was also significantly decreased during ipsolateral MCS but not with contralateral stimulation. How ever, neuron firing in SPM was significantly increased during and long after ipsolateral MCS but not with contralateral stimulation. Conclusion. Subthreshold MCS is consistently related to sensory attenuation during behavior, probably through thalamic inhibition and SPM activation.
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Cappe, C. "Intégration multisensorielle et motrice chez le primate non humain : approches anatomique, comportementale et électrophysiologique." Phd thesis, Université Paul Sabatier - Toulouse III, 2007. http://tel.archives-ouvertes.fr/tel-00170144.
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Afin d'interagir avec le monde multimodal qui nous entoure, nous devons intégrer simultanément différentes sources d'informations sensorielles (vision, audition, somesthésie...). Une question fondamentale est donc de savoir comment le cerveau intègre les éléments séparés d'un objet défini par plusieurs composantes sensorielles pour former un percept unifié. Le colliculus supérieur a été le principal modèle d'étude de l'intégration polymodale. Au niveau cortical, jusqu'à récemment, les phénomènes d'intégration polymodale paraissaient être une caractéristique que seules possédaient les aires associatives situées au sommet de la hiérarchie du traitement de l'information. Tout d'abord, notre première étude a porté sur les connexions cortico-corticales et a montré l'existence de projections directes entre aires corticales de sensorialités différentes chez le primate non humain. Ensuite, l'étude des projections entre différentes aires corticales sensorielles et motrices et le thalamus nous a permis de mettre en évidence l'existence de noyaux thalamiques qui, par leurs connexions, pourraient représenter une voie alternative pour le transfert des informations de différentes aires corticales sensorielles et/ou motrices. Le thalamus pourrait permettre un transfert plus rapide et même une intégration des informations. Par ailleurs, au niveau comportemental, l'intégration multisensorielle permet une amélioration de la perception. Une expérience que nous avons menée chez des singes macaques dans une tâche de détection de stimuli unimodaux et bimodaux a montré la présence d'un gain multisensoriel significatif qui est le plus marqué près du seuil, qui diminue pour des intensités croissantes au-dessus du seuil et qui, enfin, disparaît à fortes intensités. Enfin, chez ces animaux montrant sur le plan comportemental ce gain multisensoriel, nous avons exploré les mécanismes sous jacents de l'intégration multisensorielle au niveau des neurones du cortex auditif. Nous avons trouvé des neurones dont les propriétés de décharges reflètent une synergie multisensorielle entre audition et vision. Ainsi, par des approches anatomiques, comportementales et électrophysiologiques, nos résultats apportent des éléments fondamentaux sur les structures cérébrales impliquées dans l'intégration multisensorielle, leurs connexions et les mécanismes existant dans le cerveau pour traiter de façon efficace les différentes informations sensorielles, en vue de la genèse d'une réponse motrice.
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Lajeunesse, Francis. "Modélisation de l'intégration des entrées synaptiques excitatrices chez les cellules thalamocorticales." Thesis, Université Laval, 2011. http://www.theses.ulaval.ca/2011/28114/28114.pdf.
Full textAbstract:
Les cellules thalamocorticales (TC) du noyau ventro-postéro-latéral (VPL) du thalamus relayent l'information du système somatosensoriel (synapses excitatrices lemniscales aux dendrites proximaux) à la région correspondante du cortex, mais reçoivent également en rétro-propagation des projections du cortex (synapses excitatrices corticothalamiques aux dendrites distaux). Afin d'étudier l'intégration synaptique aux différentes parties de la cellule TC, nous avons bâti un modèle multi-compartimental à partir de reconstructions tridimensionnelles de cellules du noyau VPL, ce qui consiste en une discrétisation spatiale des dendrites en une multitude de segments associés à des circuits RC interconnectés. Nous avons pu dégager quantitativement l'impact de la géométrie cellulaire (taille d'arborisation et diamètre dendritique) sur l'amplitude et sur la durée des réponses au soma. Nous avons par la suite comparé l'intégration synaptique pour différentes distributions des entrées aux dendrites proximaux et distaux et sous différentes conditions de courants intrinsèques et de potentiel membranaire. Dans tous les cas, la sommation des entrées proximales induisait une réponse indépendante de la distribution, alors que la réponse aux entrées distales saturait lorsqu'elles étaient localisées aux mêmes branches. Nos résultats ont permis d'apporter une explication physiologique au patron d'organisation synaptique chez les cellules TC.Thalamocortical (TC) cells from the ventroposterolateral (VPL) nucleus of the thalamus relay the somatosensory inputs (excitatory lemniscal synapses at proximal dendrites) to the corresponding cortical area, but also receive feedback excitatory inputs from the cortex (corticothalamic synapses at distal dendrites). The goal of this study was to compare the synaptic integration of inputs coming to proximal vs. distal dendrites. A multicompartmental model was drawn from fully reconstructed cells of the VPL nucleus. Dendrites were spatially discretized in multiple segments associated to interconnected RC circuits. We were able to characterize the impact of neuronal size and dendritic diameter on the amplitude and on the time course of the somatic response. We also compared the synaptic integration for different distributions of proximal or distal inputs under different conditions of membrane potential and active properties. In all cases, the summation of proximal inputs was independent of their distribution, while the response induced by distal inputs saturated when those inputs were located at the same branches. The results obtained in this study suggest a physiological explanation of the synaptic pattern at TC cells.
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Reinker, Stefan. "Stochastic resonance in thalamic neurons and resonant neuron models." Thesis, 2004. http://hdl.handle.net/2429/16011.
Full textAbstract:
Neurons of the thalamus are major participants in gating sensory information for relay to the neocortex. Thalamic neurons are crucially involved in rhythmogenesis which determines the sleep/wake cycle. These roles require critical involvement of a T-type calcium current, conferring a frequency preference in response to subthreshold signals. We examine the interactions of this membrane resonance and noise using whole-cell patch clamp recordings in thalamocortical and reticular neurons of rat brain slices. We perform Monte-Carlo simulations and mathematical analysis using Hodgkin-Huxley-type and polynomial models of resonant neurons. We demonstrate stochastic resonance (SR) as maximal coherence between the input and stochastic output at intermediate noise levels. SR is measured by determining the signal-to-noise ratio under sine wave inputs, and from the reliability of detection measure under a-function inputs. In the experiments and neuron models with T-current, we demonstrate subthreshold resonance at 2-3 Hz, as well as noise dependent frequency dependence of SR for sine wave inputs. The simpler Hindmarsh-Rose model has a similar SR. This model also shows improved detection when the delay of consecutive EPSPs matches the preferred frequency. We show that the preferred frequency of the subthreshold and stochastic resonances depends on the time scale of the slow variable. The stochastic frequency preference arises from modulation of the firing probability of the fast subsystem. We develop a simple linear integrate-and-fire model with subthreshold resonance, which retains the main features of the more complicated models. An analytical solution of the stochastic equations shows that the eigenvalues determine frequency preferences in subthreshold resonance and stochastic resonance. SR can occur even with only noise. This autonomous SR depends on the resonance in our experiments and models. We demonstrate that preferred stochastic firing in the single neuron model translates into synchronized behaviour in a noisy network of resonant neuron models. With inhibitory synaptic coupling, noise can extend the parameter range of oscillations. With excitatory synaptic coupling, noise produces synchronized oscillations of the quiescent deterministic network. We speculate that combined subthreshold membrane resonance and stochastic resonance have physiological utility in coupling synaptic activity to preferred firing frequency, and in network synchronization under noise.Science, Faculty of
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