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Дисертації з теми "Inhibitory Neurons"

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Автор: Grafiati
Опубліковано: 6 вересня 2023

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1

Husson, Zoé. "Glycinergic neurons and inhibitory transmission in the cerebellar nuclei." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066279/document.

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Le cervelet, composé d'un cortex et de noyaux, est responsable du contrôle moteur fin des mouvements et de la posture. En combinant une approche génétique (basée sur l'utilisation de lignées de souris transgéniques) avec des traçages anatomiques, des marquages immunohistochimiques et des expériences d'électrophysiologie et d'optogénétique, nous établissons les caractères distinctifs des neurones inhibiteurs des noyaux cérébelleux et en détaillons la connectivité ainsi que les fonctions dans le circuit cérébelleux. Les neurones inhibiteurs glycinergiques des noyaux profonds constituent une population de neurones distincts des autres types cellulaires identifiables par leur phénotype inhibiteur mixte GABAergique/glycinergique. Ces neurones se distinguent également par leur plexus axonal qui comporte une arborisation locale dans les noyaux cérébelleux où ils contactent les neurones principaux et une projection vers le cortex cérébelleux où ils contactent les cellules de Golgi. Ces neurones inhibiteurs reçoivent également des afférences inhibitrices des cellules de Purkinje et pourraient être contactés par les fibres moussues ou les fibres grimpantes.Nous apportons ainsi la première étude d'une transmission mixte fonctionnelle par les neurones inhibiteurs des noyaux cérébelleux, projetant à la fois dans les noyaux et le cortex cérébelleux. L'ensemble de nos données établissent les neurones inhibiteurs mixtes des noyaux cérébelleux comme la troisième composante cellulaire des noyaux profonds. Leur importance dans l'organisation modulaire du cervelet, ainsi que leur impact sur l'intégration sensori-motrice, devront être confirmés par des études optogénétiques in vivo
The cerebellum is composed of a three-layered cortex and of nuclei and is responsible for the learned fine control of posture and movements. I combined a genetic approach (based on the use of transgenic mouse lines) with anatomical tracings, immunohistochemical stainings, electrophysiological recordings and optogenetic stimulations to establish the distinctive characteristics of the inhibitory neurons of the cerebellar nuclei and to detail their connectivity and their role in the cerebellar circuitry.We showed that the glycinergic inhibitory neurons of the cerebellar nuclei constitute a distinct neuronal population and are characterized by their mixed inhibitory GABAergic/glycinergic phenotype. Those inhibitory neurons are also distinguished by their axonal plexus which includes a local arborization with the cerebellar nuclei where they contact principal output neurons and a projection to the granular layer of the cerebellar cortex where they end onto Golgi cells dendrites. Finally, the inhibitory neurons of the cerebellar nuclei receive inhibitory afferents from Purkinje cells and may be contacted by mossy fibers or climbing fibers.We provided the first evidence of functional mixed transmission in the cerebellar nuclei and the first demonstration of a mixed inhibitory nucleo-cortical projection. Overall, our data establish the inhibitory neurons as the third cellular component of the cerebellar nuclei. Their importance in the modular organization of the cerebellum and their impact on sensory-motor integration need to be confirmed by optogenetic experiments in vivo
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2

Li, Yan. "Inhibitory synpatic transmission in striatal neurons after transient cerebral ischemia." Connect to resource online, 2009. http://hdl.handle.net/1805/2021.

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Thesis (Ph.D.)--Indiana University, 2009.
Title from screen (viewed on December 1, 2009). Department of Anatomy and Cell Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Zao C. Xu, Feng C. Zhou, Charles R. Yang, Theodore R. Cummins. Includes vitae. Includes bibliographical references (leaves 115-135).
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3

Bampasakis, Dimitris. "Inhibitory synaptic plasticity and gain modulation in cerebellar nucleus neurons." Thesis, University of Hertfordshire, 2016. http://hdl.handle.net/2299/17179.

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Neurons can encode information using the rate of their action potentials, making the relation between input rate and output rate a prominent feature of neuronal information processing. This relation, known as I{O function, can rapidly change in response to various factors or neuronal processes. Most noticeably, a neuron can undergo a multiplicative operation, resulting in a change of the slope of its I{O curve, also know as gain change. Gain changes represent multiplicative operations, and they are wide- spread. They have been found to play an important role in the encoding of spatial location and coordinate transformation, to signal amplification, and other neuronal functions. One of the factors found to introduce and control neuronal gain is synaptic Short Term Depression (STD). We use both integrate-and- re and conductance based neuron models to identify the effect of STD in excitatory and inhibitory modulatory input. More specifically, we are interested in the effect of STD at the inhibitory synapse from Purkinje cells to cerebellar nucleus neurons. Using a previously published, biologically realistic model, we find that the presence of STD results in a gain change. Most importantly we identify STD at the inhibitory synapse to enable excitation-mediated gain control. To isolate the mechanism that allows excitation to control gain, even though STD is applied at a different synapse, we first show that the overall effect is mediated by average conductance. Having done this, we find that the effect of STD is based on the non-linearity introduced in the relation between input rate and average conductance. We find this effect to vary, depending on the position of the I{O function on the input rate axis. Modulatory input shifts the I{O curve along the input rate axis, consequently shifting it to a position where STD has a different effect. The gain differences in the STD effects between the two positions enable excitation to perform gain control.
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4

Wang, Hui. "Structural and functional studies of the neuronal growth inhibitory factor, human metallothionein-3." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/HKUTO/record/B39559014.

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5

Wang, Hui, and 王暉. "Structural and functional studies of the neuronal growth inhibitory factor, human metallothionein-3." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B39559014.

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6

Mardinly, Alan Robert. "Regulation of Synapse Development by Activity Dependent Transcription in Inhibitory Neurons." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:10739.

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Neuronal activity and subsequent calcium influx activates a signaling cascade that causes transcription factors in the nucleus to rapidly induce an early-response program of gene expression. This early-response program is composed of transcriptional regulators that in turn induce transcription of late-response genes, which are enriched for regulators of synaptic development and plasticity that act locally at the synapse.
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7

Chik, Tai-wai David. "Global coherent activities in inhibitory neural systems Chik Tai Wai David." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31040408.

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8

Lofredi, Roxanne [Verfasser]. "Characterization of inhibitory and projection specific neurons of the presubiculum / Roxanne Lofredi." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1126505005/34.

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9

Pangalos, Maria. "Analysis of hippocampal inhibitory and excitatory neurons during sharp wave-associated ripple." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2016. http://dx.doi.org/10.18452/17590.

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Im Hippokampus gibt es verschiedene Netzwerkoszillationen mit unterschiedlichen Frequenzen. Ein Typ dieser Oszillationen sind die ”Ripple” mit einer Frequenz von etwa 200 Hz, welche in Komplexen mit einer Aktivitätswelle, der ”Sharp wave” auftreten. Sharp wave-ripple Komplexe (SWR) werden mit der Konsolidierung von Gedächtnis in Zusammenhang gebracht. Das Netzwerk, das den SWR unterliegt, hat bestimmte Mechanismen, von denen einige in der vorliegenden Arbeit näher untersucht werden. Im ersten Teil wird untersucht, wie ein hemmendes Interneuron in der hippokampalen Region CA1, das ”oriens-lacunosum moleculare” (O-LM) Interneuron, während der SWR in das Netzwerk eingebunden ist. Wir konnten zeigen, dass O-LM Zellen während der SWR starke synaptische Exzitation erhalten. Die Exzitation tritt spät während des Ripples im lokalen Feldpotential (LFP) auf und zeigt eine Phasenankopplung an die Ripple. In etwa der Hälfte der O-LM Zellen konnten wir Aktionspotentiale während der SWR zeigen, die an die Ripple-Phase im LFP gebunden sind und nach dem Ripple-Maximum auftreten. Der zweite Teil der Arbeit bezieht sich auf die hippokampale Region CA1 und vergleicht während SWR den synaptischen Eingang in zwei Untertypen von Pyramidenzellen, die tiefen und die oberflächlichen Pyramidenzellen. Beide Untertypen bekommen synaptische Eingänge während der SWR. Diese Eingänge sind eine Mischung aus exzitatorischen und inhibitorischen Eingängen, die in den Untertypen in ihrer Stärke vergleichbar sind. Im dritten Teil untersuchen wir die SWR in der Region CA2 des Hippokampus und zeigen, dass Pyramidenzellen in CA2 in das Netzwerk während SWR eingebunden sind. Wir können sowohl exzitatorische als auch inhibitorische synaptische Eingänge in den Pyramidenzellen darstellen und konnten eine Phasenkopplung der synaptischen Eingänge an die SWR im LFP zeigen. Aufgrund der Phasenverschiebung bei verschiedenen Haltepotentialen vermuten wir einen Oszillator für die Exzitation und einen für die Hemmung.
In the hippocampus there are different patterns of activity also known as network oscillations. These oscillations express different frequencies, and one oscillation is the ripple oscillation at around 200 Hz. It is associated with an activity wave called sharp wave and form a so-called sharp wave-ripple complex (SWR). SWRs are implicated in memory consolidation. In this thesis we investigate mechanisms underlying sharp wave-ripple complexes. In the first part of this thesis I examine one type of inhibitory neurons in the region CA1 of the hippocampus during SWR. Oriens-lacunosum moleculare (O-LM) interneurons receive strong excitatory synaptic input during ripples. This input arrives after the ripple maximum and is phase locked with the ripple cycles. Around half of the probed O-LM cells fire during the SWR and thereby show an active participation during SWR. The magnitude of excitation in O-LM cells and the ratio between excitation and inhibition determine if an O-LM cell is active during the SWR. Action potentials in these cells occur late during the SWR and are phase locked. In the second part the synaptic input onto excitatory pyramidal cells were investigated during ripple oscillations. Previous work has identified two different types of pyramidal cells in area CA1. We recorded from deep and superficial pyramidal cells. For both types of pyramidal cells the inhibitory and excitatory synaptic inputs temporally associated with ripples express comparable strength. In the last and third part, I recorded SWR in the CA2 region of the hippocampus and showed incidence, frequency and amplitude of ripples and SWR. Pyramidal cells in the CA2 region are integrated into the network during SWR. They receive SWR associated synaptic input during SWR. The excitatory and inhibitory synaptic inputs in CA2 pyramidal cells were investigated in detail. Phase analysis show phase locking of local field potential ripples and synaptic inputs to the ascending phase of the ripple cycle.
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10

Chik, Tai-wai David, and 戚大衛. "Global coherent activities in inhibitory neural systems: Chik Tai Wai David." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31040408.

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11

Dobie, Frederick Andrew. "Molecular and cellular mechanisms of inhibitory synapse formation in developing rat hippocampal neurons." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/41933.

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The proper functioning of the brain and central nervous system (CNS) requires the precise formation of synapses between neurons. The two main neurotransmitter systems for fast synaptic communication in the CNS are excitatory glutamate and inhibitory gamma-aminobutyric acid. A growing body of evidence has begun to uncover several shared and divergent rules for the establishment of each of these two types of synapses. At the molecular level, a number of key proteins have been shown to be involved in the initial formation and subsequent development of synaptic connection, including cell adhesion molecules (CAMs). Among the CAMs, neurexins and neuroligins are important synaptogenic proteins that act trans-synaptically to organize synapses: binding of axonal beta-neurexins by neuroligins is sufficient to cause development of a presynaptic specialization at that site, while binding of dendritic neuroligin-1 or neuroligin-2 by beta-neurexins is sufficient to cause development of postsynaptic excitatory or inhibitory specializations, respectively. In Chapter 2, we explore the role of alpha-neurexins in synapse organization. We find alpha-neurexins are able to specifically induce the formation of inhibitory synapses, presumably through clustering of postsynaptic neuroligin-2. Moreover, we find that the expression of various splice variants of alpha- and beta-neurexins is regulated both during development and by activity, suggesting a physiological role for alternative splicing in the modulation of synapse assembly. At the cellular level, it is now clear from live imaging studies that synapses and their formation are highly dynamic processes. A number of studies have established the temporal recruitment of pre- and postsynaptic components to nascent synapses and how synapse formation can influence neuron growth. However, these studies have focused on excitatory synapses. In Chapter 3, we explore the cellular mechanisms of inhibitory synapse formation and modulation. We find that entire synapses are highly mobile and can undergo dynamic structural modulation. New synapses are formed by gradual accumulation of components from diffuse cytoplasmic pools, with a significant contribution of presynaptic vesicles from previously recycling sites. These results provide new insights into the mechanisms of inhibitory synapse formation and how it is both similar and different from excitatory synapse formation.
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12

Scheimann, Jessie R. "Sex Differences in the Role of Glucocorticoid Receptors in Excitatory vs Inhibitory Neurons." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1554213356486937.

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13

Blurton-Jones, Mathew Mark. "Estrogen modulates neurotrophin systems in the brain via putative actions on inhibitory neurons /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2002. http://wwwlib.umi.com/cr/ucsd/fullcit?p3064473.

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14

Backström, Eva. "Expression of stimulatory and inhibitory molecules in interactions between natural killer cells and neurons /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-516-6.

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15

Doolin, Richard Edward. "An odorant-suppressible chloride conductance mediates inhibitory receptor potentials in lobster olfactory receptor neurons." [Gainesville, Fla.] : University of Florida, 2002. http://purl.fcla.edu/fcla/etd/UFE1001136.

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16

Austin, Mason. "Is the lateral septum's inhibitory influence on the amygdala mediated by GABA-ergic neurons?" Diss., Connect to the thesis, 2004. http://hdl.handle.net/10066/741.

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17

Jalil, Sajiya Jesmin. "Stability Analysis of Phase-Locked Bursting in Inhibitory Neuron Networks." Digital Archive @ GSU, 2012. http://digitalarchive.gsu.edu/math_diss/7.

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Networks of neurons, which form central pattern generators (CPGs), are important for controlling animal behaviors. Of special interest are configurations or CPG motifs composed of reciprocally inhibited neurons, such as half-center oscillators (HCOs). Bursting rhythms of HCOs are shown to include stable synchrony or in-phase bursting. This in-phase bursting can co-exist with anti-phase bursting, commonly expected as the single stable state in HCOs that are connected with fast non-delayed synapses. The finding contrasts with the classical view that reciprocal inhibition has to be slow or time-delayed to synchronize such bursting neurons. Phase-locked rhythms are analyzed via Lyapunov exponents estimated with variational equations, and through the convergence rates estimated with Poincar\'e return maps. A new mechanism underlying multistability is proposed that is based on the spike interactions, which confer a dual property on the fast non-delayed reciprocal inhibition; this reveals the role of spikes in generating multiple co-existing phase-locked rhythms. In particular, it demonstrates that the number and temporal characteristics of spikes determine the number and stability of the multiple phase-locked states in weakly coupled HCOs. The generality of the multistability phenomenon is demonstrated by analyzing diverse models of bursting networks with various inhibitory synapses; the individual cell models include the reduced leech heart interneuron, the Sherman model for pancreatic beta cells, the Purkinje neuron model and Fitzhugh-Rinzel phenomenological model. Finally, hypothetical and experiment-based CPGs composed of HCOs are investigated. This study is relevant for various applications that use CPGs such as robotics, prosthetics, and artificial intelligence.
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18

Ng, Yu Pong. "Leukemia inhibitory factor receptor signaling in NGF-induced neuronal differentiation of PC12 cells /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BICH%202004%20NG.

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Анотація:
Thesis (Ph. D.)--Hong Kong University of Science and Technology, 2004.
Includes bibliographical references (leaves 134-172). Also available in electronic version. Access restricted to campus users.
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19

Chéry, Nadège. "Inhibitory control of neurons in the marginal zone (lamina I) of the rat spinal cord." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0032/NQ64534.pdf.

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20

McDougal, Robert A. "Excitatory-Inhibitory Interactions as the Basis of Working Memory." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1313004219.

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21

Beebe, Nichole L. "Perineuronal nets and the inhibitory circuitry of the auditory midbrain: evidence for subtypes of GABAergic neurons." Kent State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=kent1468938365.

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22

Layne, Robert Michael. "The AIB interneurons are modulated by excitatory and inhibitory signaling pathways to shape aversive behaviors in response to 1-octanol." University of Toledo / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1445452178.

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23

Guilbert, Erin. "Inhibitory role of d-series resolvins in the cellular response to painful stimuli in trigeminal ganglion neurons." Thesis, Boston University, 2012. https://hdl.handle.net/2144/12405.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Resolvins (Rv) are molecules that are responsible for the active resolution of inflammation. Recent studies have suggested that the resolvins are capable of inhibiting pain associated with inflammation. Our goal was to determine the effects of RvD1, aspirin triggered (AT)-RvD1, and RvD2 on the intracellular calcium concentration ([Ca2+]i) response to the painful stimulus, capsaicin, in cultured trigeminal ganglion neurons. Neuronal cells of the rat trigeminal ganglia were isolated and cultured on 35 mm glass bottom dishes that had been treated with poly-D lysine and laminin. Cells were incubated in the presence or absence of RvD1 , RvD2, or AT-RvD1. Cells were then loaded with Fura-2 to detect changes in [Ca2+]i..[Ca2+]i was measured in response to capsaicin administration. RvD1, AT-RvD1, and RvD2 significantly inhibited the increase in [Ca2+]i in response to capsaicin. In addition the localization of lipoxin A4 (ALX) receptor that can be used by RvD1 and AT-RvD1 and nestin that indicates neurons was detected in the plated cells using immunofluorescence microscopy. The ability of D-series resolvins to inhibit the Ca2+i response to capsaicin suggests that this type of resolvin has the potential to be effective endogenous analgesics in pain conditions of the face and head. The presence of the ALX receptor on the cells of the trigeminal ganglion supports the hypothesis that RvD1 and AT-RvD1 could inhibit pain through interaction with ALX.
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24

Kaplan, Eitan S. "Visual cortical plasticity : the role of parvalbumin expressing inhibitory neurons and abnormalities in models of neurodevelopmental disorders." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/103210.

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Анотація:
Thesis: Ph. D. in Neuroscience, Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 2016.
Cataloged from PDF version of thesis. Vita.
Includes bibliographical references (pages 121-134).
The roles played by cortical inhibitory neurons in experience-dependent plasticity and learning are not well understood. Here we evaluate the participation of parvalbumin-expressing (PV+) GABAergic neurons in two forms of experience-dependent modification of primary visual cortex (V1) in adult mice: ocular dominance (OD) plasticity resulting from monocular deprivation and stimulus-selective response potentiation (SRP) resulting from supplemental visual experience. These two forms of plasticity are triggered by different events but lead to a similar increase in visual cortical response. Both also require the NMDA class of glutamate receptor (NMDAR). However, we find that PV+ inhibitory neurons in V1 play a critical role in the expression of SRP and its behavioral correlate of familiarity recognition, but not in the expression of OD plasticity. Furthermore, NMDARs expressed within PV+ cells play a critical role in SRP, but not in the induction or expression of adult OD plasticity. We also explore the use of visual cortical plasticity paradigms to better understand the function of proteins implicated in autism spectrum disorders (ASDs) and schizophrenia. We find that NMDAR-dependent long-term depression (LTD) and deprived-eye depression in layer 4 of V1 require metabotropic glutamate receptor 5 (mGluR5) signaling during postnatal development. Additionally, schizophrenia-associated protein neurogranin overexpression in V1 disrupts juvenile ocular dominance plasticity. Finally, we evaluate SRP in two models of ASDs associated with excitatory/ inhibitory imbalance: Rett syndrome (RTT) and tuberous sclerosis complex (TSC). Surprisingly, mouse models of RTT and TSC exhibit abnormal SRP phenotypes, but in opposite directions.
by Eitan S. Kaplan.
Ph. D. in Neuroscience
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25

Baca, Serapio Michael. "Inhibitory motor neurons are essential for the production of local bending in the medicinal leech (Hirudo medicinalis) /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3167858.

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26

Bihun, Marzena Maria. "Functional relevance of inhibitory and disinhibitory circuits in signal propagation in recurrent neuronal networks." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31148.

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Cell assemblies are considered to be physiological as well as functional units in the brain. A repetitive and stereotypical sequential activation of many neurons was observed, but the mechanisms underlying it are not well understood. Feedforward networks, such as synfire chains, with the pools of excitatory neurons unidirectionally connected and facilitating signal transmission in a cascade-like fashion were proposed to model such sequential activity. When embedded in a recurrent network, these were shown to destabilise the whole network’s activity, challenging the suitability of the model. Here, we investigate a feedforward chain of excitatory pools enriched by inhibitory pools that provide disynaptic feedforward inhibition. We show that when embedded in a recurrent network of spiking neurons, such an augmented chain is capable of robust signal propagation. We then investigate the influence of overlapping two chains on the signal transmission as well as the stability of the host network. While shared excitatory pools turn out to be detrimental to global stability, inhibitory overlap implicitly realises the motif of lateral inhibition, which, if moderate, maintains the stability but if substantial, it silences the whole network activity including the signal. Addition of a disinhibitory pathway along the chain proves to rescue the signal transmission by transforming a strong inhibitory wave into a disinhibitory one, which specifically guards the excitatory pools from receiving excessive inhibition and thereby allowing them to remain responsive to the forthcoming activation. Disinhibitory circuits not only improve the signal transmission, but can also control it via a gating mechanism. We demonstrate that by manipulating a firing threshold of the disinhibitory neurons, the signal transmission can be enabled or completely blocked. This mechanism corresponds to cholinergic modulation, which was shown to be signalled by volume as well as phasic transmission and variably target classes of neurons. Furthermore, we show that modulation of the feedforward inhibition circuit can promote generating spontaneous replay at the absence of external inputs. This mechanism, however, tends to also cause global instabilities. Overall, these results underscore the importance of inhibitory neuron populations in controlling signal propagation in cell assemblies as well as global stability. Specific inhibitory circuits, when controlled by neuromodulatory systems, can robustly guide or block the signals and invoke replay. This mounts to evidence that the population of interneurons is diverse and can be best categorised by neurons’ specific circuit functions as well as their responsiveness to neuromodulators.
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27

Ure, Daren Raymond. "Retrograde signaling and retrograde axonal transport of leukemia inhibitory factor and nerve growth factor by cultured sympathetic neurons." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21648.pdf.

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28

Fujiyama, Tomoyuki. "Inhibitory and excitatory subtypes of cochlear nucleus neurons are defined by distinct bHLH transcription factors, Ptf1a and Atoh1." Kyoto University, 2012. http://hdl.handle.net/2433/157456.

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29

Miyazaki, Yoshiya. "Xenon Has Greater Inhibitory Effects on Spinal Dorsal Horn Neurons than Nitrous Oxide in Spinal Cord Transected Cats." Kyoto University, 2000. http://hdl.handle.net/2433/181269.

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30

Whittaker, Maximilian Anthony Erik. "Modulation of fast-spiking interneurons using two-pore channel blockers." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31252.

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The balance between excitatory and inhibitory synaptic transmission within and across neurons in active networks is crucial for cortical function and may allow for rapid transitions between stable network states. GABAergic interneurons mediate the majority of inhibitory transmission in the cortex, and therefore contribute to the global balance of activity in neuronal networks. Disruption in the network balance due to impaired inhibition has been implicated in several neuropsychiatric diseases (Marin 2012). Both schizophrenia and autism are two highly heritable cognitive disorders with complex genetic aetiologies but overlapping behavioural phenotypes that share common imbalances in neuronal network activity (Gao & Penzes 2015). An increasing body of evidence suggests that functional abnormalities in a particular group of cortical GABAergic interneurons expressing the calcium-binding protein parvalbumin (PV) are involved in the pathology of these disorders (Marin 2012). As deficits in this neuronal population have been linked to these disorders it could be useful to target them and increase their activity. A conserved feature in PV cells is their unusually low input resistance compared to other neuronal populations. This feature is regulated by the expression of leak K+ channels, believed to be mediated in part by TASK and TREK subfamily two-pore K+ channels (Goldberg et al. 2011). The selective blockade of specific leak K+ channels could therefore be applied to increase the activity of PV cells. In this thesis, specific TASK-1/3 and TREK-1 channel blockers were applied in cortical mouse slices in an attempt to increase the output of PV cells. The blockade of either channel did not successfully increase the amplitude of PV cell-evoked inhibitory postsynaptic currents (IPSCs) onto principal cells. However, while the blockade of TASK-1/3 channels failed to depolarise the membrane or alter the input resistance, the blockade of TREK-1 channels resulted in a small but significant depolarisation of the membrane potential in PV cells. Interestingly, TREK-1 channel blockade also increased action potential firing of PV cells in response to given current stimuli, suggesting that TREK-1 could be a useful target for PV cell modulation. These results demonstrate for the first time the functional effects of using specific two-pore K+ channel blockers in PV cells. Furthermore, these data provide electrophysiological evidence against the functional expression of TASK-1/3 in PV cells. It could therefore be interesting to further characterise the precise subtypes of leak K+ channels responsible for their low resistivity. This would help to classify the key contributors of the background K+ conductances present in PV cells in addition to finding suitable targets to increase their activity.
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31

Cleland, Thomas A. "Inhibitory glutamate receptor channels : characterization and modulation in cultured lobster stomatogastric neurons : or it's amazing it works at all /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1997. http://wwwlib.umi.com/cr/ucsd/fullcit?p9724889.

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32

Delgado, Arriagada Ricardo Alfonso [Verfasser]. "Molecular components involved in the inhibitory responses and Ca2+ clearance from the cilia of olfactory receptor neurons / Ricardo Alfonso Delgado Arriagada." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover (TIB), 2011. http://d-nb.info/1019723386/34.

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33

Pangalos, Maria [Verfasser], Richard [Gutachter] Kempter, Dietmar [Gutachter] Schmitz, and Nikolai [Gutachter] Axmacher. "Analysis of hippocampal inhibitory and excitatory neurons during sharp wave-associated ripple / Maria Pangalos ; Gutachter: Richard Kempter, Dietmar Schmitz, Nikolai Axmacher." Berlin : Lebenswissenschaftliche Fakultät, 2016. http://d-nb.info/1113686162/34.

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34

Avigdor, Mauricio. "Natural Neuronal Variation in a Complex Neuroendocrine Pathway: Effect of Selection for Photoperiod Responsiveness on the Density and Location of Mature GNRH-Releasing Neurons in Inhibitory and Excitatory Photoperiods." W&M ScholarWorks, 2004. https://scholarworks.wm.edu/etd/1539626458.

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35

Painter, Palak Rajeshkumar. "Quantitative analysis of glycinergic neurons including Ia inhibitory interneurons in the ventral spinal cord using a BAC-GlyT2-eGFP transgenic mouse model." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1347911464.

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36

Bredack, Christoph [Verfasser], Sonja [Akademischer Betreuer] Wojcik, Erwin [Akademischer Betreuer] Neher, and Ahmed [Akademischer Betreuer] Mansouri. "Genetic Targeting and Analysis of Parvalbumin and VGLUT3 Expressing Inhibitory Neurons / Christoph Bredack. Gutachter: Sonja Wojcik ; Erwin Neher ; Ahmed Mansouri. Betreuer: Sonja Wojcik." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2012. http://d-nb.info/1042305536/34.

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37

Marx, Manuel [Verfasser]. "Intralaminar and translaminar microcircuits involving excitatory and inhibitory neurons in layer 6B of the somatosensory rat barrel cortex : a morphological, physiological and immunofluorescence study / Manuel Marx." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2014. http://d-nb.info/1051528771/34.

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38

Duguid, Ian Charles. "Inhibitory synaptic plasticity in the cerebellum." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368689.

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39

Nakamizo, Tomoki. "Phosphodiesterase inhibitors are neuroprotective to cultured spinal motor neurons." Kyoto University, 2003. http://hdl.handle.net/2433/148692.

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40

Chow, Wei-Yan. "Inhibitory neuron lamination in the developing zebrafish retina." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708976.

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41

Tarczy-Hornoch, Kristina. "Physiology of synaptic inputs to layer IV of cat visual cortex." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337608.

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42

De, Sousa Sara Luisa Mellor. "Effects of the general anaesthetics isoflurane and xenon on synaptic transmission in isolated hippocampal neurones." Thesis, Imperial College London, 1999. http://hdl.handle.net/10044/1/8593.

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43

Landucci, Elisa. "Modeling Rett syndrome with iPSCs-derived neurons." Doctoral thesis, Università di Siena, 2018. http://hdl.handle.net/11365/1051069.

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Rett syndrome is a severe neurodevelopmental disorder. The condition affects approximately one in every 10.000 females and is only rarely seen in males. Causative mutations in the transcriptional regulator MeCP2 have been identified in more than 95% of classic Rett patients; mutations in CDKL5 are responsible for the early onset seizures Rett variant and mutations in FOXG1 gene lead to the congenital Rett variant. To shed light on molecular mechanisms underlying Rett syndrome onset and progression in disease-relevant cells, we took advantage of the breakthrough genetic reprogramming technology and we investigated changes in iPSC-derived neurons from patients with different MECP2 and FOXG1 mutations and in the brain of Foxg1+/- mice. In total brains from Foxg1+/ − mutants we noticed a statistically significant overexpression of a group of neuropeptides expressed in the basal ganglia, cortex, hippocampus and hypothalamus: Oxytocin (Oxt), Arginine vasopressin (Avp) and Neuronatin (Nnat).Moreover, in iPSC-derived neuronal precursors and neurons mutated in FOXG1 and in Foxg1+/− mouse embryonic brain (E11.5) compared to wild type controls we found an increase in the expression of GluD1 and inhibitory synaptic markers, such as GAD67 and GABA AR-α1 and a decreased expression of excitatory synaptic markers, such as VGLUT1, GluA1, GluN1 and PSD-95, suggesting an excitation/inhibition imbalance in the developing brain of the congenital RTT variant. Furthermore, we investigated transcriptome changes in neurons differentiated from MECP2 mutated iPSC-derived neurons and we noticed a prominent GABAergic circuit disruption and a perturbation of cytoskeleton dynamics. In particular, in MECP2-mutated neurons we identified a significant decrease of acetylated α-tubulin which can be reverted by treatment with a selective inhibitor of HDAC6, the main α-tubulin deacetylase. Taken togheter, these findings contribute to shed light on Rett pathogenic mechanisms and provide hints for the definition of new therapeutic strategies for Rett syndrome.
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44

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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45

Zeki, Mustafa. "DISCRETE ANALYSIS OF SYNCHRONIZED OSCILLATIONS IN EXCITATORY-INHIBITORY NEURONAL NETWORKS." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1282065976.

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46

Chan, Yuen-man, and 陳婉文. "Effect of caspase inhibitors on the survival and regeneration of injured spinal motoneurons." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31242893.

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47

Ngo, Dung. "Elucidating the Cellular and Molecular Changes of Dopaminergic Neurons by Rotenone-Induced Neurodegeneration in Zebrafish." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37921.

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Chemical-induced models have revealed the crucial role of oxidative stress and mito-chondrial dysfunction in the development of Parkinson’s Disease. In this project, firstly, we in-vestigated the mechanism of action of rotenone, a commercialized pesticide that was previously described to reproduce the bradykinetic dopaminergic neurodegeneration symptoms of Parkin-son’s Disease in zebrafish by inhibition of the mitochondrial complex I. We found out that rote-none caused change in the morphology of the zebrafish dopaminergic mitochondrial network. We also observed the altered expression of various genes involves in mitochondrial fusion and fission in response to rotenone exposure. Secondly, to develop the use of adult zebrafish as a toxin-based model for Parkinson’s Disease, we sought to minimize any off-target effects by exposure of rotenone specifically to the brain. We demonstrated that microinjection of rotenone into the forebrain ventricular zone of adult zebrafish decreases the number of dopaminergic neurons. However, behavioural tests suggested that did not translate into locomotor impairment in these fish. Taken together, these results gave us more information about the potential use of zebrafish to study the physiological mechanism leading to dopaminergic degeneration and allow for the development of therapeutic strategies for Parkinson’s Disease.
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48

Yaraghi, Zahra. "The Neuronal Apoptosis Inhibitory Protein, NAIP, analysis of human and murine genetics." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0021/NQ46555.pdf.

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49

Jordan, Russell S. (Russell Stall). "Investigation of Inhibitory Influences in Neuronal Monolayer Networks Cultured from Mouse Spinal Cord." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc500431/.

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The effects of the inhibitory neurotransmitters gammaamino butyric acid (GABA) and glycine were characterized on spontaneous activity recorded from mouse spinal cord cultures. The GABA concentration which completely inhibited burst activity was chosen as a quantifiable measure of culture drug response and was used to 1) assess interculture and intraculture variability, 2) determine the influence of culture age and initial activity on GABA responses, and 3) compare the GABA responses between networks obtained from whole spinal cord and ventral half spinal cord. Results showed that 1) no significant variability existed either within or among cultures, 2) the initial culture activity directly affected GABA responses, 3) the culture age had no effect on GABA responses, and 4) there was no significant difference in GABA responses between the two spinal cord tissues.
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50

Bricker, Rebecca L. "Q-VE-OPh, a control caspase inhibitor for analyzing neuronal death." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1340647107.

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