Relevant bibliographies by topics / Interneurone cortical

Academic literature on the topic 'Interneurone cortical'

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Published: 2 March 2024

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Journal articles on the topic "Interneurone cortical"

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Somogyi, Peter, and Thomas Klausberger. "Defined types of cortical interneurone structure space and spike timing in the hippocampus." Journal of Physiology 562, no. 1 (December 22, 2004): 9–26. http://dx.doi.org/10.1113/jphysiol.2004.078915.

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Yang, Panzao, Joanne O. Davidson, Tania M. Fowke, Robert Galinsky, Guido Wassink, Rashika N. Karunasinghe, Jaya D. Prasad, et al. "Connexin Hemichannel Mimetic Peptide Attenuates Cortical Interneuron Loss and Perineuronal Net Disruption Following Cerebral Ischemia in Near-Term Fetal Sheep." International Journal of Molecular Sciences 21, no. 18 (September 4, 2020): 6475. http://dx.doi.org/10.3390/ijms21186475.

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Perinatal hypoxia-ischemia is associated with disruption of cortical gamma-aminobutyric acid (GABA)ergic interneurons and their surrounding perineuronal nets, which may contribute to persisting neurological deficits. Blockade of connexin43 hemichannels using a mimetic peptide can alleviate seizures and injury after hypoxia-ischemia. In this study, we tested the hypothesis that connexin43 hemichannel blockade improves the integrity of cortical interneurons and perineuronal nets. Term-equivalent fetal sheep received 30 min of bilateral carotid artery occlusion, recovery for 90 min, followed by a 25-h intracerebroventricular infusion of vehicle or a mimetic peptide that blocks connexin hemichannels or by a sham ischemia + vehicle infusion. Brain tissues were stained for interneuronal markers or perineuronal nets. Cerebral ischemia was associated with loss of cortical interneurons and perineuronal nets. The mimetic peptide infusion reduced loss of glutamic acid decarboxylase-, calretinin-, and parvalbumin-expressing interneurons and perineuronal nets. The interneuron and perineuronal net densities were negatively correlated with total seizure burden after ischemia. These data suggest that the opening of connexin43 hemichannels after perinatal hypoxia-ischemia causes loss of cortical interneurons and perineuronal nets and that this exacerbates seizures. Connexin43 hemichannel blockade may be an effective strategy to attenuate seizures and may improve long-term neurological outcomes after perinatal hypoxia-ischemia.
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Qiu, Fang, Xingfeng Mao, Penglai Liu, Jinyun Wu, Yuan Zhang, Daijing Sun, Yueyan Zhu, et al. "microRNA Deficiency in VIP+ Interneurons Leads to Cortical Circuit Dysfunction." Cerebral Cortex 30, no. 4 (November 4, 2019): 2229–49. http://dx.doi.org/10.1093/cercor/bhz236.

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Abstract Genetically distinct GABAergic interneuron subtypes play diverse roles in cortical circuits. Previous studies revealed that microRNAs (miRNAs) are differentially expressed in cortical interneuron subtypes, and are essential for the normal migration, maturation, and survival of medial ganglionic eminence-derived interneuron subtypes. How miRNAs function in vasoactive intestinal peptide expressing (VIP+) interneurons derived from the caudal ganglionic eminence remains elusive. Here, we conditionally removed Dicer in postmitotic VIP+ interneurons to block miRNA biogenesis. We found that the intrinsic and synaptic properties of VIP+ interneurons and pyramidal neurons were concordantly affected prior to a progressive loss of VIP+ interneurons. In vivo recording further revealed elevated cortical local field potential power. Mutant mice had a shorter life span but exhibited better spatial working memory and motor coordination. Our results demonstrate that miRNAs are indispensable for the function and survival of VIP+ interneurons, and highlight a key role of VIP+ interneurons in cortical circuits.
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Fishell, Gord, and Adam Kepecs. "Interneuron Types as Attractors and Controllers." Annual Review of Neuroscience 43, no. 1 (July 8, 2020): 1–30. http://dx.doi.org/10.1146/annurev-neuro-070918-050421.

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Cortical interneurons display striking differences in shape, physiology, and other attributes, challenging us to appropriately classify them. We previously suggested that interneuron types should be defined by their role in cortical processing. Here, we revisit the question of how to codify their diversity based upon their division of labor and function as controllers of cortical information flow. We suggest that developmental trajectories provide a guide for appreciating interneuron diversity and argue that subtype identity is generated using a configurational (rather than combinatorial) code of transcription factors that produce attractor states in the underlying gene regulatory network. We present our updated three-stage model for interneuron specification: an initial cardinal step, allocating interneurons into a few major classes, followed by definitive refinement, creating subclasses upon settling within the cortex, and lastly, state determination, reflecting the incorporation of interneurons into functional circuit ensembles. We close by discussing findings indicating that major interneuron classes are both evolutionarily ancient and conserved. We propose that the complexity of cortical circuits is generated by phylogenetically old interneuron types, complemented by an evolutionary increase in principal neuron diversity. This suggests that a natural neurobiological definition of interneuron types might be derived from a match between their developmental origin and computational function.
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Lukomska, Agnieszka, Grzegorz Dobrzanski, Monika Liguz-Lecznar, and Malgorzata Kossut. "Somatostatin receptors (SSTR1-5) on inhibitory interneurons in the barrel cortex." Brain Structure and Function 225, no. 1 (December 23, 2019): 387–401. http://dx.doi.org/10.1007/s00429-019-02011-7.

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AbstractInhibitory interneurons in the cerebral cortex contain specific proteins or peptides characteristic for a certain interneuron subtype. In mice, three biochemical markers constitute non-overlapping interneuron populations, which account for 80–90% of all inhibitory cells. These interneurons express parvalbumin (PV), somatostatin (SST), or vasoactive intestinal peptide (VIP). SST is not only a marker of a specific interneuron subtype, but also an important neuropeptide that participates in numerous biochemical and signalling pathways in the brain via somatostatin receptors (SSTR1-5). In the nervous system, SST acts as a neuromodulator and neurotransmitter affecting, among others, memory, learning, and mood. In the sensory cortex, the co-localisation of GABA and SST is found in approximately 30% of interneurons. Considering the importance of interactions between inhibitory interneurons in cortical plasticity and the possible GABA and SST co-release, it seems important to investigate the localisation of different SSTRs on cortical interneurons. Here, we examined the distribution of SSTR1-5 on barrel cortex interneurons containing PV, SST, or VIP. Immunofluorescent staining using specific antibodies was performed on brain sections from transgenic mice that expressed red fluorescence in one specific interneuron subtype (PV-Ai14, SST-Ai14, and VIP-Ai14 mice). SSTRs expression on PV, SST, and VIP interneurons varied among the cortical layers and we found two patterns of SSTRs distribution in L4 of barrel cortex. We also demonstrated that, in contrast to other interneurons, PV cells did not express SSTR2, but expressed other SSTRs. SST interneurons, which were not found to make chemical synapses among themselves, expressed all five SSTR subtypes.
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Ying, Guoxin, Sen Wu, Ruiqing Hou, Wei Huang, Mario R. Capecchi, and Qiang Wu. "The Protocadherin Gene Celsr3 Is Required for Interneuron Migration in the Mouse Forebrain." Molecular and Cellular Biology 29, no. 11 (March 30, 2009): 3045–61. http://dx.doi.org/10.1128/mcb.00011-09.

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ABSTRACT Interneurons are extremely diverse in the mammalian brain and provide an essential balance for functional neural circuitry. The vast majority of murine cortical interneurons are generated in the subpallium and migrate tangentially over a long distance to acquire their final positions. By using a mouse line with a deletion of the Celsr3 (Flamingo, or Fmi1) gene and a knock-in of the green fluorescent protein reporter, we find that Celsr3, a member of the nonclustered protocadherin (Pcdh) family, is predominantly expressed in the cortical interneurons in adults and in the interneuron germinal zones in embryos. We show that Celsr3 is crucial for interneuron migration in the developing mouse forebrain. Specifically, in Celsr3 knockout mice, calretinin-positive interneurons are reduced in the developing neocortex, accumulated in the corticostriatal boundary, and increased in the striatum. Moreover, the laminar distribution of cortical calbindin-positive cells is altered. Finally, we found that expression patterns of NRG1 (neuregulin-1) and its receptor ErbB4, which are essential for interneuron migration, are changed in Celsr3 mutants. These results demonstrate that the protocadherin Celsr3 gene is essential for both tangential and radial interneuron migrations in a class-specific manner.
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Lamsa, Karri, and Tomi Taira. "Use-Dependent Shift From Inhibitory to Excitatory GABAA Receptor Action in SP-O Interneurons in the Rat Hippocampal CA3 Area." Journal of Neurophysiology 90, no. 3 (September 2003): 1983–95. http://dx.doi.org/10.1152/jn.00060.2003.

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Cortical inhibitory interneurons set the pace of synchronous neuronal oscillations implicated in synaptic plasticity and various cognitive functions. The hyperpolarizing nature of inhibitory postsynaptic potentials (IPSPs) in interneurons has been considered crucial for the generation of oscillations at β (15–30 Hz) and γ (30–100 Hz) frequency. Hippocampal basket cells and axo-axonic cells in stratum pyramidale-oriens (S-PO) play a central role in the synchronization of the local interneuronal network as well as in pacing of glutamatergic principal cell firing. A lack of conventional forms of plasticity in excitatory synapses onto interneurons facilitates their function as stable neuronal oscillators. We have used gramicidin-perforated and whole cell clamp recordings to study properties of GABAAR-mediated transmission in CA3 SP-O interneurons and in CA3 pyramidal cells in rat hippocampal slices during electrical 5- to 100-Hz stimulation and during spontaneous activity. We show that GABAergic synapses onto SP-O interneurons can easily switch their mode from inhibitory to excitatory during heightened activity. This is based on a depolarizing shift in the GABAA reversal potential ( EGABA-A), which is much faster and more pronounced in interneurons than in pyramidal cells. We also found that the shift in interneuronal function was frequency dependent, being most prominent at 20- to 40-Hz activation of the GABAergic synapses. After 40-Hz tetanic stimulation (100 pulses), GABAA responses remained depolarizing for ∼45 s in the interneurons, promoting bursting in the GABAergic network. Hyperpolarizing EGABA-A was restored >60 s after the stimulus train. Similar but spontaneous GABAergic bursting was induced by application of 4-aminopyridine (100 μM) to slices. A shift to depolarizing IPSPs by the GABAAR permeant weak acid anion formate provoked interneuronal population bursting, supporting the role of GABAergic excitation in burst generation. Furthermore, depolarizing GABAergic potentials and synchronous interneuronal bursting were enhanced by pentobarbital (100 μM), a positive allosteric modulator of GABAARs, and were blocked by picrotoxin (100 μM). Intriguingly, GABAergic bursts displayed short (<1 s) oscillations at 15–40 Hz, even though only depolarizing GABAA responses were seen in the SP-O interneurons. This β-γ rhythmicity in the interneuron network was dependent on electrotonic coupling, and was abolished by blockade of gap junctions with carbenoxolone (200 μM). Results here implicate the rapid activity-dependent degradation of hyperpolarizing IPSPs in SP-O interneurons in setting the temporal limits for a given interneuron to participate in β-γ oscillations synchronized by GABAergic synapses. Furthermore, they imply that mutual GABAergic excitation provided by interneurons may be an integral part in the function of neuronal networks. We suggest that the use-dependent change in EGABA-A could represent a form of short-term plasticity in interneurons promoting coherent and sustained activation of local GABAergic networks.
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Howard, MacKenzie A., and Scott C. Baraban. "Synaptic integration of transplanted interneuron progenitor cells into native cortical networks." Journal of Neurophysiology 116, no. 2 (August 1, 2016): 472–78. http://dx.doi.org/10.1152/jn.00321.2016.

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Interneuron-based cell transplantation is a powerful method to modify network function in a variety of neurological disorders, including epilepsy. Whether new interneurons integrate into native neural networks in a subtype-specific manner is not well understood, and the therapeutic mechanisms underlying interneuron-based cell therapy, including the role of synaptic inhibition, are debated. In this study, we tested subtype-specific integration of transplanted interneurons using acute cortical brain slices and visualized patch-clamp recordings to measure excitatory synaptic inputs, intrinsic properties, and inhibitory synaptic outputs. Fluorescently labeled progenitor cells from the embryonic medial ganglionic eminence (MGE) were used for transplantation. At 5 wk after transplantation, MGE-derived parvalbumin-positive (PV+) interneurons received excitatory synaptic inputs, exhibited mature interneuron firing properties, and made functional synaptic inhibitory connections to native pyramidal cells that were comparable to those of native PV+ interneurons. These findings demonstrate that MGE-derived PV+ interneurons functionally integrate into subtype-appropriate physiological niches within host networks following transplantation.
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Cruz-Santos, Maria, Lucia Fernandez Cardo, and Meng Li. "A Novel LHX6 Reporter Cell Line for Tracking Human iPSC-Derived Cortical Interneurons." Cells 11, no. 5 (March 1, 2022): 853. http://dx.doi.org/10.3390/cells11050853.

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GABAergic interneurons control the neural circuitry and network activity in the brain. The dysfunction of cortical interneurons, especially those derived from the medial ganglionic eminence, contributes to neurological disease states. Pluripotent stem cell-derived interneurons provide a powerful tool for understanding the etiology of neuropsychiatric disorders, as well as having the potential to be used as medicine in cell therapy for neurological conditions such as epilepsy. Although large numbers of interneuron progenitors can be readily induced in vitro, the generation of defined interneuron subtypes remains inefficient. Using CRISPR/Cas9-assisted homologous recombination in hPSCs, we inserted the coding sequence of mEmerald and mCherry fluorescence protein, respectively, downstream that of the LHX6, a gene required for, and a marker of medial ganglionic eminence (MGE)-derived cortical interneurons. Upon differentiation of the LHX6-mEmerald and LHX6-mCherry hPSCs towards the MGE fate, both reporters exhibited restricted expression in LHX6+ MGE derivatives of hPSCs. Moreover, the reporter expression responded to changes of interneuron inductive cues. Thus, the LHX6-reporter lines represent a valuable tool to identify molecules controlling human interneuron development and design better interneuron differentiation protocols as well as for studying risk genes associated with interneuronopathies.
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Nestor, Michael W., Samson Jacob, Bruce Sun, Deborah Prè, Andrew A. Sproul, Seong Im Hong, Chris Woodard, et al. "Characterization of a subpopulation of developing cortical interneurons from human iPSCs within serum-free embryoid bodies." American Journal of Physiology-Cell Physiology 308, no. 3 (February 1, 2015): C209—C219. http://dx.doi.org/10.1152/ajpcell.00263.2014.

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Production and isolation of forebrain interneuron progenitors are essential for understanding cortical development and developing cell-based therapies for developmental and neurodegenerative disorders. We demonstrate production of a population of putative calretinin-positive bipolar interneurons that express markers consistent with caudal ganglionic eminence identities. Using serum-free embryoid bodies (SFEBs) generated from human inducible pluripotent stem cells (iPSCs), we demonstrate that these interneuron progenitors exhibit morphological, immunocytochemical, and electrophysiological hallmarks of developing cortical interneurons. Finally, we develop a fluorescence-activated cell-sorting strategy to isolate interneuron progenitors from SFEBs to allow development of a purified population of these cells. Identification of this critical neuronal cell type within iPSC-derived SFEBs is an important and novel step in describing cortical development in this iPSC preparation.
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Dissertations / Theses on the topic "Interneurone cortical"

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Touzot, Audrey. "Migration et spécification des interneurones GABAergiques corticaux issus de la CGE au cours du développement chez la souris." Thesis, Nice, 2014. http://www.theses.fr/2014NICE4089/document.

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Chez les rongeurs, les interneurones (INs) corticaux sont issus de l’éminence ganglionnaire (EG) médiale (MGE) et caudale (CGE), expriment une combinaison de facteurs définis et migrent tangentiellement puis radialement pour atteindre leur position laminaire définitive. La diversité et la spécification des sous-types d’INs provenant de la MGE ont suscité de nombreuses études, en revanche les mécanismes moléculaires contrôlant la migration et la spécification des INs issus de la CGE demeurent toujours obscurs. Dans cette étude, les voies de migration de ces INs ont été examinées grâce à une lignée de souris rapportrices des interneurones issus de la CGE avant d’analyser le rôle de deux facteurs de transcription, COUP-TFI et COUP-TFII, hautement exprimés dans la CGE. Deux voies de migration non précédemment caractérisées ont alors été identifiées : une voie dorsale (CLMS) où les INs migrent vers l’EG latérale (LGE) et une voie ventrale (CMMS) où les INs migrent vers la MGE. Le CLMS et le CMMS ont donc été analysés, ainsi que la voie de migration caudale (CMS), à différents stades de développement et l’expression spécifique de certains gènes a pu être identifiée. En inactivant conditionnellement COUP-TFI et/ou COUP-TFII dans les INs, les voies de migration sont altérées ainsi que l’expression des marqueurs moléculaires. Comme probable conséquence, les souris mutantes adultes montrent une distribution altérée des sous-populations d’INs en particulier de celles issues de la CGE. Mon étude a donc permis d’identifier et de caractériser deux nouvelles voies de migration pour les INs provenant de la CGE et a montré que COUP-TFs contribuent à leur modulation
In rodents, cortical interneurons (INs) originate from the medial (MGE) and caudal ganglionic eminence (CGE) according to precise temporal schedules, express a defined combination of factors, and reach their final laminar position through tangential and radial cell migration. The diversity and fate-specification of MGE-derived interneuron subtypes are well characterized however the molecular mechanisms controlling the migration and specification of CGE-derived INs are still vague. In this study, I have first investigated the migratory paths of cortical INs using a reporter line specific to the CGE, and then I have assessed the involvement of COUP-TFI and COUP-TFII, which are highly expressed in the embryonic CGE during development, in these paths. My data unravelled two major previously non-characterized migratory streams from the subpallium to the pallium: a dorsal stream (CLMS) in which CGE-derived cells migrate to the lateral GE (LGE), and a ventral one (CMMS) in which CGE-derived cells migrate to the MGE. I have characterized both streams and the already well-described caudal stream (CMS) during different stages of development and identified a series of genes expressed in the migrating cells. By inactivating COUP-TFI and/or COUP-TFII in the developing INs, these streams together with their molecular marker expression are perturbed. As a consequence, adult mutant mice have an altered distribution of interneuron subpopulations, particularly the ones derived from the CGE. Taken together, my study identified and characterized two novel CGE-derived interneuron migratory routes to the cortex and showed that COUP-TFs contribute in modulating these paths
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Wilmet, Baptiste. "Analyses des dysfonctions neuronales d’un modèle murin de Paraplégie Spastique Héréditaire." Thesis, Paris Sciences et Lettres (ComUE), 2019. http://www.theses.fr/2019PSLEP045.

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Les Paraplégies Spastiques Héréditaires sont un groupe de maladies du motoneurone caractérisées par une dégénérescence de l’axe corticospinal menant à la spasticité et une paralysie progressive des membres parfois associés à des troubles cognitifs. Des mutations dans le gène SPG11 codant pour la Spatacsine sont la majeure cause de ces formes complexes de HSP. Pour mieux comprendre les mécanismes responsables de la pathologie liée à SPG11, notre équipe a généré un modèle de souris Knock-out pour ce gène, mimant les déficits cognitifs et moteurs observés chez les patients, corrélés à des altérations histologiques (J.Branchu & al. ; 2017). Etant donné que les troubles moteurs apparaissent avant les premières pertes neuronales, nous avons émis l’hypothèse qu’il existait des dysfonctions neuronales précédant la mort des neurones et mesurables par des techniques d’électrophysiologie. Des enregistrements EEG in vivo du cortex moteur des souris Spg11-/- nous ont permis d’observer l’émergence de décharges pointe-onde (DPO), survenant avant la mort des neurones corticaux NeuN+. Ces signaux sont semblables à ceux observés dans une forme particulière d’épilepsie : l’épilepsie d’absence et suggérent une perturbation de l’excitabilité corticale. Ces signaux ne semblent pas se propager dans le thalamus mais ces DPO répondent de manière dose dépendante à des drogues pro et anti Epilepsie d’Absence. Aucune différence significative n’a été observée dans le nombre d’interneurones GABAergiques, suggérant que l’inhibition corticale médiée par ces derniers n’est pas atteinte. Nous n’avons pas réussi à mettre en évidence de modification de l’expression de gènes liés à l’épilepsie d’absence. Cependant, des expériences de Patch clamp sur des neurones corticaux embryonnaires ont révélé une perturbation de la densité du courant sodique et d’excitabilité dans les neurones Spg11-/-. Des enregistrements ex vivo de l’hippocampe des souris Spg11-/- révèlent une perte de potentialisation à long et à court terme, corrélés avec une perte de mémoire spatiale, suggérant une atteinte d’un ou plusieurs éléments synaptiques. Ces pertes de plasticité hippocampiques ne sont pas observées durant le développement malgré ce qui semble être un défaut de synaptogénèse dans les collatérales de Schaffer. A terme, ces résultats vont étoffer nos connaissances sur les rôles de l’absence de Spatacsine dans la pathogénèse de l’HSP et des maladies du motoneurone et nous fourniront une mesure intéressante et non invasive (EEG) pour l’évaluation de l’efficacité de futur d’essais thérapeutiques
Hereditary Spastic Paraplegia is a group of Motor Neuron Disease characterized by the degeneration of cortico-spinal tract leading to a progressive spasticity and paralysis of lower limbs sometimes associated with cognitive deficits. Mutations in SPG11 gene coding for Spatacsin are a major cause of these complex forms. For a better understanding of SPG11-related HSP mechanisms, our team generated a Knock-Out mouse model (spg11-/-) mimicking the cognitive and motor deficits correlated with histological alterations (J.Branchu & al.; 2017). As motor impairments precede the first neuronal losses, we hypothesized that there may exist some neuronal dysfunctions primary to neuronal death observable with electrophysiological methods. In Vivo EEG recordings of spg11-/- motor cortex highlighted the emergence of spike and wave discharges events (SWD), occurring before the cortical NeuN+ cells loss and suggesting a disturbance of excitability of cortical networks. No propagation to thalamus was found, but these SWLD seems to response in a dose dependent manner to pro and anti-Absence Epilepsy drugs. With our IHC experiments, we didn’t observe any change in GABAergic interneurons number, suggesting no change in cortical inhibition mediated by interneurons. Ex vivo Electrophysiological recordings of adult spg11-/- hippocampi displayed reduced short and long-term potentiation, correlated with a loss of spatial and fear-related memories, suggesting an impairment in synaptic elements. We did not observe those alterations during development although there seem to be a shift from mature to immature dendritic spines. mRNA quantification couldn’t highlight any modification in epilepsy-related gene expression. However, in vitro intracellular recordings of embryonic cortical neurons revealed impairments in sodic current density and excitability in Spg11-/- neurons. Altogether, the results of these experiments will decipher the roles of Spatacsin in the pathogenesis of Motorneurons Diseases and give us a useful and non-invasive read-out for the evaluation of therapeutical assays
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Fleitas, Pérez Catherine. "FLRT proteins act as guidance cues for migrating cortical interneurons." Doctoral thesis, Universitat de Lleida, 2015. http://hdl.handle.net/10803/378646.

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The establishment of functional neuronal connectivity starts during development and depends on neuronal migration and the correct positioning of newborn neurons which integrate into specific layers of the cortex. The fibronectin and leucine-rich family of transmembrane proteins (FLRT) have evolved as new regulators of several aspects during nervous system development, including neuronal migration. This work is focused on the study of in vivo FLRTs involvement in the tangential migration of interneurons. For this, we have analyzed nervous system specific knockout animals for FLRT2 and FLRT3, single mutants as well as the double mutants The simultaneous suppression of FLRT2 and FLRT3, resulted in the appearance of several defects related to interneuron migration. Finally, was addressed the intracellular mechanisms involved in FLRT function and was assessed the relationship between FLRT3 and the Rho GTPase Rnd3. The results suggest a possible functional interaction between FLRTs and Rnds in the central nervous system.
L’establiment de les connectivitats neuronals a l’escorça en desenvolupament depèn de la migració i del correcte posicionament de les noves neurones que integren específicament les diferents capes corticals. Les proteïnes transmembrana riques en fibronectina i leucina (FLRT) han estat identificades com a nous reguladors de diversos aspectes en el desenvolupament del sistema nerviós, incloent la migració neuronal. El present treball de tesi està centrat en l’estudi in vivo de la implicació dels FLRTs en la migració tangencial de les interneurones. Amb aquest propòsit, hem analitzat animals knockout de FLRT2 i FLRT3, específics de sistema nerviós, com a mutants simples i també, com a dobles mutants. La supressió simultània de FLRT2 i FLRT3, produeix diversos defectes relacionats amb la migració de les interneurones. Finalment, es van abordar els mecanismes intracel•lulars implicats en la funció de FLRT, descrivint la relació entre FLRT3 i RhoGTPase Rnd3. Això suggereix una interacció funcional entre els FLRTs i els Rnds en el sistema nerviós.
El establecimiento de las conectividad neuronal comienza durante el desarrollo y depende de la migración neuronal y del correcto posicionamiento de las nuevas neuronas, las cuales se integran dentro de capas específicas de la corteza. Las proteínas transmembrana ricas en fibronectina y leucina (FLRT) han evolucionado como nuevos reguladores de varios aspectos durante el desarrollo del sistema nervioso, incluyendo la migración neuronal. Este trabajo se centra en el estudio de la implicación in vivo de FLRTs en la migración tangencial de las interneuronas. Para ello, hemos analizado animales knockout (KO) específicos del sistema nervioso para FLRT2 y FLRT3, simples mutantes y dobles KOs (DKO). La supresión simultánea de FLRT2 y FLRT3, resultó en la aparición de varios defectos relacionados con la migración de las interneuronas. Por último, se abordaron los mecanismos intracelulares implicados en la función de FLRT y se evaluó la relación entre FLRT3 y Rho GTPase Rnd3. Los resultados sugieren una posible interacción funcional entre FLRTs y Rnds en este sistema.
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Leclech, Claire. "Etude de l'influence de la topographie du microenvironnement sur la migration des interneurones corticaux par l'utilisation de substrats microstructurés." Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS245/document.

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Dans le cerveau en développement, les interneurones corticaux effectuent une longue migration avant de se positionner dans le cortex et s’intégrer dans les réseaux corticaux dont ils régulent l’activité. Différents facteurs chimiques ont été impliqués dans le guidage de ces cellules, mais l’influence des propriétés physiques de l’environnement dans lequel ils naviguent reste peu connue. Il a été montré que les indices topographiques peuvent guider le mouvement de nombreux types cellulaires, un processus appelé guidage par contact. Mes travaux de thèse ont ainsi cherché à tester et comprendre l’influence de la topographie de l’environnement sur la migration des interneurones corticaux. En utilisant un système expérimental de substrats microstructurés, nous avons mis en évidence pour la première fois l’existence du guidage par contact pour ces cellules. En testant deux types de micro-plots, nous avons établi qu’un changement de forme des structures influence de manière importante l’orientation, la morphologie, l’organisation du cytosquelette et le comportement dynamique des cellules. En particulier, les interneurones en migration entre des plots carrés adoptent majoritairement une morphologie allongée et peu branchée, associée à un mouvement lent et dirigé. A l’inverse, des cellules entre des plots ronds sont plus courtes et montrent un branchement important associé à un mouvement dynamique mais aléatoire. Plus généralement, nous montrons in vitro que la topographie génère des contraintes spatiales globales qui promeuvent la mise en place de différents états cellulaires morphologiques et dynamiques, soulignant ainsi la potentielle importance de ce type d’indices in vivo
In the developing brain, cortical interneurons undergo a long distance migration to reach the cortex where they integrate into cortical networks and regulate their activity in the adult. Different chemical factors have been involved in the guidance of these cells, but the influence of the physical parameters of the environment in which they navigate remains unclear. It has been shown that topographical cues are able to influence and guide the migration of several cell types, a process called contact guidance. This work therefore aimed at testing and understanding the influence of the topography of the environment in the migration of cortical interneurons. By using an experimental system of microstructured substrates, we demonstrated for the first time the existence of contact guidance for these cells. By testing two types of micron-sized pillars, we showed that a change in the shape of the structures could greatly impact cell orientation, morphology, cytoskeleton organization and dynamic behavior. In particular, most interneurons migrating in between square pillars adopt an elongated, unbranched morphology associated with a slow and directed movement, whereas the majority of cells among round pillars exhibit a short and branched morphology associated with a dynamic but wandering movement. Overall, we show that micron-sized topography provides global spatial constraints promoting the establishment of different morphological and migratory states in vitro, highlighting the potential importance of these types of cues in vivo
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Skowronski-Lutz, Ethan M. (Ethan Mikael). "Interneuron networks and cortical dynamics : emulated whisking drives SOM interneurons in the ketamine anesthetized mouse SI neocortex." Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/95858.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 2014.
Cataloged from PDF version of thesis.
Includes bibliographical references.
In the core of this thesis I test and confirm the hypothesis that separate classes of interneurons respond differentially to sensory stimulation independent of volitional or other top-down control on the part of the animal. I also test and confirm the hypothesis that, based only on bottom-up sensory stimulation the activity of two major classes of interneurons (adapting Parvalbumin positive and facilitating Somatostatin positive interneurons) predominates during different phases of what corresponds to natural sensing cycles in a behaving rodent. These questions are addressed using an in vivo mouse model with intrinsically fluorescent, but differentiable, interneuron populations combined with 2-photon imaging, Ca²+-sensitive dyes. Anesthesia and electrical control of facial muscles allowed for naturalistic stimulation without the confounds presented by volitional whisking and unknown top-down or behavioral states. Additional chapters in this thesis focus on ancillary work related to computational modeling of neural systems and systems' level perspectives on maturation and disease.
by Ethan M. Skowronski-Lutz.
Ph. D.
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Courtin, Julien. "Role of cortical parvalbumin interneurons in fear behaviour." Thesis, Bordeaux 2, 2013. http://www.theses.fr/2013BOR22045/document.

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Les processus d'apprentissage et de mémoire sont contrôlés par des circuits et éléments neuronaux spécifiques. De nombreuses études ont récemment mis en évidence que les circuits corticaux jouent un rôle important dans la régulation des comportements de peur, cependant, leurs caractéristiques anatomiques et fonctionnelles restent encore largement inconnues. Au cours de ma thèse, en utilisant des enregistrements unitaires et des approches optogénétiques chez la souris libre de se comporter, nous avons pu montrer que les interneurones inhibiteurs du cortex auditif et du cortex préfrontal médian forment un microcircuit désinhibiteur permettant respectivement l'acquisition et l'expression de la mémoire de peur conditionnée. Dans les deux cas, les interneurones parvalbuminergiques constituent l'élément central du circuit et sont inhibés de façon phasique. D’un point de vue fonctionnel, nous avons démontré que cette inhibition était associée à la désinhibition des neurones pyramidaux par un mécanisme de réduction de l'inhibition continue exercée par les interneurones parvalbuminergiques. Ainsi, les interneurones parvalbuminergiques peuvent contrôler temporellement l'excitabilité des neurones pyramidaux. En particulier, nous avons montré que l'acquisition de la mémoire de peur conditionnée dépend du recrutement d'un microcircuit désinhibiteur localisé dans le cortex auditif. En effet, au cours du conditionnement de peur, la présentation du choc électrique induit l'inhibition des interneurones parvalbuminergiques, ce qui a pour conséquence de désinhiber les neurones pyramidaux du cortex auditif et de permettre l’apprentissage du conditionnement de peur. Dans leur ensemble, ces données suggèrent que la désinhibition est un mécanisme important dans l'apprentissage et le traitement de l'information dans les circuits corticaux. Dans un second temps, nous avons montré que l'expression de la peur conditionnée requière l'inhibition phasique des interneurones parvalbuminergiques du cortex préfrontal médian. En effet, leur inhibition désinhibe les cellules pyramidales préfrontales et synchronise leur activité en réinitialisant les oscillations thêta locales. Ces résultats mettent en évidence deux mécanismes neuronaux complémentaires induits par les interneurones parvalbuminergiques qui coordonnent et organisent avec précision l’activité neuronale des neurones pyramidaux du cortex préfrontal pour contrôler l'expression de la peur conditionnée. Ensemble, nos données montrent que la désinhibition joue un rôle important dans les comportements de peur en permettant l’association entre des informations comportementalement pertinentes, en sélectionnant les éléments spécifiques du circuit et en orchestrant l'activité neuronale des cellules pyramidales
Learning and memory processes are controlled by specific neuronal circuits and elements. Numerous recent reports highlighted the important role of cortical circuits in the regulation of fear behaviour, however, the anatomical and functional characteristics of their neuronal components remain largely unknown. During my thesis, we used single unit recordings and optogenetic manipulations of specific neuronal elements in behaving mice, to show that both the auditory cortex and the medial prefrontal cortex contain a disinhibitory microcircuit required respectively for the acquisition and the expression of conditioned fear memory. In both cases, parvalbumin-expressing interneurons constitute the central element of the circuit and are phasically inhibited during the presentation of the conditioned tone. From a functional point of view, we demonstrated that this inhibition induced the disinhibition of cortical pyramidal neurons by releasing the ongoing perisomatic inhibition mediated by parvalbumin-expressing interneurons onto pyramidal neurons. Thereby, this disinhibition allows the precise temporal regulation of pyramidal neurons excitability. In particular, we showed that the acquisition of associative fear memories depend on the recruitment of a disinhibitory microcircuit in the auditory cortex. Fear-conditioning-associated disinhibition in auditory cortex is driven by foot-shock-mediated inhibition of parvalbumin-expressing interneurons. Importantly, pharmacological or optogenetic blockade of pyramidal neuron disinhibition abolishes fear learning. Together, these data suggest that disinhibition is an important mechanism underlying learning and information processing in cortical circuits. Secondly, in the medial prefrontal cortex, we demonstrated that expression of fear behaviour is causally related to the phasic inhibition of prefrontal parvalbumin-expressing interneurons. Inhibition of parvalbumin-expressing interneuron activity disinhibits prefrontal pyramidal neurons and synchronizes their firing by resetting local theta oscillations, leading to fear expression. These results identify two complementary neuronal mechanisms both mediated by prefrontal parvalbumin-expressing interneurons that precisely coordinate and enhance the neuronal efficiency of prefrontal pyramidal neurons to drive fear expression. Together these data highlighted the important role played by neuronal disinhibition in fear behaviour by binding behavioural relevant information, selecting specific circuit elements and orchestrating pyramidal neurons activity
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Chang, Melissa McKenzie. "Secreted factors FGF and WNT in cortical interneuron specification." Thesis, New York University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3665119.

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Cortical Interneurons are an incredibly diverse population of locally connecting GABAergic inhibitory neurons. In rodents, cortical interneurons originate from the ventral telencephalon during embryogenesis, and migrate tangentially into the neocortex following their specification. Despite our understanding of the early patterning of the telencephalon, established through sonic hedgehog (SHH), fibroblast growth factor (FGF) signaling, and wingless-int (WNT) we still know very little about the downstream effectors responsible for establishing interneuron diversity. This work has aimed to elucidate the role of secreted morphogens in interneuron specification, specifically FGF and WNT.

I began by investigating the role of FGF signaling in the specification of cortical interneurons by targeting downstream effectors, a critical adaptor protein, and receptors for FGF signaling. In particular, I examined the role of two candidate transcription factors classically found downstream of FGF: Ets1 and Ets2. Previously identified by microarray as enriched in cortical interneurons at developmental timepoints, Ets1 and Ets2 single and double mutants had no obvious defects in interneuron specification as assessed by immunohistochemistry. Using both forebrain and interneuron specific Cre recombinase drivers, I also generated conditional knockouts of the adaptor protein FRS2α, which is critical for FGF signaling through the MAP kinase and PI3 kinase signaling pathways (Hadari et al, 2001). Interestingly, pan-forebrain loss of FRS2α, failed to replicate the phenotype of forebrain removal of FGF receptors 1, 2 and 3. Similarly, interneuron specific removal of FRS2α, did not affect interneuron migration or fate. Additionally, through a complex set of genetic crosses, I generated an interneuron specific triple knockout of FGFRs 1, 2, and 3; this animal also did not exhibit any gross interneuron specification defects. These results together suggest that the development of cortical interneurons is likely not regulated by FGF signaling, at least not after their initial specification.

Previous work in the developing spinal cord has shown that cell identity can be conferred by exposure to diffusible morphogen gradients. Despite previous attempts, delineation of cell types by morphogen gradient in a "spinal cord" fashion has not yet been discovered in the forebrain. We have discovered a novel rostral-caudal regionality within the medial ganglionic eminence (MGE) that delineates the specification of the two main classes of cortical interneuron subtypes based on their exposure to a non-canonical WNT signaling gradient. Caudally located MGE progenitors receiving high levels of WNT signaling give rise to cortical interneurons labeled by somatostatin (SST). Parvalbumin (PV) expressing basket cells, in contrast, originate primarily from the most rostral region of the MGE, and do not signal highly through WNT pathways. Interestingly, canonical WNT signaling through β-catenin is not required for this process. WNT signals transmitted via cleavage of the intracellular domain of the non-canonical WNT receptor RYK, however, are sufficient to drive interneuron progenitors to a SST fate.

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Dupper, Amy Contole. "Altered cortical calbindin-immunoreactive interneuron populations associated with schizophrenia." Kent State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=kent1381416068.

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9

Jin, Xiaoming. "Dendritic development of GABAergic cortical interneurons revealed by biolistic transfection with GFP." Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2626.

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Thesis (Ph. D.)--West Virginia University, 2002.
Title from document title page. Document formatted into pages; contains vii, 218 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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10

Leclerq, Pascale. "Quantitative post-mortem study of cortical interneurons in chronic schizophrenia." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300445.

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Books on the topic "Interneurone cortical"

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Gallerani, Nicholas Edmund. The spatial distribution of cortical interneurons: The role of clustered protocadherins. [New York, N.Y.?]: [publisher not identified], 2021.

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Traub, Roger D. Fast oscillations in cortical circuits. Cambridge, Mass: MIT Press, 1999.

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Zecevic, Nada, Zsófia Maglóczky, and Filip Barinka, eds. At The Top of the Interneuronal Pyramid – Calretinin Expressing Cortical Interneurons. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-708-8.

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Cauli, Bruno, Yoshiyuki Kubota, and Ludovic Tricoire, eds. Cortical NO interneurons: from embryogenesis to functions. Frontiers Media SA, 2014. http://dx.doi.org/10.3389/978-2-88919-175-8.

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Traub, Roger D., John G. R. Jefferys, and Miles A. Whittington. Fast Oscillations in Cortical Circuits. MIT Press, 1999.

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Ziemann, Ulf. Pharmacology of TMS measures. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0013.

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This article discusses various aspects of the pharmacology of transcranial magnetic stimulator (TMS) measures. TMS measures reflect axonal, or excitatory or inhibitory synaptic excitability in distinct interneuron circuits. TMS measures can be employed to study the effects of a drug with unknown or multiple modes of action, and hence to determine its main mode of action at the systems level of the motor cortex. TMS experiments can also study acute drug effects that may be different from chronic drug effects. TMS or repetitive TMS may induce changes in endogenous neurotransmitter or neuromodulator systems. This allows for the study of neurotransmission along defined neuronal projections in health and disease. This article describes pharmacological experiments that have characterized the physiology of TMS measures of motor cortical excitability. Pharmacological challenging of TMS measures has opened a broad window into human cortical physiology.
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Mason, Peggy. From Movement to Action. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0023.

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Tracts descending from motor control centers in the brainstem and cortex target motor interneurons and in select cases motoneurons. The mechanisms and constraints of postural control are elaborated and the effect of body mass on posture discussed. Feed-forward reflexes that maintain posture during standing and other conditions of self-motion are described. The role of descending tracts in postural control and the pathological posturing is described. Pyramidal (corticospinal and corticobulbar) and extrapyramidal control of body and face movements is contrasted. Special emphasis is placed on cortical regions and tracts involved in deliberate control of facial expression; these pathways are contrasted with mechanisms for generating emotional facial expressions. The signs associated with lesions of either motoneurons or motor control centers are clearly detailed. The mechanisms and presentation of cerebral palsy are described. Finally, understanding how pre-motor cortical regions generate actions is used to introduce apraxia, a disorder of action.
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Book chapters on the topic "Interneurone cortical"

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Miyoshi, Goichi, Robert P. Machold, and Gord Fishell. "Specification of GABAergic Neocortical Interneurons." In Cortical Development, 89–126. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54496-8_5.

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Murakami, Fujio, Daisuke Tanaka, Mitsutoshi Yanagida, and Emi Yamazaki. "Intracortical Multidirectional Migration of Cortical Interneurons." In Cortical Development: Genes and Genetic Abnormalities, 116–29. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470994030.ch9.

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Cuomo, Dario, Paola Platania, Giuseppina Martella, Graziella Madeo, Giuseppe Sciamanna, Annalisa Tassone, and Antonio Pisani. "Cholinergic Interneuron and Parkinsonism." In Cortico-Subcortical Dynamics in Parkinson¿s Disease, 1–11. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-252-0_7.

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Fishell, Gordon. "Perspectives on the Developmental Origins of Cortical Interneuron Diversity." In Cortical Development: Genes and Genetic Abnormalities, 21–44. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470994030.ch3.

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Geiger, J. R. P., A. Roth, B. Taskin, and P. Jonas. "Glutamate-Mediated Synaptic Excitation of Cortical Interneurons." In Ionotropic Glutamate Receptors in the CNS, 363–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-08022-1_11.

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Maroof, Asif, and Stewart Anderson. "The Origins and Specification of Cortical Interneurons." In Developmental Plasticity of Inhibitory Circuitry, 13–26. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-1243-5_2.

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Murakami, Fujio. "Cell Migration Analysis of Cortical Interneurons After Electroporation." In Electroporation Methods in Neuroscience, 81–92. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2459-2_6.

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Cook, Kieona, and Stewart A. Anderson. "Genesis and Migration of Cerebral Cortical Inhibitory Interneurons: An Overview." In Neuroscience in the 21st Century, 291–305. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-88832-9_186.

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Cook, Kieona, and Stewart A. Anderson. "Genesis and Migration of Cerebral Cortical Inhibitory Interneurons: An Overview." In Neuroscience in the 21st Century, 1–15. New York, NY: Springer New York, 2022. http://dx.doi.org/10.1007/978-1-4614-6434-1_186-1.

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Braz, João M., and Allan I. Basbaum. "Intraspinal Transplantation of Precursors of Cortical GABAergic Interneurons to Treat Neuropathic Pain." In Neuromethods, 159–70. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2039-7_9.

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Conference papers on the topic "Interneurone cortical"

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Pendyam, Sandeep, Dongbeom Kim, Gregory J. Quirk, and Satish S. Nair. "Acquisition of Fear and Extinction in Lateral Amygdala: A Modeling Study." In ASME 2010 Dynamic Systems and Control Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/dscc2010-4218.

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The lateral nucleus of amygdala (LA) is known to be a critical storage site for conditioned fear memory. Synaptic plasticity at auditory inputs to the dorsal LA (LAd) is critical for the formation and storage of auditory fear memories. Recent evidence suggests that two different cell populations (transient- and long-term plastic cells) are present in LAd and are responsible for fear learning. However, the mechanisms involved in the formation and storage of fear are not well understood. As an extension of previous work, a biologically realistic computational model of the LAd circuitry is developed to investigate these mechanisms. The network model consists of 52 LA pyramidal neurons and 13 interneurons. Auditory and somatosensory information reaches LA from both thalamic and cortical inputs. The model replicated the tone responses observed in the two LAd cell populations during conditioning and extinction. The model provides insights into the role of thalamic and cortical inputs in fear memory formation and storage.
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Martini, Lorenzo, Roberta Bardini, and Stefano Di Carlo. "Meta-Analysis of cortical inhibitory interneurons markers landscape and their performances in scRNA-seq studies." In 2021 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2021. http://dx.doi.org/10.1109/bibm52615.2021.9669888.

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