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Relevant bibliographies by topics / GABAergic

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Academic literature on the topic 'GABAergic'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 June 2023

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Journal articles on the topic "GABAergic"

1

Charvet, Christine J., Goran Šimić, Ivica Kostović, Vinka Knezović, Mario Vukšić, Mirjana Babić Leko, Emi Takahashi, Chet C. Sherwood, Marnin D. Wolfe, and Barbara L. Finlay. "Coevolution in the timing of GABAergic and pyramidal neuron maturation in primates." Proceedings of the Royal Society B: Biological Sciences 284, no. 1861 (August 30, 2017): 20171169. http://dx.doi.org/10.1098/rspb.2017.1169.

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The cortex of primates is relatively expanded compared with many other mammals, yet little is known about what developmental processes account for the expansion of cortical subtype numbers in primates, including humans. We asked whether GABAergic and pyramidal neuron production occurs for longer than expected in primates than in mice in a sample of 86 developing primate and rodent brains. We use high-resolution structural, diffusion MR scans and histological material to compare the timing of the ganglionic eminences (GE) and cortical proliferative pool (CPP) maturation between humans, macaques, rats, and mice. We also compare the timing of post-neurogenetic maturation of GABAergic and pyramidal neurons in primates (i.e. humans, macaques) relative to rats and mice to identify whether delays in neurogenesis are concomitant with delayed post-neurogenetic maturation. We found that the growth of the GE and CPP are both selectively delayed compared with other events in primates. By contrast, the timing of post-neurogenetic GABAergic and pyramidal events (e.g. synaptogenesis) are predictable from the timing of other events in primates and in studied rodents. The extended duration of GABAergic and pyramidal neuron production is associated with the amplification of GABAerigc and pyramidal neuron numbers in the human and non-human primate cortex.

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2

Crawley, Jacqueline N. "GABAergic Antidepressants." Contemporary Psychology: A Journal of Reviews 32, no. 10 (October 1987): 876–77. http://dx.doi.org/10.1037/026430.

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MINCHIN, M., A. WHITE, and K. LLOYD. "GABAERGIC ANTIDEPRESSANTS." Behavioural Pharmacology 3, Supplement (April 1992): 3. http://dx.doi.org/10.1097/00008877-199204001-00001.

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4

Gottlieb, David I. "GABAergic Neurons." Scientific American 258, no. 2 (February 1988): 82–89. http://dx.doi.org/10.1038/scientificamerican0288-82.

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5

Cristofolini, Michela, Roberto De Luca, Anne Venner, Loris Ferrari, Kevin Grace, Patrick Fuller, and Elda Arrigoni. "074 Basal Forebrain GABAergic Neurons Promote Arousal by Disinhibiting the Orexin Neurons via Local GABAergic Interneurons." Sleep 44, Supplement_2 (May 1, 2021): A31. http://dx.doi.org/10.1093/sleep/zsab072.073.

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Abstract Introduction Optogenetic and chemogenetic studies have shown that activation of basal forebrain (BF) GABAergic neurons rapidly wakes up mice from non-REM (NREM) sleep. These wake-promoting responses have been attributed to BF GABAergic neurons projecting to the cerebral cortex and more specifically to the inhibition of cortical fast-spiking interneurons. Tracing studies have however found that BF GABAergic neurons also densely innervate the lateral hypothalamus (LH) perifornical area, although the role of this pathway in behavioral state control remains mostly unexplored. Methods We conducted in vivo and in vitro optogenetic studies. We selectively expressed channelrhodopsin-2 (ChR2) in BF GABAergic neurons by injecting a cre-dependent viral vector encoding for ChR2 into the BF of VGAT-cre mice. We photostimulated the BF GABAergic input to the LH with optical fibers placed into the LH of EEG instrumented mice. For in vitro recordings we expressed ChR2 in BF GABAergic neurons and we fluorescently labeled orexin or LH GABAergic neurons. We recorded in brain slices from identified orexin neurons or GABA neurons while photostimulating the BF GABAergic input. Results Optogenetic stimulation of the BF GABAergic fibers in the LH produced rapid arousals from NREM sleep. The same stimulation however did not wake up the mice if they were in REM sleep. We conducted additional studies in brain slices to identify the postsynaptic neurons in the LH targeted by the BF GABAergic input. We found that while optogenetic stimulation of the BF GABAergic input did not produce opto-evoked synaptic responses in the orexin neurons, it produced short-latency opto-evoked inhibitory postsynaptic currents (IPSCs) in LH GABAergic neurons. These opto-evoked IPSCs were GABAA receptor-mediated and were maintained in tetrodotoxin (TTX) indicating monosynaptic connectivity. We have previously found that orexin neurons are inhibited by local LH GABAergic neurons. Our hypothesis is that these local GABAergic interneurons are the target of the BF GABAergic arousal input. Conclusion BF GABAergic neurons drive arousal through projections to the LH. We propose that this arousal response is due to the inhibition of local GABAergic interneurons which in turn disinhibit the LH wake-promoting neurons including the orexin neurons. Support (if any) NS091126 and HL149630

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Uusisaari, M., and T. Knöpfel. "GABAergic synaptic communication in the GABAergic and non-GABAergic cells in the deep cerebellar nuclei." Neuroscience 156, no. 3 (October 2008): 537–49. http://dx.doi.org/10.1016/j.neuroscience.2008.07.060.

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Wenner, Peter. "Mechanisms of GABAergic Homeostatic Plasticity." Neural Plasticity 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/489470.

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Homeostatic plasticity ensures that appropriate levels of activity are maintained through compensatory adjustments in synaptic strength and cellular excitability. For instance, excitatory glutamatergic synapses are strengthened following activity blockade and weakened following increases in spiking activity. This form of plasticity has been described in a wide array of networks at several different stages of development, but most work and reviews have focussed on the excitatory inputs of excitatory neurons. Here we review homeostatic plasticity of GABAergic neurons and their synaptic connections. We propose a simplistic model for homeostatic plasticity of GABAergic components of the circuitry (GABAergic synapses onto excitatory neurons, excitatory connections onto GABAergic neurons, cellular excitability of GABAergic neurons): following chronic activity blockade there is a weakening of GABAergic inhibition, and following chronic increases in network activity there is a strengthening of GABAergic inhibition. Previous work on GABAergic homeostatic plasticity supports certain aspects of the model, but it is clear that the model cannot fully account for some results which do not appear to fit any simplistic rule. We consider potential reasons for these discrepancies.

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Frank, J. G., H. S. Jameson, C. Gorini, and D. Mendelowitz. "Mapping and Identification of GABAergic Neurons in Transgenic Mice Projecting to Cardiac Vagal Neurons in the Nucleus Ambiguus Using Photo-Uncaging." Journal of Neurophysiology 101, no. 4 (April 2009): 1755–60. http://dx.doi.org/10.1152/jn.91134.2008.

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The neural control of heart rate is determined primarily by the activity of preganglionic parasympathetic cardiac vagal neurons (CVNs) originating in the nucleus ambiguus (NA) in the brain stem. GABAergic inputs to CVNs play an essential role in determining the activity of these neurons including a robust inhibition during each inspiratory burst. The origin of GABAergic innervation has yet to be determined however. A transgenic mouse line expressing green florescent protein (GFP) in GABAergic cells was used in conjunction with caged glutamate to identify both clusters and individual GABAergic neurons that evoke inhibitory GABAergic synaptic responses in CVNs. Transverse slices were taken with CVNs patch-clamped in the whole cell configuration. Sections containing both the pre-Botzinger complex as well as the calamus scriptorius were divided into ∼90 quadrants, each 200 × 200 μm and were sequentially photostimulated. Inhibitory post synaptic currents (IPSCs) were recorded in CVNs after a 5-ms photostimulation of 50 μM caged glutamate. The four areas that contained GABAergic cells projecting to CVNs were 200 μm medial, 400 μm medial, 200 μm ventral, and 1,200 μm dorsal and 1,000 μm medial to patched CVNs. Once foci of GABAergic cells projecting to CVNs were determined, photostimulation of individual GABAergic neurons was conducted. The results from this study suggest that GABAergic cells located in four specific areas project to CVNs, and that these cells can be individually identified and stimulated using photouncaging to recruit GABAergic neurotransmission to CVNs.

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Shimizu-Okabe, Chigusa, Shiori Kobayashi, Jeongtae Kim, Yoshinori Kosaka, Masanobu Sunagawa, Akihito Okabe, and Chitoshi Takayama. "Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord." International Journal of Molecular Sciences 23, no. 2 (January 13, 2022): 834. http://dx.doi.org/10.3390/ijms23020834.

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Gamma-aminobutyric acid (GABA) and glycine act as inhibitory neurotransmitters. Three types of inhibitory neurons and terminals, GABAergic, GABA/glycine coreleasing, and glycinergic, are orchestrated in the spinal cord neural circuits and play critical roles in regulating pain, locomotive movement, and respiratory rhythms. In this study, we first describe GABAergic and glycinergic transmission and inhibitory networks, consisting of three types of terminals in the mature mouse spinal cord. Second, we describe the developmental formation of GABAergic and glycinergic networks, with a specific focus on the differentiation of neurons, formation of synapses, maturation of removal systems, and changes in their action. GABAergic and glycinergic neurons are derived from the same domains of the ventricular zone. Initially, GABAergic neurons are differentiated, and their axons form synapses. Some of these neurons remain GABAergic in lamina I and II. Many GABAergic neurons convert to a coreleasing state. The coreleasing neurons and terminals remain in the dorsal horn, whereas many ultimately become glycinergic in the ventral horn. During the development of terminals and the transformation from radial glia to astrocytes, GABA and glycine receptor subunit compositions markedly change, removal systems mature, and GABAergic and glycinergic action shifts from excitatory to inhibitory.

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Bracci, Enrico, and Stefano Panzeri. "Excitatory GABAergic Effects in Striatal Projection Neurons." Journal of Neurophysiology 95, no. 2 (February 2006): 1285–90. http://dx.doi.org/10.1152/jn.00598.2005.

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The ability of synaptically released GABA to facilitate action potential generation in striatal projection neurons was studied in brain slices using current-clamp, gramicidin-perforated whole cell recordings. Evoked GABAergic postsynaptic potentials (PSPs) were pharmacologically isolated with ionotropic glutamate receptor antagonists. Subthreshold depolarizing current injections were paired with GABAergic PSPs at different intervals. GABAergic PSPs were able to convert current injection-induced depolarizations from subthreshold to suprathreshold, but only when they preceded the current injection by an appropriate interval; accordingly, action potentials were observed 4–140 ms after the onset of the GABAergic PSP, and their likelihood was maximal after 50–60 ms. The GABAergic excitatory effects were fully blocked by the GABAA receptor antagonist bicuculline. Appropriately timed GABA PSPs decreased the time taken by current injections to depolarize projection neurons, causing an apparent reduction in the spike threshold. In control solution, the ability of evoked PSPs (comprising both glutamatergic and GABAergic components) to reach spike threshold was often impaired by bicuculline. We conclude that GABAergic PSPs can exert excitatory effects on projection neurons and that this ability crucially depends on the timing between the GABAergic event and a concomitant depolarizing input.

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Dissertations / Theses on the topic "GABAergic"

1

Gabor, Ronnie. "GABAergic mechanisms in adrenal enzyme regulation." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=63939.

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Benini, Ruba Sayed. "GABAergic signalling in temporal lobe epilepsy." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111818.

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Earlier studies on temporal lobe epilepsy (TLE), by focusing on the anatomical and electrophysiological abnormalities of the hippocampus, have attributed a major role to this limbic structure in the process of epileptogenesis and seizure generation. Recently however, there has been increasing evidence from both animal and human studies that other limbic structures, including the subiculum, the entorhinal cortex (EC, perirhinal cortex (PC) as well as the amygdala, are possibly involved in the process of epileptogenesis. With the help of both acute and chronic models of limbic seizures, I have used an electrophysiological approach to gain more insight into the mechanisms through which these structures could participate in the establishment of hyperexcitable neuronal networks. Particularly, my investigations have focused on assessing the role played by the subiculum, the amygdala and the PC in epileptiform synchronization in vitro. My findings demonstrate that seizure-induced cell damage in chronically epileptic mice results in a change in limbic network interactions whereby EC ictogenesis is sustained via a reverberant EC-subiculum pathway ( Chapter 1). Furthermore, I have discovered that the subiculum, which holds an anatomically strategic position within the hippocampus, is capable of gating hippocampul output activity via a GABAA-receptor mediated mechanism (Chapter 2). My investigations in the amygdala have confirmed that this limbic structure contributes to epileptiform synchronization (Chapter 3). Moreover, using a chronic rat model of TLE, I have found novel evidence suggesting that alterations in inhibitory mechanisms play a role in the increased excitability of the lateral amygdalar nucleus (Chapter 4). Finally, my studies in chronically epileptic rats have also led to preliminary data signifying hyperexcitability of the PC as well alterations in the interactions between the amygdala and this cortical structure (Chapter 5).

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Cobb, Stuart Robert. "Synaptic interaction of hippocampal gabaergic neurones." Thesis, University of Oxford, 1996. http://ora.ox.ac.uk/objects/uuid:527682b7-2146-458a-b821-5dca9733e32f.

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Current concepts of hippocampal circuitry assume a large population of excitatory principal neurones whose activity is largely governed by a network of local-circuit GABAergic interneurones. The diversity of hippocampal local-circuit neurones and their synaptic control over principal cell activity was investigated in vitro, in order to define their synaptic connections and functional roles. Single and dual intracellular recordings were made from local-circuit neurones and pyramidal cells in area CA1 of the rat hippocampal slice. Interneurones were tentatively distinguished from pyramidal cells based on their firing as well as their membrane properties. Intracellular labelling of recorded cells with the marker biocytin revealed a diversity of cell types based on differential dendritic and axonal morphology and synaptic connections. The physiological data revealed that all types of interneurone tested evoked inhibitory postsynaptic potentials (IPSPs) in simultaneously recorded pyramidal cells. The IPSPs had fast rise and decay kinetics and the ones tested pharmacologically, were mediated by GABA_A receptors. Similarly, individual interneurones were also shown to innervate other local-circuit interneurones in addition to pyramidal cells, the evoked effects being qualitatively similar in both types of postsynaptic targets. The postsynaptic effect and functional role of one type of hippocampal interneurone, the basket cell, was investigated in greater detail. Basket cell-evoked IPSPs were reliable, but showed some frequency-dependent attenuation. Moreover, basket cell IPSPs were found to interact with intrinsic pyramidal cell conductances to elicit rebound depolarisations and facilitate action potential generation. More detailed investigation showed that basket and axo-axonic cells were particularly effective in entraining pyramidal cell firing and sub-threshold membrane potential oscillations. Through these powerfully tuned mechanisms, sub-types of local-circuit interneurone provide a powerful mechanism to synchronise the activity of pyramidal cells. These results demonstrate a remarkable diversity of GABAergic local-circuit neurones in the hippocampal CA1 area and suggest that specific subtypes of cell mediate different functions.

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Nasrallah, Fatma Faculty of Medicine UNSW. "A metabolic approach to the GABAergic system." Publisher:University of New South Wales, 2008. http://handle.unsw.edu.au/1959.4/43413.

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Here, we investigated the effects of modulation of the GABAergic system using a targeted neuropharmacological, 1H/13C NMR spectroscopy and metabolomic approach in Guinea pig cortical brain slices. The effects of exogenous GABA, agonists, antagonists and allosteric modulators at GABAA receptors were described and classified on the basis of metabolic activity; this corresponded to receptor location rather than pharmacology. The effects of agonists and antagonists at the GABAB receptor were described and classified into inhibitory and excitatory components, consistent with context dependent outcomes of receptor activity. Metabolic evidence for GABAC mediated activity in the cerebral cortex was identified for the first time indicating a strong role for this receptor in the control of neuronal activity. Inhibition of GABA uptake was examined using inhibitors of these transporters. The major effect of individual transporter subtype blockade was increased synaptic inhibition. The paradoxical activity of the GABA-transaminase inhibitor vigabatrin was resolved, with a direct demonstration of a single inhibitory mechanism mediated via this drug, via a mechanism also induced by antagonists at the GABAC receptor. These data were then integrated using multivariate statistics to identify 5 subclasses of activity which corresponded to receptor location (e.g. synaptic or extrasynaptic) rather than receptor pharmacology. This represents a novel and powerful new approach to the study of brain metabolism and the GABAergic system.

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Nicholson, Martin William. "Diazepam-dependent modulation of GABAergic inhibitory synapses." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10046265/.

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Diazepam is an allosteric modulator of GABAA receptors which potentiates GABAA receptor activity resulting in enhanced inhibitory synaptic transmission. Diazepam is used to treat anxiety, insomnia and seizures, however, its use is limited due to the development of tolerance. Here I show that prolonged treatment of cortical neurones with diazepam triggers endocytosis and subsequent downregulation of cell-surface GABAA receptors. Using pharmacological reagents, I have demonstrated that diazepam triggers PLC-dependent release of calcium from the endoplasmic reticulum which activates the phosphatase calcineurin resulting in dephosphorylation of the γ2 subunit of GABAA receptors and their endocytosis. This was elucidated using a combination of biochemical and cell biological approaches. In addition, I have developed HEK293 cell lines stably expressing various subtypes of GABAA receptors to investigate further diazepam and isoguvacine-dependent regulation of GABAA receptors. The same calcium-dependent signalling pathway that regulates cell-surface stability of GABAA receptors in neurones was found to operate in HEK293 cells. Subsequently, I focused on a key component of this signalling pathway; PLCδ1. Using biochemical techniques I have demonstrated that PLCδ1 binds directly to the GABAA receptor β3 subunit at two independent sites. This binding was confirmed by coimmunoprecipitation of PLCδ1 and GABAA receptors from cortical neuronal lysates. Interestingly, upon diazepam treatments, PLCδ1 was shown to dissociate from GABAA receptors, thus leading to mobilisation of calcium from the intracellular stores and activation of calcineurin. To assess how changes in cell-surface expression of GABAA receptors affect the stability of GABAergic synapses, I characterised the size and number of post-synaptic GABAA receptor clusters and the number of presynaptic GABA-releasing terminals following chronic diazepam treatment. I observed a reduction in the size and number of post-synaptic GABAA receptor clusters and a reduction in the number of GABA-releasing terminals. These data are consistent with the loss of cell-surface GABAA receptors following long-term treatments of cortical neurones with diazepam. These changes correlated with an increase in the expression of the early apoptosis marker, cleaved-caspase 3, in glutamatergic neurones suggesting indirect cytotoxic effects of diazepam treatments. The loss of inhibitory GABAergic synapses following chronic diazepam treatment may contribute to the well-known development of tolerance to these clinically important therapies for stress- and anxiety- related neurological disorders.

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Ma, Wenqian. "Dlx Gene Regulation of Zebrafish GABAergic Interneuron Development." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19970.

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Abstract The Dlx genes play an important role in the differentiation and migration of gamma-aminobutyric acid (GABA) interneurons of mice. GABAergic interneurons are born in the proliferative zones of the ventral telencephalon and migrate to the cortex early during mouse development. Single Dlx mutant mice show only subtle phenotypes. However, the migration of immature interneurons is blocked in the ventral telencephalon of Dlx1/Dlx2 double mutant mice leading to reduction of GABAergic interneurons in the cortex. Also, Dlx5/Dlx6 expression is almost entirely absent in the forebrain, most probably due to cross-regulatory mechanisms. In zebrafish, the role of dlx genes in GABAergic interneuron development is unknown. By injecting Morpholino, we double knocked down dlx1 and dlx2 genes in wildtype zebrafish to investigate the function of the two genes in zebrafish GABAergic interneuron development. By comparing different subsets of GABAergic interneuron development in wildtype and dlx1/2 morphant zebrafish forebrain, we found out that at 3dpf, 4dpf and 7dpf, double knockdown of dlx1 and dlx2 genes in zebrafish remarkably reduced the number of Calbindin-, Somatostatin- and Parvalbumin-positive GABAergic neurons, whereas the development of Calretinin-positive neurons is slightly affected. These results suggest that in zebrafish, dlx1a and dlx2a genes are important for the development of certain subtypes of GABAergic interneurons (Calbindin-, Somatostatin- and Parvalbumin-positive neurons) and may have minor influence on Calretinin-positive neuron development. This also suggests that different regulatory mechanisms are involved in the development of the different subtypes of GABAergic interneurons.

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Garden, Derek Leonard Frank. "GABAergic transmission in the perirhinal cortex in vitro." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274770.

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Huff, Courtney L. M. S. "MDMA and Glutamate: Implications for Hippocampal GABAergic Neurotoxicity." University of Cincinnati / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1460444662.

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Mabey, Jennifer Kei. "Synaptic Plasticity in GABAergic Inhibition of VTA Neurons." BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/5256.

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Past research has demonstrated that the motivational effects of opiates causes a change in ventral tegmental area (VTA) γ-amino butyric acid (GABA) subtype A receptor [GABA(A)R] complexes in opiate-dependent animals, which switch from a GABA-induced hyperpolarization of VTA GABA neurons to a GABA-induced depolarization. Previously shown in naïve animals, superfusion of ethanol (IC50 = 30 mM) and the GABA(A)R agonist muscimol (IC50 = 100 nM) decreased VTA GABA neuron firing rate in a dose-dependent manner. The aim of this study was to evaluate VTA GABA neuron excitability, GABA synaptic transmission to VTA GABA neurons, and a potential switch in GABA(A)R functionality produced by alcohol dependence. To accomplish these studies, we used standard whole-cell, perforated patch, and attached-cell mode electrophysiological techniques to evaluate chronic ethanol effects on VTA GABA neurons in CD-1 GAD GFP mice, which enable the visual identification of GABA neurons in the slice preparation. In order to more conclusively demonstrate synaptic plasticity in VTA neurons associated with alcohol dependence, three studies were proposed to elucidate the mechanism underlying the switch in GABA synaptic function with dependence. First, we evaluated the effects of withdrawal from chronic ethanol exposure on muscimol-induced inhibition of VTA GABA neuron firing rate. Second, we evaluated the effects of withdrawal from chronic ethanol exposure on GABA(A)R-mediated synaptic responses in VTA GABA neurons by looking at eIPSCs, and corresponding changes in VTA DA neuron firing rate. Third, we evaluated chloride reversal potentials in VTA GABA neurons using perforated patch recordings in VTA GABA neurons.Through these studies, we found that there was less sensitivity to muscimol in animals treated with ethanol versus air-exposed controls. However, it is yet to be shown more conclusively if VTA GABA neurons undergo a switch in GABA(A)R function with chronic ethanol.

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COLACI, FRANCESCO. "GABAergic synaptic protein dynamics measured by spectroscopic approaches." Doctoral thesis, Università degli studi di Genova, 2018. http://hdl.handle.net/11567/929825.

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The activity dependent adjustment of synaptic strength (synaptic plasticity) involves the reorganization of post-synaptic proteins. The fast diffusion of synaptic proteins has been shown to play an important role in such molecular rearrangements. Taking advantage of single particle tracking (SPT) and fluorescence recovery after photobleaching (FRAP) techniques, it has been demonstrated that during inhibitory long-term potentiation (iLTP) the scaffold protein gephyrin and GABAA receptors are accumulated and immobilized at post-synaptic inhibitory sites.

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Books on the topic "GABAergic"

1

L, Erdő Sándor, and Bowery N. G, eds. GABAergic mechanisms in the mammalian periphery. New York: Raven Press, 1986.

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2

Giovanni, Biggio, Concas Alessandra, and Costa Erminio, eds. GABAergic synaptic transmission: Molecular, pharmacological, and clinical aspects. New York: Raven Press, 1992.

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L, Alkon Daniel, and National Institute of Neurological and Communicative Disorders and Stroke, eds. Long-term transformation of an inhibitory into an excitatory GABAergic synaptic response. [Bethesda, Md.?: National Institute of Neurological and Communicative Disorders and Stroke, 1993.

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L, Alkon Daniel, and National Institute of Neurological and Communicative Disorders and Stroke, eds. Long-term transformation of an inhibitory into an excitatory GABAergic synaptic response. [Bethesda, Md.?: National Institute of Neurological and Communicative Disorders and Stroke, 1993.

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L, Alkon Daniel, and National Institute of Neurological and Communicative Disorders and Stroke, eds. Long-term transformation of an inhibitory into an excitatory GABAergic synaptic response. [Bethesda, Md.?: National Institute of Neurological and Communicative Disorders and Stroke, 1993.

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L, Alkon Daniel, and National Institute of Neurological and Communicative Disorders and Stroke., eds. Long-term transformation of an inhibitory into an excitatory GABAergic synaptic response. [Bethesda, Md.?: National Institute of Neurological and Communicative Disorders and Stroke, 1993.

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SanCartier, Nancy A. The role of the GABAergic system in the production of ultrasonic vocalization in rats. St. Catharines, Ont: Brock University, Dept. of Psychology, 2000.

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Buzsáki, G. Abstracts of papers presented at the 2006 meeting on the GABAergic system: December 6-December 9, 2006. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 2006.

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Giovanni, Biggio, Costa Erminio, and Capo Boi Conference on Neuroscience (4th : 1985 : Villasimius, Italy), eds. GABAergic transmission and anxiety. New York: Raven Press, 1986.

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10

Barberis, Andrea, and Alberto Bacci, eds. Plasticity of GABAergic Synapses. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-732-3.

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Book chapters on the topic "GABAergic"

1

Manji, Husseini K., Jorge Quiroz, R. Andrew Chambers, Anthony Absalom, David Menon, Patrizia Porcu, A. Leslie Morrow, et al. "GABAergic Transmission." In Encyclopedia of Psychopharmacology, 549. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1398.

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Rudolph, Uwe. "GABAergic System." In Encyclopedia of Molecular Pharmacology, 1–6. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_61-1.

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Rudolph, Uwe. "GABAergic System." In Encyclopedia of Molecular Pharmacology, 679–84. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57401-7_61.

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4

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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Avoli, Massimo. "GABAergic Mechanisms and Epileptic Discharges." In Neurotransmitters and Cortical Function, 187–205. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0925-3_12.

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6

Taniyama, K., N. Saito, S. Matsuyama, K. Takeda, and C. Tanaka. "GABAergic Mechanisms and Cardiovascular Function." In GABA Outside the CNS, 261–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76915-3_18.

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7

Sassoè-Pognetto, Marco. "Development of Glutamatergic and GABAergic Synapses." In Essentials of Cerebellum and Cerebellar Disorders, 155–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-24551-5_17.

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Schilling, Karl. "Specification and Development of GABAergic Interneurons." In Handbook of the Cerebellum and Cerebellar Disorders, 207–35. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-1333-8_11.

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Sassoè-Pognetto, Marco, and Annarita Patrizi. "Development of Glutamatergic and GABAergic Synapses." In Handbook of the Cerebellum and Cerebellar Disorders, 237–55. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-1333-8_12.

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White, Edward L. "GABAergic Inhibition in the Cerebral Cortex." In Cortical Circuits, 150–58. Boston, MA: Birkhäuser Boston, 1989. http://dx.doi.org/10.1007/978-1-4684-8721-3_6.

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Conference papers on the topic "GABAergic"

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Tsetsos, Konstantinos, Thomas Pfeffer, Christoffer Gahnström, and Tobias H. Donner. "GABAergic Competition Boosts the Irrationality of Protracted Decisions." In 2019 Conference on Cognitive Computational Neuroscience. Brentwood, Tennessee, USA: Cognitive Computational Neuroscience, 2019. http://dx.doi.org/10.32470/ccn.2019.1347-0.

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Fu, Peng, Yin Liu, Liang Zhu, Mengqi Wang, Weijie Zhang, Hequn Zhang, Anna Wang Roe, and Wang Xi. "Two-photon imaging of GABAergic and non-GABAergic neuronal calcium activity induced by infrared neural stimulation in awake mouse cortex." In Optogenetics and Optical Manipulation 2023, edited by Samarendra K. Mohanty, Anna W. Roe, and Shy Shoham. SPIE, 2023. http://dx.doi.org/10.1117/12.2657654.

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Xu, Qiuling, Fengyuan Bai, and Tao Liu. "GABAergic Neuron-related DNA Methylation Modification and Chronic Pain." In BIBE2021: The Fifth International Conference on Biological Information and Biomedical Engineering. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3469678.3469698.

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"Whole-genome analysis of epigenetic control of human GABAergic interneuron differentiation." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-064.

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LI, XIANGNING, GENG ZHU, WEI ZHOU, SHAOQUN ZENG, and QINGMING LUO. "CULTURE OF GABAERGIC NEURONS FROM TRANSGENIC MICE ON MULTI-ELECTRODE ARRAY." In Proceedings of the 6th International Conference on Photonics and Imaging in Biology and Medicine (PIBM 2007). WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812832344_0036.

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Wu, Qing, Ben Foote-Huth, Stephan Steidl, Hui Ye, and Wenbing Zhao. "EEG analysis reveals reduced seizure activity by optogenetic inhibition of GABAergic interneurons." In 2017 IEEE International Conference on Systems, Man and Cybernetics (SMC). IEEE, 2017. http://dx.doi.org/10.1109/smc.2017.8123184.

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Anunoby, Ifeoma, Vovanti Jones, Alexander Brown, and Carmen M. Cirstea. "Cortical tonic GABAergic inhibition – preliminary insights from MR Spectroscopy of subacute stroke." In 2020 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2020. http://dx.doi.org/10.1109/bibm49941.2020.9313112.

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Neman, Josh, John Termini, Claudia M. Kowolik, Amanda C. Hambrecht, Rahul Jandial, and Eugene Roberts. "Abstract A21: Human breast-to-brain metastases display GABAergic properties in the neural niche." In Abstracts: AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a21.

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"Alterations of glutamatergic/GABAergic systems during healthy aging and Alzheimer’s disease-like pathology in rats." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-613.

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Hirota, JA, W. Lu, and MD Inman. "GABAergic Signaling in Airway Epithelium Is Associated with Goblet Cell Metaplasia in Chronic Allergen Exposure Models." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4241.

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Reports on the topic "GABAergic"

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Bonci, Antonello. Plasticity of GABAergic Synapses in the Ventral Tegmental Area During Withdrawal from In Vivo Ethanol Administration. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407409.

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