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1

Liu, Tao, Tsugumi Fujita, and Eiichi Kumamoto. "Acetylcholine and norepinephrine mediate GABAergic but not glycinergic transmission enhancement by melittin in adult rat substantia gelatinosa neurons." Journal of Neurophysiology 106, no. 1 (2011): 233–46. http://dx.doi.org/10.1152/jn.00838.2010.

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GABAergic and glycinergic inhibitory synaptic transmissions in substantia gelatinosa (SG; lamina II of Rexed) neurons of the spinal dorsal horn play an important role in regulating nociceptive transmission from the periphery. It has not yet been well known whether each of the inhibitory transmissions plays a distinct role in the regulation. We report an involvement of neurotransmitters in GABAergic but not glycinergic transmission enhancement produced by the PLA2 activator melittin, where the whole-cell patch-clamp technique is applied to the SG neurons of adult rat spinal cord slices. Glycine
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2

Zhu, Ping Jun, and Vincent A. Chiappinelli. "Nicotine Modulates Evoked GABAergic Transmission in the Brain." Journal of Neurophysiology 82, no. 6 (1999): 3041–45. http://dx.doi.org/10.1152/jn.1999.82.6.3041.

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The effects of nicotine on evoked GABAergic synaptic transmission were examined using whole cell recordings from neurons of the lateral spiriform nucleus in embryonic chick brain slices. All synaptic activities were abolished by the GABAA receptor antagonist, bicuculline (20 μM). Under voltage-clamp with KCl-filled pipettes (holding potential −70 mV), nicotine (0.1–1.0 μM) increased the frequency of spontaneous GABAergic currents in a dose-dependent manner. Nicotine enhanced electrically evoked GABAergic transmission only at relatively low concentrations of 50–100 nM (but not 25 nM), which app
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3

Donato, Roberta, and Andrea Nistri. "Relative Contribution by GABA or Glycine to Cl−-Mediated Synaptic Transmission on Rat Hypoglossal Motoneurons In Vitro." Journal of Neurophysiology 84, no. 6 (2000): 2715–24. http://dx.doi.org/10.1152/jn.2000.84.6.2715.

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The relative contribution by GABA and glycine to synaptic transmission of motoneurons was investigated using an hypoglossus nucleus slice preparation from neonatal rats. Spontaneous, miniature, or electrically evoked postsynaptic currents (sPSCs, mPSCs, ePSCs, respectively) mediated by glycine or GABA were recorded under whole cell voltage clamp after blocking excitatory glutamatergic transmission with kynurenic acid. The overall majority of Cl−-mediated sPSCs was glycinergic, while only one-third was GABAergic; 70 ± 10% of mPSCs were glycinergic while 22 ± 8% were GABAergic. Tetrodotoxin (TTX
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4

Rao, G. Prasad. "Anxiety Disorders and Gabaergic Transmission." Indian Journal of Psychological Medicine 28, no. 1 (2006): 5–6. http://dx.doi.org/10.1177/0975156420060101.

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5

Sergeeva, Olga A. "GABAergic transmission in hepatic encephalopathy." Archives of Biochemistry and Biophysics 536, no. 2 (2013): 122–30. http://dx.doi.org/10.1016/j.abb.2013.04.005.

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6

Gafurov, Boris, and Suzanne B. Bausch. "GABAergic transmission facilitates ictogenesis and synchrony between CA3, hilus, and dentate gyrus in slices from epileptic rats." Journal of Neurophysiology 110, no. 2 (2013): 441–55. http://dx.doi.org/10.1152/jn.00679.2012.

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The impact of regional hippocampal interactions and GABAergic transmission on ictogenesis remain unclear. Cortico-hippocampal slices from pilocarpine-treated epileptic rats were compared with controls to investigate associations between seizurelike events (SLE), GABAergic transmission, and neuronal synchrony within and between cortico-hippocampal regions. Multielectrode array recordings revealed more prevalent hippocampal SLE in epileptic tissue when excitatory transmission was enhanced and GABAergic transmission was intact [removal of Mg2+ (0Mg)] than when GABAergic transmission was blocked [
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7

Schubert, Timm, Daniel Kerschensteiner, Erika D. Eggers, et al. "Development of Presynaptic Inhibition Onto Retinal Bipolar Cell Axon Terminals Is Subclass-Specific." Journal of Neurophysiology 100, no. 1 (2008): 304–16. http://dx.doi.org/10.1152/jn.90202.2008.

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Synaptic integration is modulated by inhibition onto the dendrites of postsynaptic cells. However, presynaptic inhibition at axonal terminals also plays a critical role in the regulation of neurotransmission. In contrast to the development of inhibitory synapses onto dendrites, GABAergic/glycinergic synaptogenesis onto axon terminals has not been widely studied. Because retinal bipolar cells receive subclass-specific patterns of GABAergic and glycinergic presynaptic inhibition, they are a good model for studying the development of inhibition at axon terminals. Here, using whole cell recording
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8

Vázquez-Gómez, Elizabeth, Andy Hernández-Abrego, Jassiel Mejía-Piedras, and Jesús García-Colunga. "Regulation of Hippocampal GABAergic Transmission by Fluoxetine and Its Metabolite Norfluoxetine." Receptors 3, no. 1 (2024): 1–12. http://dx.doi.org/10.3390/receptors3010001.

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Major depression is related to dysfunction of the GABAergic pathway. Interestingly, the antidepressant fluoxetine modifies GABAergic neurotransmission in human and animal models of depression. However, the effects of norfluoxetine (the main metabolite of fluoxetine) on GABAergic neurotransmission have not yet been studied. Therefore, we explored whether fluoxetine and/or norfluoxetine may regulate GABAergic transmission and whether these substances interact with GABAA receptors in hippocampal CA1 stratum radiatum interneurons. For these purposes, we recorded the firing profile, GABAergic spont
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9

Rubi, Lena, and Jean-Marc Fritschy. "Increased GABAergic transmission in neuropeptide Y-expressing neurons in the dopamine-depleted murine striatum." Journal of Neurophysiology 123, no. 4 (2020): 1496–503. http://dx.doi.org/10.1152/jn.00059.2020.

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As the main input nucleus of the basal ganglia, the striatum plays a central role in planning, control, and execution of movement and motor skill learning. More than 90% of striatal neurons, so-called medium spiny neurons (MSN), are GABAergic projection neurons, innervating primarily the substantia nigra pars reticulata or the globus pallidus internus. The remaining neurons are GABAergic and cholinergic interneurons, synchronizing and controlling striatal output by reciprocal connections with MSN. Besides prominent local cholinergic influence, striatal function is globally regulated by dopamin
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10

Petukhova, Elena, Daria Ponomareva, Karin Rustler, Burkhard Koenig, and Piotr Bregestovski. "Action of the Photochrome Glyght on GABAergic Synaptic Transmission in Mouse Brain Slices." International Journal of Molecular Sciences 23, no. 18 (2022): 10553. http://dx.doi.org/10.3390/ijms231810553.

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Glyght is a new photochromic compound described as an effective modulator of glycine receptors at heterologous expression, in brain slices and in zebrafish larvae. Glyght also caused weak inhibition of GABAA-mediated currents in a cell line expressing α1/β2/γ2 GABAA receptors. However, the effects of Glyght on GABAergic transmission in the brain have not been analysed, which does not allow a sufficiently comprehensive assessment of the effects of the compound on the nervous system. Therefore, in this study using whole-cell patch-clamp recording, we analysed the Glyght (100 µM) action on evoked
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11

Jo, Young-Hwan, and Lorna W. Role. "Cholinergic Modulation of Purinergic and GABAergic Co-Transmission at In Vitro Hypothalamic Synapses." Journal of Neurophysiology 88, no. 5 (2002): 2501–8. http://dx.doi.org/10.1152/jn.00352.2002.

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The lateral hypothalamus (LH) is an important center for the integration of autonomic and limbic information and is implicated in the modulation of visceral motor and sensory pathways, including those underlying feeding and arousal behaviors. LH neurons in vitro release both ATP and GABA. The control of ATP and GABA co-transmission in LH may underlie the participation of LH in basic aspects of arousal and reinforcement. LH neurons receive cholinergic input from the pedunculopontine and laterodorsal tegmental nuclei as well as from cholinergic interneurons within the LH per se. This study prese
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12

Okada, Motohiro, and Kouji Fukuyama. "Interaction between Mesocortical and Mesothalamic Catecholaminergic Transmissions Associated with NMDA Receptor in the Locus Coeruleus." Biomolecules 10, no. 7 (2020): 990. http://dx.doi.org/10.3390/biom10070990.

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Noncompetitive N-methyl-D-aspartate/glutamate receptor (NMDAR) antagonists contribute to the pathophysiology of schizophrenia and mood disorders but improve monoaminergic antidepressant-resistant mood disorder and suicidal ideation. The mechanisms of the double-edged sword clinical action of NMDAR antagonists remained to be clarified. The present study determined the interaction between the NMDAR antagonist (MK801), α1 adrenoceptor antagonist (prazosin), and α2A adrenoceptor agonist (guanfacine) on mesocortical and mesothalamic catecholaminergic transmission, and thalamocortical glutamatergic
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13

Nieto Mendoza, Elizabeth, and Elizabeth Hernández Echeagaray. "Dopaminergic Modulation of Striatal Inhibitory Transmission and Long-Term Plasticity." Neural Plasticity 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/789502.

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Dopamine (DA) modulates glutamatergic synaptic transmission and its plasticity in the striatum; however it is not well known how DA modulates long-term plasticity of striatal GABAergic inhibitory synapses. This work focused on the analysis of both dopaminergic modulation of inhibitory synapses and the synaptic plasticity established between GABAergic afferents to medium spiny neurons (MSNs). Our results showed that low and high DA concentrations mainly reduced the amplitude of inhibitory synaptic response; however detailed analysis of the D1 and D2 participation in this modulation displayed a
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14

Kauer, J. A., and L. L. McMahon. "Depressing transmission in GABAergic hippocampal neurons." Molecular Psychiatry 2, no. 6 (1997): 434–36. http://dx.doi.org/10.1038/sj.mp.4000283.

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15

Burket, Jessica A., Maria R. Urbano, and Stephen I. Deutsch. "Sugarcoated Perineuronal Nets Regulate “GABAergic” Transmission." Clinical Neuropharmacology 40, no. 3 (2017): 120–30. http://dx.doi.org/10.1097/wnf.0000000000000209.

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16

Saitow, Fumihito. "Modulation of Cerebellar GABAergic Synaptic Transmission." Nihon Ika Daigaku Igakkai Zasshi 5, no. 3 (2009): 152–58. http://dx.doi.org/10.1272/manms.5.152.

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17

Zhan, Yang. "Harnessing GABAergic Transmission for Slow Oscillations." Neuroscience Bulletin 32, no. 5 (2016): 501–2. http://dx.doi.org/10.1007/s12264-016-0058-1.

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18

Sebe, Joy Y., Erika D. Eggers, and Albert J. Berger. "Differential Effects of Ethanol on GABAA and Glycine Receptor-Mediated Synaptic Currents in Brain Stem Motoneurons." Journal of Neurophysiology 90, no. 2 (2003): 870–75. http://dx.doi.org/10.1152/jn.00119.2003.

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Ethanol potentiates glycinergic synaptic transmission to hypoglossal motoneurons (HMs). This effect on glycinergic transmission changes with postnatal development in that juvenile HMs (P9–13) are more sensitive to ethanol than neonate HMs (P1–3). We have now extended our previous study to investigate ethanol modulation of synaptic GABAA receptors (GABAARs), because both GABA and glycine mediate inhibitory synaptic transmission to brain stem motoneurons. We tested the effects of ethanol on GABAergic and glycinergic miniature inhibitory postsynaptic currents (mIPSCs) recorded from neonate and ju
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19

Ehrlich, David E., Steven J. Ryan, Rimi Hazra, Ji-Dong Guo, and Donald G. Rainnie. "Postnatal maturation of GABAergic transmission in the rat basolateral amygdala." Journal of Neurophysiology 110, no. 4 (2013): 926–41. http://dx.doi.org/10.1152/jn.01105.2012.

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Many psychiatric disorders, including anxiety and autism spectrum disorders, have early ages of onset and high incidence in juveniles. To better treat and prevent these disorders, it is important to first understand normal development of brain circuits that process emotion. Healthy and maladaptive emotional processing involve the basolateral amygdala (BLA), dysfunction of which has been implicated in numerous psychiatric disorders. Normal function of the adult BLA relies on a fine balance of glutamatergic excitation and GABAergic inhibition. Elsewhere in the brain GABAergic transmission change
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20

Donato, Roberta, and Andrea Nistri. "Differential Short-Term Changes in GABAergic or Glycinergic Synaptic Efficacy on Rat Hypoglossal Motoneurons." Journal of Neurophysiology 86, no. 2 (2001): 565–74. http://dx.doi.org/10.1152/jn.2001.86.2.565.

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Using whole cell patch-clamp recording from hypoglossal motoneurons of a neonatal rat brain slice preparation, we investigated short-term changes in synaptic transmission mediated by GABA or glycine. In 1.5 mM extracellular Ca2+[Ca2+]o, pharmacologically isolated GABAergic or glycinergic currents were elicited by electrical stimulation of the reticular formation. At low stimulation frequency, glycinergic currents were larger and faster than GABAergic ones. GABAergic currents were strongly facilitated by pulse trains at 5 or 10 Hz without apparent depression. This phenomenon persisted after pha
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21

Li, Ke Y., Yan-zhong Guan, Kresimir Krnjević, and Jiang H. Ye. "Propofol Facilitates Glutamatergic Transmission to Neurons of the Ventrolateral Preoptic Nucleus." Anesthesiology 111, no. 6 (2009): 1271–78. http://dx.doi.org/10.1097/aln.0b013e3181bf1d79.

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Background There is much evidence that the sedative component of anesthesia is mediated by gamma-aminobutyric acid type A (GABA(A)) receptors on hypothalamic neurons responsible for arousal, notably in the tuberomammillary nucleus. These GABA(A) receptors are targeted by gamma-aminobutyric acid-mediated (GABAergic) neurons in the ventrolateral preoptic area (VLPO): When these neurons become active, they inhibit the arousal-producing nuclei and induce sleep. According to recent studies, propofol induces sedation by enhancing VLPO-induced synaptic inhibition, making the target cells more respons
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22

Saitow, Fumihito, Shin'Ichiro Satake, Junko Yamada та Shiro Konishi. "β-Adrenergic Receptor-Mediated Presynaptic Facilitation of Inhibitory GABAergic Transmission at Cerebellar Interneuron-Purkinje Cell Synapses". Journal of Neurophysiology 84, № 4 (2000): 2016–25. http://dx.doi.org/10.1152/jn.2000.84.4.2016.

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Norepinephrine (NE) has been shown to elicit long-term facilitation of GABAergic transmission to rat cerebellar Purkinje cells (PCs) through β-adrenergic receptor activation. To further examine the locus and adrenoceptor subtypes involved in the NE-induced facilitation of GABAergic transmission, we recorded inhibitory postsynaptic currents (IPSCs) evoked by focal stimulation with paired-pulse (PP) stimuli from PCs in rat cerebellar slices by whole cell recordings and analyzed the PP ratio of the IPSC amplitude. NE increased the IPSC amplitude with a decease in the variance of the PP ratio, whi
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23

Jeong, Hyo-Jin, Il-Sung Jang, Junichi Nabekura, and Norio Akaike. "Adenosine A1 Receptor-Mediated Presynaptic Inhibition of GABAergic Transmission in Immature Rat Hippocampal CA1 Neurons." Journal of Neurophysiology 89, no. 3 (2003): 1214–22. http://dx.doi.org/10.1152/jn.00516.2002.

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In the mechanically dissociated rat hippocampal CA1 neurons with native presynaptic nerve endings, namely “synaptic bouton” preparation, the purinergic modulation of spontaneous GABAergic miniature inhibitory postsynaptic currents (mIPSCs) was investigated using whole-cell recording mode under the voltage-clamp conditions. In immature neurons, adenosine (10 μM) reversibly decreased GABAergic mIPSC frequency without affecting the mean current amplitude. The inhibitory effect of adenosine transmission was completely blocked by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 100 nM), a selective Α1 re
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24

Park, Chungwon, Xingxiang Chen, Chong-Li Tian, et al. "Unique dynamics and exocytosis properties of GABAergic synaptic vesicles revealed by three-dimensional single vesicle tracking." Proceedings of the National Academy of Sciences 118, no. 9 (2021): e2022133118. http://dx.doi.org/10.1073/pnas.2022133118.

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Maintaining the balance between neuronal excitation and inhibition is essential for proper function of the central nervous system. Inhibitory synaptic transmission plays an important role in maintaining this balance. Although inhibitory transmission has higher kinetic demands compared to excitatory transmission, its properties are poorly understood. In particular, the dynamics and exocytosis of single inhibitory vesicles have not been investigated, due largely to both technical and practical limitations. Using a combination of quantum dots (QDs) conjugated to antibodies against the luminal dom
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25

Dickinson, Robert, Sara L. M. de Sousa, William R. Lieb, and Nicholas P. Franks. "Selective Synaptic Actions of Thiopental and Its Enantiomers." Anesthesiology 96, no. 4 (2002): 884–92. http://dx.doi.org/10.1097/00000542-200204000-00016.

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Background There is conflicting evidence concerning the extent to which the intravenous general anesthetic thiopental acts by enhancing inhibitory gamma-aminobutyric acid-mediated (GABAergic) synaptic transmission or by inhibiting excitatory glutamatergic transmission. Yet there are remarkably few studies on the effects of thiopental on functional synapses. In addition, the degree of stereoselectivity of thiopental acting at synapses has yet to be tested. Methods The actions of thiopental and its enantiomers on GABAergic and glutamatergic synapses were investigated using voltage clamp techniqu
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26

Xiao, Zhaoyang, Pan-Yue Deng, Chuanxiu Yang, and Saobo Lei. "Modulation of GABAergic Transmission by Muscarinic Receptors in the Entorhinal Cortex of Juvenile Rats." Journal of Neurophysiology 102, no. 2 (2009): 659–69. http://dx.doi.org/10.1152/jn.00226.2009.

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Whereas the entorhinal cortex (EC) receives profuse cholinergic innervations from the basal forebrain and activation of cholinergic receptors has been shown to modulate the activities of the principal neurons and promote the intrinsic oscillations in the EC, the effects of cholinergic receptor activation on GABAergic transmission in this brain region have not been determined. We examined the effects of muscarinic receptor activation on GABAA receptor-mediated synaptic transmission in the superficial layers of the EC. Application of muscarine dose-dependently increased the frequency and amplitu
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27

Kirmse, Knut, Christian A. Hübner, Dirk Isbrandt, Otto W. Witte, and Knut Holthoff. "GABAergic Transmission during Brain Development: Multiple Effects at Multiple Stages." Neuroscientist 24, no. 1 (2017): 36–53. http://dx.doi.org/10.1177/1073858417701382.

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In recent years, considerable progress has been achieved in deciphering the cellular and network functions of GABAergic transmission in the intact developing brain. First, in vivo studies in non-mammalian and mammalian species confirmed the long-held assumption that GABA acts as a mainly depolarizing neurotransmitter at early developmental stages. At the same time, GABAergic transmission was shown to spatiotemporally constrain spontaneous cortical activity, whereas firm evidence for GABAergic excitation in vivo is currently missing. Second, there is a growing body of evidence indicating that d
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28

Nakamura, Michiko, Il-Sung Jang, Hitoshi Ishibashi, Shigenori Watanabe, and Norio Akaike. "Possible Roles of Kainate Receptors on GABAergic Nerve Terminals Projecting to Rat Substantia Nigra Dopaminergic Neurons." Journal of Neurophysiology 90, no. 3 (2003): 1662–70. http://dx.doi.org/10.1152/jn.01165.2002.

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GABAergic afferent inputs are thought to play an important role in the control of the firing pattern of substantia nigra pars compacta (SNc) dopaminergic neurons. We report here the actions of presynaptic kainite (KA) receptors in GABAergic transmission of rat SNc dopaminergic neurons. In mechanically dissociated rat SNc dopaminergic neurons attached with native presynaptic nerve terminals, GABAergic miniature inhibitory postsynaptic currents (mIPSCs) were recorded by use of conventional whole cell patch recording mode. In the voltage-clamp condition, KA (3 μM) significantly increased GABAergi
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29

Tyagarajan, Shiva K., Himanish Ghosh, Gonzalo E. Yévenes та ін. "Regulation of GABAergic synapse formation and plasticity by GSK3β-dependent phosphorylation of gephyrin". Proceedings of the National Academy of Sciences 108, № 1 (2010): 379–84. http://dx.doi.org/10.1073/pnas.1011824108.

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Postsynaptic scaffolding proteins ensure efficient neurotransmission by anchoring receptors and signaling molecules in synapse-specific subcellular domains. In turn, posttranslational modifications of scaffolding proteins contribute to synaptic plasticity by remodeling the postsynaptic apparatus. Though these mechanisms are operant in glutamatergic synapses, little is known about regulation of GABAergic synapses, which mediate inhibitory transmission in the CNS. Here, we focused on gephyrin, the main scaffolding protein of GABAergic synapses. We identify a unique phosphorylation site in gephyr
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30

Sebe, Joy Y., Johannes F. van Brederode, and Albert J. Berger. "Inhibitory Synaptic Transmission Governs Inspiratory Motoneuron Synchronization." Journal of Neurophysiology 96, no. 1 (2006): 391–403. http://dx.doi.org/10.1152/jn.00086.2006.

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Neurons within the intact respiratory network produce bursts of action potentials that cause inspiration or expiration. Within inspiratory bursts, activity is synchronized on a shorter timescale to generate clusters of action potentials that occur in a set frequency range and are called synchronous oscillations. We investigated how GABA and glycine modulate synchronous oscillations and respiratory rhythm during postnatal development. We recorded inspiratory activity from hypoglossal nerves using the in vitro rhythmically active mouse medullary slice preparation from P0–P11 mice. Average oscill
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31

Henderson, L. P., C. A. A. Penatti, B. L. Jones, P. Yang, and A. S. Clark. "Anabolic androgenic steroids and forebrain GABAergic transmission." Neuroscience 138, no. 3 (2006): 793–99. http://dx.doi.org/10.1016/j.neuroscience.2005.08.039.

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32

Schlichting, Joyce L. "Modulation and polytypic signaling in GABAergic transmission." Neurochemical Research 15, no. 2 (1990): 131–43. http://dx.doi.org/10.1007/bf00972203.

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33

Daghfous, Gheylen, François Auclair, Felix Clotten, et al. "GABAergic modulation of olfactomotor transmission in lampreys." PLOS Biology 16, no. 10 (2018): e2005512. http://dx.doi.org/10.1371/journal.pbio.2005512.

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Saitow, Fumihito, and Hidenori Suzuki. "GABAergic Synaptic Transmission in the Cerebellar Cortex." Nihon Ika Daigaku Igakkai Zasshi 3, no. 2 (2007): 56–57. http://dx.doi.org/10.1272/manms.3.56.

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35

Rabenstein, Michael, Nico Murr, Andreas Hermann, Arndt Rolfs, and Moritz J. Frech. "Alteration of GABAergic Input Precedes Neurodegeneration of Cerebellar Purkinje Cells of NPC1-Deficient Mice." International Journal of Molecular Sciences 20, no. 24 (2019): 6288. http://dx.doi.org/10.3390/ijms20246288.

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Niemann-Pick Disease Type C1 (NPC1) is a rare hereditary neurodegenerative disease belonging to the family of lysosomal storage disorders. NPC1-patients suffer from, amongst other symptoms, ataxia, based on the dysfunction and loss of cerebellar Purkinje cells. Alterations in synaptic transmission are believed to contribute to a pathological mechanism leading to the progressive loss of Purkinje cells observed in NPC1-deficient mice. With regard to inhibitory synaptic transmission, alterations of GABAergic synapses are described but functional data are missing. For this reason, we have examined
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Losi, Gabriele, Letizia Mariotti, and Giorgio Carmignoto. "GABAergic interneuron to astrocyte signalling: a neglected form of cell communication in the brain." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1654 (2014): 20130609. http://dx.doi.org/10.1098/rstb.2013.0609.

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GABAergic interneurons represent a minority of all cortical neurons and yet they efficiently control neural network activities in all brain areas. In parallel, glial cell astrocytes exert a broad control of brain tissue homeostasis and metabolism, modulate synaptic transmission and contribute to brain information processing in a dynamic interaction with neurons that is finely regulated in time and space. As most studies have focused on glutamatergic neurons and excitatory transmission, our knowledge of functional interactions between GABAergic interneurons and astrocytes is largely defective.
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Shimizu-Okabe, Chigusa, Shiori Kobayashi, Jeongtae Kim, et al. "Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord." International Journal of Molecular Sciences 23, no. 2 (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 foc
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38

Zheng, Zhongfan, Xiumei Zhang, Junqiang Liu, et al. "GABAergic synapses suppress intestinal innate immunity via insulin signaling in Caenorhabditis elegans." Proceedings of the National Academy of Sciences 118, no. 20 (2021): e2021063118. http://dx.doi.org/10.1073/pnas.2021063118.

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GABAergic neurotransmission constitutes a major inhibitory signaling mechanism that plays crucial roles in central nervous system physiology and immune cell immunomodulation. However, its roles in innate immunity remain unclear. Here, we report that deficiency in the GABAergic neuromuscular junctions (NMJs) of Caenorhabditis elegans results in enhanced resistance to pathogens, whereas pathogen infection enhances the strength of GABAergic transmission. GABAergic synapses control innate immunity in a manner dependent on the FOXO/DAF-16 but not the p38/PMK-1 pathway. Our data reveal that the insu
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39

Awatramani, Gautam B., Rostislav Turecek, and Laurence O. Trussell. "Staggered Development of GABAergic and Glycinergic Transmission in the MNTB." Journal of Neurophysiology 93, no. 2 (2005): 819–28. http://dx.doi.org/10.1152/jn.00798.2004.

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Maturation of some brain stem and spinal inhibitory systems is characterized by a shift from GABAergic to glycinergic transmission. Little is known about how this transition is expressed in terms of individual axonal inputs and synaptic sites. We have explored this issue in the rat medial nucleus of the trapezoid body (MNTB). Synaptic responses at postnatal days 5–7 (P5–P7) were small, slow, and primarily mediated by GABAA receptors. By P8–P12, an additional, faster glycinergic component emerged. At these ages, GABAA, glycine, or both types of receptors mediated transmission, even at single sy
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Baspinar, Emre, Martina Simonti, Hadi Srour, Mathieu Desroches, Daniele Avitabile, and Massimo Mantegazza. "GABAergic neurons can facilitate the propagation of cortical spreading depolarization: experiments in mouse neocortical slices and a novel neural field computational model." PLOS Computational Biology 21, no. 6 (2025): e1013099. https://doi.org/10.1371/journal.pcbi.1013099.

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Cortical spreading depolarization (CSD) is a wave of depolarization with local onset and extended propagation implicated in several pathological conditions. Its mechanisms have been extensively investigated, including our recent studies showing with experimental and computational approaches that the hyperactivity of GABAergic neurons’ can initiate migraine-related CSD because of spiking-generated extracellular potassium (K+) build-up. However, less is known about the role played by GABAergic neurons in CSD propagation. Here we studied mechanisms of CSD propagation, focusing on the role of GABA
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Uchida, Soko, Eiichiro Noda, Yasuhiro Kakazu, Yoshihito Mizoguchi, Norio Akaike, and Junichi Nabekura. "Allopregnanolone enhancement of GABAergic transmission in rat medial preoptic area neurons." American Journal of Physiology-Endocrinology and Metabolism 283, no. 6 (2002): E1257—E1265. http://dx.doi.org/10.1152/ajpendo.00049.2002.

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γ-Aminobutyric acid (GABA)-mediated transmission in the medial preoptic area (MPOA) of the hypothalamus plays an important role in functions such as sex steroid hormone dynamics and control of body temperature. The action of allopregnanolone, the primary metabolite of progesterone, on GABAergic transmission was investigated by employing patch clamp whole cell recording on acutely dissociated rat MPOA neurons with the functional connection of presynaptic terminals. Allopregnanolone enhanced spontaneous GABA release on the MPOA neurons and induced prolonged decay of miniature GABAergic-inhibitor
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Lüscher, Bernhard, and Hanns Möhler. "Brexanolone, a neurosteroid antidepressant, vindicates the GABAergic deficit hypothesis of depression and may foster resilience." F1000Research 8 (May 29, 2019): 751. http://dx.doi.org/10.12688/f1000research.18758.1.

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The GABAergic deficit hypothesis of depression states that a deficit of GABAergic transmission in defined neural circuits is causal for depression. Conversely, an enhancement of GABA transmission, including that triggered by selective serotonin reuptake inhibitors or ketamine, has antidepressant effects. Brexanolone, an intravenous formulation of the endogenous neurosteroid allopregnanolone, showed clinically significant antidepressant activity in postpartum depression. By allosterically enhancing GABAA receptor function, the antidepressant activity of allopregnanolone is attributed to an incr
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Hosseinzadeh Sahafi, Oveis, Maryam Sardari, Sakineh Alijanpour, and Ameneh Rezayof. "Shared Mechanisms of GABAergic and Opioidergic Transmission Regulate Corticolimbic Reward Systems and Cognitive Aspects of Motivational Behaviors." Brain Sciences 13, no. 5 (2023): 815. http://dx.doi.org/10.3390/brainsci13050815.

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The functional interplay between the corticolimbic GABAergic and opioidergic systems plays a crucial role in regulating the reward system and cognitive aspects of motivational behaviors leading to the development of addictive behaviors and disorders. This review provides a summary of the shared mechanisms of GABAergic and opioidergic transmission, which modulate the activity of dopaminergic neurons located in the ventral tegmental area (VTA), the central hub of the reward mechanisms. This review comprehensively covers the neuroanatomical and neurobiological aspects of corticolimbic inhibitory
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Gomes, Francisco Isaac Fernandes, Maria Gerusa Brito Aragão, Mirna Marques Bezerra, and Hellíada Vasconcelos Chaves. "GABAergic transmission and modulation of anxiety: A review on molecular aspects." Brazilian Journal of Biological Sciences 6, no. 12 (2019): 9–16. http://dx.doi.org/10.21472/bjbs.061202.

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Stress responses activate protective mechanisms to achieve homeostasis, but they can be detrimental when such responses become maladaptive. Anxiety relates to risk assessment of a potential threat and involves uncertainty regarding the anticipation of a threatening situation and it dampers quality of life. Gamma-Aminobutyric Acid (GABA) is the major inhibitory system in the central nervous system and plays a key role in the regulation of neuronal transmission in the brain, affecting many physiological and psychological processes. This mini-review aims to summarize key points concerned with the
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Tang, Bo, Jiali Tang та Yuguang Huang. "Dexmedetomidine Reduces Presynaptic γ-Aminobutyric Acid Release and Prolongs Postsynaptic Responses in Layer 5 Pyramidal Neurons in the Primary Somatosensory Cortex of Mice". International Journal of Molecular Sciences 26, № 5 (2025): 1931. https://doi.org/10.3390/ijms26051931.

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Dexmedetomidine (DEX) exhibits notable sedative, analgesic, and anesthetic-sparing properties. While growing evidence suggests these effects are linked to the modulation of γ-aminobutyric acid (GABA) system, the precise pre- and postsynaptic mechanisms of DEX action on cortical GABAergic signaling remain unclear. In this study, we applied whole-cell patch-clamp recording to investigate the impact of DEX on GABAergic transmission in layer 5 pyramidal neurons of the mouse primary somatosensory cortex. We recorded spontaneous inhibitory postsynaptic currents (sIPSCs), miniature IPSCs (mIPSCs), an
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Hernández-Vázquez, Fabiola, Julieta Garduño, and Salvador Hernández-López. "GABAergic modulation of serotonergic neurons in the dorsal raphe nucleus." Reviews in the Neurosciences 30, no. 3 (2019): 289–303. http://dx.doi.org/10.1515/revneuro-2018-0014.

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Abstract The dorsal raphe nucleus (DRN), located in the brainstem, is involved in several functions such as sleep, temperature regulation, stress responses, and anxiety behaviors. This nucleus contains the largest population of serotonin expressing neurons in the brain. Serotonergic DRN neurons receive tonic γ-aminobutyric acid (GABA)inhibitory inputs from several brain areas, as well as from interneurons within the same nucleus. Serotonergic and GABAergic neurons in the DRN can be distinguished by their size, location, pharmacological responses, and electrophysiological properties. GABAergic
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Imbrosci, Barbara, and Thomas Mittmann. "Functional Consequences of the Disturbances in the GABA-Mediated Inhibition Induced by Injuriesin the Cerebral Cortex." Neural Plasticity 2011 (2011): 1–14. http://dx.doi.org/10.1155/2011/614329.

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Cortical injuries are often reported to induce a suppression of the intracortical GABAergic inhibition in the surviving, neighbouring neuronal networks. Since GABAergic transmission provides the main source of inhibition in the mammalian brain, this condition may lead to hyperexcitability and epileptiform activity of cortical networks. However, inhibition plays also a crucial role in limiting the plastic properties of neuronal circuits, and as a consequence, interventions aiming to reestablish a normal level of inhibition might constrain the plastic capacity of the cortical tissue. A promising
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Baba, Hiroshi, Peter A. Goldstein, Manabu Okamoto, et al. "Norepinephrine Facilitates Inhibitory Transmission in Substantia Gelatinosa of Adult Rat Spinal Cord (Part 2)." Anesthesiology 92, no. 2 (2000): 485. http://dx.doi.org/10.1097/00000542-200002000-00031.

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Background It has been reported previously that norepinephrine, when applied to the spinal cord dorsal horn, excites a subpopulation of dorsal horn neurons, presumably inhibitory interneurons. In the current study, the authors tested whether norepinephrine could activate inhibitory interneurons, specifically those that are "GABAergic." Methods A transverse slice was obtained from a segment of the lumbar spinal cord isolated from adult male Sprague-Dawley rats. Whole-cell patch-clamp recordings were made from substantia gelatinosa neurons using the blind patch-clamp technique. The effects of no
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Jo, Young-Hwan. "Endogenous BDNF regulates inhibitory synaptic transmission in the ventromedial nucleus of the hypothalamus." Journal of Neurophysiology 107, no. 1 (2012): 42–49. http://dx.doi.org/10.1152/jn.00353.2011.

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Output from steroidogenic factor-1 (SF-1) neurons in the ventromedial nucleus of the hypothalamus (VMH) is anorexigenic. SF-1 neurons express brain-derived neurotrophic factor (BDNF) that contributes to the regulation of food intake and body weight. Here I show that regulation of GABAergic inputs onto SF-1 neurons by endogenous BDNF determines the anorexigenic outcome from the VMH. Single-cell RT-PCR analysis reveals that one-third of SF-1 neurons express BDNF and that only a subset of BDNF-expressing SF-1 neurons coexpresses the melanocortin receptor type 4. Whole cell patch-clamp analysis of
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Dunning, D. D., C. L. Hoover, I. Soltesz, M. A. Smith та D. K. O'Dowd. "GABAA Receptor–Mediated Miniature Postsynaptic Currents and α-Subunit Expression in Developing Cortical Neurons". Journal of Neurophysiology 82, № 6 (1999): 3286–97. http://dx.doi.org/10.1152/jn.1999.82.6.3286.

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Previous studies have described maturational changes in GABAergic inhibitory synaptic transmission in the rodent somatosensory cortex during the early postnatal period. To determine whether alterations in the functional properties of synaptically localized GABAAreceptors (GABAARs) contribute to development of inhibitory transmission, we used the whole cell recording technique to examine GABAergic miniature postsynaptic currents (mPSCs) in developing cortical neurons. Neurons harvested from somatosensory cortices of newborn mice showed a progressive, eightfold increase in GABAergic mPSC frequen
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