Relevant bibliographies by topics / GABAergic transmissioni

Academic literature on the topic 'GABAergic transmissioni'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "GABAergic transmissioni"

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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 (July 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. Glycinergic but not GABAergic spontaneous inhibitory postsynaptic current (sIPSC) was increased in frequency and amplitude by melittin in the presence of nicotinic, muscarinic acetylcholine, and α1-adrenergic receptor antagonists (mecamylamine, atropine, and WB-4101, respectively). GABAergic transmission enhancement produced by melittin was unaffected by the 5-hydroxytryptamine 3 receptor and P2X receptor antagonists (ICS-205,930 and pyridoxalphosphate-6-azophenyl-2′,4′-disulphonic acid, respectively). Nicotinic and muscarinic acetylcholine receptor agonists [(−)-nicotine and carbamoylcholine, respectively] and norepinephrine, as well as melittin, increased GABAergic sIPSC frequency and amplitude. A repeated application of (−)-nicotine, carbamoylcholine, and norepinephrine, but not melittin, at an interval of 30 min produced a similar transmission enhancement. These results indicate that melittin produces the release of acetylcholine and norepinephrine, which activate (nicotinic and muscarinic) acetylcholine and α1-adrenergic receptors, respectively, resulting in GABAergic but not glycinergic transmission enhancement in SG neurons. The desensitization of a system leading to the acetylcholine and norepinephrine release is slow in recovery. This distinction in modulation between GABAergic and glycinergic transmissions may play a role in regulating nociceptive transmission.
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Zhu, Ping Jun, and Vincent A. Chiappinelli. "Nicotine Modulates Evoked GABAergic Transmission in the Brain." Journal of Neurophysiology 82, no. 6 (December 1, 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 approximate the concentrations of nicotine in the blood produced by cigarette smoking. At higher concentrations nicotine had either no effect (0.25 μM) or diminished (0.5–1.0 μM) evoked GABAergic neurotransmission. Nicotine had no significant effect on the postsynaptic current induced by exogenous GABA (30–50 μM). These data imply that nicotine levels attained in smokers are sufficient to enhance evoked GABAergic transmission in the brain, and that this effect is most likely mediated through activation of presynaptic nicotinic receptors.
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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 (December 1, 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) application dramatically reduced the frequency (and slightly the amplitude) of GABAergic events without changing frequency or amplitude of glycinergic sPSCs. These results indicate that, unlike spontaneous GABAergic transmission, glycine-mediated neurotransmission was essentially independent of network activity. There was a consistent difference in the kinetics of GABAergic and glycinergic responses as GABAergic events had significantly slower rise and decay times than glycinergic ones. Such a difference was always present whenever sPSCs, mPSCs, or ePSCs were measured. Finally, GABAergic and glycinergic mPSCs were differentially modulated by activation of glutamate metabotropic receptors (mGluRs), which are abundant in the hypoglossus nucleus. In fact, the broad-spectrum mGluR agonist (±)-1-aminocyclopentane- trans-1,3-dicarboxylic acid (50 μM), which in control solution increased the frequency of both GABAergic and glycinergic sPSCs, enhanced the frequency of glycinergic mPSCs only. These results indicate that on brain stem motoneurons, Cl−-mediated synaptic transmission is mainly due to glycine rather than GABA and that GABAergic and glycinergic events differ in terms of kinetics and pharmacological sensitivity to mGluR activation or TTX.
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Rao, G. Prasad. "Anxiety Disorders and Gabaergic Transmission." Indian Journal of Psychological Medicine 28, no. 1 (January 2006): 5–6. http://dx.doi.org/10.1177/0975156420060101.

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Sergeeva, Olga A. "GABAergic transmission in hepatic encephalopathy." Archives of Biochemistry and Biophysics 536, no. 2 (August 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 (July 15, 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 [removal of Mg2+ + bicuculline methiodide (0Mg+BMI)]. When activity within individual regions was analyzed, spectral and temporal slow oscillation/SLE correlations and cross-correlations were highest within the hilus of epileptic tissue during SLE but were similar in 0Mg and 0Mg+BMI. GABAergic facilitation of spectral “slow” oscillation and ripple correlations was most prominent within CA3 of epileptic tissue during SLE. When activity between regions was analyzed, slow oscillation and ripple coherence was highest between the hilus and dentate gyrus as well as between the hilus and CA3 of epileptic tissue during SLE and was significantly higher in 0Mg than 0Mg+BMI. High 0Mg-induced SLE cross-correlations between the hilus and dentate gyrus as well as between the hilus and CA3 were reduced or abolished in 0Mg+BMI. SLE cross-correlation lag measurements provided evidence for a monosynaptic connection from the hilus to the dentate gyrus during SLE. Findings implicate the hilus as an oscillation generator, whose impact on other cortico-hippocampal regions is mediated by GABAergic transmission. Data also suggest that GABAA receptor-mediated transmission facilitates back-propagation from CA3/hilus to the dentate gyrus and that this back-propagation augments SLE in epileptic hippocampus.
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Schubert, Timm, Daniel Kerschensteiner, Erika D. Eggers, Thomas Misgeld, Martin Kerschensteiner, Jeff W. Lichtman, Peter D. Lukasiewicz, and Rachel O. L. Wong. "Development of Presynaptic Inhibition Onto Retinal Bipolar Cell Axon Terminals Is Subclass-Specific." Journal of Neurophysiology 100, no. 1 (July 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 methods and transgenic mice in which subclasses of retinal bipolar cells are labeled, we determined the temporal sequence and patterning of functional GABAergic and glycinergic input onto the major subclasses of bipolar cells. We found that the maturation of GABAergic and glycinergic synapses onto the axons of rod bipolar cells (RBCs), on-cone bipolar cells (on-CBCs) and off-cone bipolar cells (off-CBCs) were temporally distinct: spontaneous chloride-mediated currents are present in RBCs earlier in development compared with on- and off-CBC, and RBCs receive GABAergic and glycinergic input simultaneously, whereas in off-CBCs, glycinergic transmission emerges before GABAergic transmission. Because on-CBCs show little inhibitory activity, GABAergic and glycinergic events could not be pharmacologically distinguished for these bipolar cells. The balance of GABAergic and glycinergic input that is unique to RBCs and off-CBCs is established shortly after the onset of synapse formation and precedes visual experience. Our data suggest that presynaptic modulation of glutamate transmission from bipolar cells matures rapidly and is differentially coordinated for GABAergic and glycinergic synapses onto distinct bipolar cell subclasses.
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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 (April 1, 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 dopamine (DA) from the nigrostriatal pathway. Little is known about whether DA depletion, as occurs in Parkinson’s disease, affects the activity of striatal interneurons. Here we focused on neuropeptide Y (NPY)-expressing interneurons, which are among the major subgroups of GABAergic interneurons in the striatum. We investigated the effects of striatal DA depletion on GABAergic transmission in NPY interneurons by electrophysiologically recording GABAergic spontaneous (s) and miniature (m) inhibitory postsynaptic currents (IPSCs) in identified NPY interneurons in slices from 6-hydroxydopamine (6-OHDA)- and vehicle-injected transgenic NPY-humanized Renilla green fluorescent protein (hrGFP) mice with the whole cell patch-clamp technique. We report a significant increase in sIPSC and mIPSC frequency as well as the occurrence of giant synaptic and burst sIPSCs in the 6-OHDA group, suggesting changes in GABAergic circuit activity and synaptic transmission. IPSC kinetics remained unchanged, pointing to mainly presynaptic changes in GABAergic transmission. These results show that chronic DA depletion following 6-OHDA injection causes activity-dependent and -independent increase of synaptic GABAergic inhibition onto striatal NPY interneurons, confirming their involvement in the functional impairments of the DA-depleted striatum. NEW & NOTEWORTHY Neuropeptide Y (NPY) interneurons regulate the function of striatal projection neurons and are upregulated upon dopamine depletion in the striatum. Here we investigated how dopamine depletion affects NPY circuits and show electrophysiologically that it leads to the occurrence of giant synaptic and burst GABAergic spontaneous inhibitory postsynaptic currents (IPSCs) and to an activity-independent increase in GABAergic miniature IPSC frequency in NPY neurons. We suggest that degeneration of dopaminergic terminals in the striatum causes functional changes in striatal GABAergic function.
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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 (September 12, 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 GABAergic inhibitory postsynaptic currents (eIPSCs) in mice hippocampal slices. Two populations of cells were found: the first responded by reducing the GABAergic eIPSCs’ amplitude, whereas the second showed no sensitivity to the compound. Glyght did not affect the ionic currents’ amplitude induced by GABA application, suggesting the absence of action on postsynaptic GABA receptors. Additionally, Glyght had no impact on the paired-pulse modulation of GABAergic eIPSCs, indicating that Glyght does not modulate the neurotransmitter release mechanisms. In the presence of strychnine, an antagonist of glycine receptors, the Glyght effect on GABAergic synaptic transmission was absent. Our results suggest that Glyght can modulate GABAergic synaptic transmission via action on extrasynaptic glycine receptors.
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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 (November 1, 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 presents evidence for nicotinic acetylcholine receptor (nAChR)-mediated enhancement of GABAergic, but not of purinergic, transmission despite the co-transmission of ATP and GABA at LH synapses in vitro. Facilitation of GABAergic transmission by nicotine is inhibited by antagonists of (αβ)*-containing nAChRs, but is unaffected by an α7-selective antagonist, consistent with a nAChR-mediated enhancement of GABA release mediated by non-α7-containing nAChRs. Activation of muscarinic ACh receptors enhances the release of ATP while concomitantly depressing GABAergic transmission. The independent modulation of ATP/GABAergic transmission may provide a new level of synaptic flexibility in which individual neurons utilize more than one neurotransmitter but retain independent control over their synaptic activity.
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Dissertations / Theses on the topic "GABAergic transmissioni"

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MAURI, MARIO. "Cellule staminali mesenchimali: potenziali modulatori del sistema nervoso centrale." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/39835.

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Bone marrow-derived mesenchymal stem cells (MSCs) account for a small population of cells of the non-hematopoietic component of bone marrow. MSCs are multipotent stem cells endowed with neurotrophic potential combined to immunological properties, making them a promising therapeutic tool for neurodegenerative disorders. Although the mechanisms by which they act are still largely unknown, trans-differentiation, paracrine and autocrine actions have been hypothesized. Here we focus on the study of the effects exerted by rat MSCs on CNS neurons and oligodendrocytes by using a simplified in vitro co-culture system that precludes any direct contact between different cell types. The analysis of hippocampal synaptogenesis, synaptic vesicle recycling and electrical activity show that MSCs by themselves, efficiently support morphological and functional neuronal differentiation. Our observations demonstrate that MSCs selectively and directly increased hippocampal GABAergic presynapses and inhibitory transmission. In fact, this increment correlated to a higher expression of the potassium/chloride KCC2 cotransporter and to an enhancement of both the frequency and the amplitude of mIPSC and sIPSC. The decreased of GABA synapses following the treatment with a widely used Trk-neurotrophin receptor blocker, K252a, and the more specific TrkB receptor bodies prompt for the involvement of the brain derived neurotrophic factor (BDNF) in mediating such effects. The involvement of this neurotrophin is also strengthened by test ELISA on the culture medium collected from MSC-neuron co-cultures in which an higher BDNF concentration was detected, when compared to astrocyte-neuron co-cultures. The results obtained indicate that MSC-secreted factors induce glial-dependent neuronal survival and directly trigger an augmented GABAergic transmission in hippocampal cultures, highlighting a new effect by which MSCs could cooperate in CNS repair. Additionally, MSCs have been described to improve the clinical course of some demyelinating pathologies and to promote tissue repair through immunological mechanisms and neuroprotective effects. Following these evidences we performed in vitro and in vivo experiments to assess whether MSCs exert their actions through the support of oligodendrocytes (OLs), the myelinating CNS cells, and participate in the regulation of their proliferation and maturation. Through the analysis of specific proteins typically used as markers of the different stages of proliferation, maturation and differentiation (specifically, the membrane glycoprotein O4, the proteoglycan NG2 and myelin basic protein MBP, respectively), it has been noticed that MSCs are capable to prolong the proliferation phase of OPCs and also to anticipate OL differentiation, with respect to standard astrocyte/OL co-cultures. Moreover we investigated a possible molecular mechanism underlying these phenomena focusing on neurotrophin pathways. Trk receptors activation was analyzed in order to find out a possible role of neurotrophins in MSC-mediated effects on OLs, as it happens in neuronal cultures. We focused on the changes in the phosphorylation level of ERK (Extracellular signaling-regulated kinases), one of the activated effectors by TrK receptors. Our observations show that, in OLs co-cultured with MSCs, ERK is highly phosphorylated with respect to astrocyte/OL co-cultures, suggesting a MSC-induced activation of the pathways regulated by this protein. These data, although preliminary, suggest that MSCs positively act on the regulation of proliferation and maturation of OLs and, due to the observed effects on the regulation of synaptogenesis (see above), make these cells an interesting model for the identification of molecules involved in MSC neuroprotective processes. This may open new therapeutic approaches in the treatment of neurodegenerative diseases involving not only a synaptic imbalance, as it happens in various forms of epilepsy, but also in demyelinating diseases. Thus, in this research project, we aimed at characterising the molecular mechanisms underlying MSC actions that could participate in the recovery of neurological disorders or demyelinating pathologies.
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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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Mellor, Jack Robert. "Electrophysiological investigation of the mechanisms underlying GABAergic synaptic transmission." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624122.

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Fan, Kai Yoon. "GABAergic synaptic transmission, plasticity and integration in the subthalamic nucleus." Thesis, University of Sheffield, 2012. http://etheses.whiterose.ac.uk/3167/.

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Diana, Marco Alberto. "Charakterisierung von einer retrograden Modulation inhibitorischer synaptischer Transmission im Kleinhirn der Ratte." Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=971021988.

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Asseri, Khalid. "Effects of AMBD and isovaline on GABAergic transmission in thalamic neurons." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/35078.

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In central neurons, the endogenous amino acid γ-aminobutyric acid (GABA) exerts synaptic inhibition mediated through ionotropic GABAA-, or metabotropic GABAB-receptors. These receptors exist on both pre- and postsynaptic membranes. The synthetic structural analogues of GABA, 6-aminomethyl-3-methyl-4H-1,2,4-benzothiadiazine-1,1-dioxide (AMBD) and R-isovaline have received little study on synaptic inhibition in the mammalian thalamus. AMBD was originally proposed as a taurine antagonist whereas R-isovaline is a non-biogenic amino acid that increases postsynaptic K⁺ conductance of thalamocortical neurons. The aim of this work was to assess the prediction that AMBD and R-isovaline would affect presynaptic release of GABA onto neurons of ventrobasal nuclei. AMBD and R-isovaline were applied by perfusion of thalamic slices obtained from juvenile Sprague-Dawley rats (P10 -13). During whole-cell patch clamp recording from thalamocortical neurons, we voltage-clamped neurons at a holding potential of -70 mV. Miniature inhibitory postsynaptic currents (mIPSCs) were recorded in the presence of tetrodotoxin (TTX). Kynurenic acid and internal Cs⁺ were used to block postsynaptic glutamate receptors and K⁺ conductances. We used the GABAA antagonist bicuculline to identify GABAergic mIPSCs, without affecting a possible presynaptic GABAB-component. Applied alone at 250 μM, AMBD had no effect on the passive and active membrane properties of neurons. In the range of 10 µM to 1 mM, AMBD had no effect on amplitude or decay time constant of GABAergic mIPSCs. Acting with an IC₅₀ of 232 μM, AMBD reversibly reduced the frequency of GABAergic mIPSCs. The above observations implied that AMBD reduced presynaptic release of GABA. In a range of 25 to 200 µM, R-isovaline had no effect on the holding current or frequency, amplitude and decay time constant of GABAergic mIPSCs. Hence, R-isovaline did not affect release of GABA and did not affect receptors on nerve terminals. In summary, AMBD reversibly decreased the presynaptic release of GABA, likely by an action on nerve terminals while having no effects on postsynaptic membrane properties that could account for the reduced frequency of GABAergic mIPSCs. The exact mechanism whereby AMBD decreased GABA release remains unclear. R-isovaline had no effect on GABA release in ventrobasal nuclei.
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Cao, Zhiwen, and 曹志文. "GABAergic transmission in developmental establishment of a gravity-related spatial reference." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47151304.

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In rats, the subnuclei of the inferior olive (IO) and thalamus exist topographic spatial representation to sinusoidal horizontal linear translations along either the antero-posterior or interaural direction. To examine the effect of GABAergic neurotransmission within the vestibular nucleus on the establishment of gravity-related topographic spatial representation in relay station of the central vestibular pathway, GABAA receptor antagonist bicuculline was used to chronically perturb GABA transmission within the vestibular nucleus of postnatal rats. Implantation of bicuculline-loaded or saline-loaded Elvax slice onto the dorsal surface of vestibular nucleus was performed in P1 rats which were allowed to recover into adulthood. Fos protein expression was used as an indicator to identify central neurons responsive to horizontal linear accelerations. In stationary or labyrinthectomized rats, Fos-immunoreactive (ir) neurons were either absent or sporadically scattered throughout the IO and thalamic subnuclei, indicating that the Fos expression in these neural area was otolithic in origin. In the saline control group, Fos expression induced by horizontal antero-posterior linear acceleration was observed in both the IO and thalamus. Responsive IO subnuclei include β subnucleus of IO and dorsomedial cell column while those in the thalamus include central medial nucleus, paracentral nucleus, mediodorsal nucleus, central lateral nucleus, zona incerta and subparafascicular nucleus of thalamus. For-ir neurons responsive to horizontal interaural linear acceleration were found in those IO subnuclei and thalamic subnuclei. When compared with the saline-treated group, the number of Fos-ir IO neurons responsive to horizontal linear acceleration was significantly lower in adult rats perturbed with bicuculline at P1. Besides, the pattern of Fos expression in both the IO and thalamus was altered in adult rats pretreated with bicuculline. In the utricle-related thalamic subnuclei, the postnatal time when Fos-ir neurons were found triggered by otolithic stimulation was delayed and the number of these Fos-ir neurons was fewer in the bicuculline-treated group than those in the saline-treated group. To investigate whether there exists a critical period for postnatal establishment of topographic spatial representation in the IO and thalamus, implantation of bicuculline-loaded Elvax slice onto the vestibular nucleus was carried out in P14 rats. The topographic spatial representation in IO and thalamus of those rats were unchanged as compared with adult rats pretreated with saline at P14. These results indicate that the GABAergic neuronal circuit in the vestibular nucleus plays an important role in postnatal establishment of topographic spatial representation in the central vestibular system. Most importantly, we documented the occurrence of a postnatal critical period (between P1 and P14) during which GABAergic transmission regulated the formation of a gravity-related spatial framework in the brain.
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Ma, Ying [Verfasser]. "Effects of enhancing GABAergic transmission on sleep-associated memory consolidation / Ying Ma." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2012. http://d-nb.info/1021331007/34.

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Yuan, Ning. "DISTINCT MODULATORY EFFECTS OF DOPAMINE ON EXCITATORY CHOLINERGIC AND INHIBITORY GABAERGIC SYNAPTIC TRANSMISSION IN DROSOPHILA." Ohio University / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1149001533.

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Seiscio, Andrew R. "The Role of GABAergic Transmission in Mediation of Striatal Local Field Potentials (LFPs)." Digital Archive @ GSU, 2008. http://digitalarchive.gsu.edu/psych_theses/63.

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In the present study, electrophysiological and behavioral effects of compromised Gama-Aminobutyric Acid (GABAergic) transmission were investigated in adult Rhesus macaque monkeys (N=2). GABAergic transmission was perturbed in the putamen by administration of a GABAa receptor antagonist, gabazine (10 and 500 μM), via a microdialysis-local field potential (MD-LFP) probe. Resultant changes in striatal local field potentials (LFPs) were measured as an assay of synchrony. Gabazine perfusion evoked discrete large amplitude spikes in LFPs in all subjects, and the frequency and shape of individual spikes were concentration-dependent. Pre-treatment with the GABAa receptor agonist, muscimol (100 μM) blocked the gabazine-induced events, confirming a role for GABAa receptors in the effects. Behavioral manifestations of gabazine treatment were observed only at the maximum concentration. Unusual facial movements suggested aberrant electrical activity was propagated from striatum to motor cortex, perhaps via reentrant circuits. These results support a role for GABAergic transmission in segregation of striatal circuits.
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Books on the topic "GABAergic transmissioni"

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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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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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Biggio, Giovanni, and Alessandra Concas. Gabaergic Synaptic Transmission: Molecular, Pharmacological, and Clinical Aspects (Advances in Biochemical Psychopharmacology). Raven Pr, 1992.

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Giovanni, Giuseppe Di, Adam C. Errington, and Vincenzo Crunelli. Extrasynaptic GABAA Receptors. Springer, 2014.

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Giovanni, Giuseppe Di, Adam C. Errington, and Vincenzo Crunelli. Extrasynaptic GABAA Receptors. Springer, 2016.

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Giovanni, Giuseppe Di, Adam C. Errington, and Vincenzo Crunelli. Extrasynaptic GABAA Receptors. Springer, 2014.

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Book chapters on the topic "GABAergic transmissioni"

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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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Gaiarsa, Jean-Luc, and Yezekiel Ben-Ari. "Ontogenesis of Gabaergic and Glutamatergic Synaptic Transmission." In Advances in Behavioral Biology, 45–54. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/0-306-47612-6_5.

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Bartos, Marlene, Jonas-Frederic Sauer, Imre Vida, and Ákos Kulik. "Fast and Slow GABAergic Transmission in Hippocampal Circuits." In Springer Series in Computational Neuroscience, 159–200. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-99103-0_5.

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Bartos, Marlene, Jonas-Frederic Sauer, Imre Vida, and Ákos Kulik. "Fast and Slow GABAergic Transmission in Hippocampal Circuits." In Hippocampal Microcircuits, 129–61. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0996-1_5.

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Sipilä, Sampsa T., and Kai K. Kaila. "GABAergic Transmission and Neuronal Network Events During Hippocampal Development." In Developmental Plasticity of Inhibitory Circuitry, 115–36. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-1243-5_7.

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Dieudonné, Stéphane, and Marco Alberto Diana. "Postsynaptic Determinants of Inhibitory Transmission at Mixed GABAergic/Glycinergic Synapses." In Co-Existence and Co-Release of Classical Neurotransmitters, 1–27. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-09622-3_7.

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Costa, E., C. Ferrarese, A. Guidotti, M. Miyata, and I. Mocchetti. "Multiple Signal in GABAergic Transmission: A New Family of Modulatory Peptides." In Receptor-Receptor Interactions, 363–71. London: Palgrave Macmillan UK, 1987. http://dx.doi.org/10.1007/978-1-349-08949-9_29.

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Costa, E., C. Ferrarese, A. Guidotti, M. Miyata, and I. Mocchetti. "Multiple Signal in GABAergic Transmission: A New Family of Modulatory Peptides." In Receptor-Receptor Interactions, 363–71. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5415-4_29.

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Maneuf, Y. P., and J. M. Brotchie. "Cannabinoid Receptor-Mediated Modulation of Gabaergic Transmission in the Basal Ganglia." In Advances in Behavioral Biology, 183–89. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0194-1_21.

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Woodin, Melanie A., and Mu-ming Poo. "Activity-Dependent Modification of Cation-Chloride Cotransporters Underlying Plasticity of Gabaergic Synaptic Transmission." In Excitatory-Inhibitory Balance, 89–97. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0039-1_6.

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Conference papers on the topic "GABAergic transmissioni"

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Li, Guoshi, Stacy Cheng, Frank Ko, Scott L. Raunch, Gregory Quirk, and Satish S. Nair. "Computational Modeling of Lateral Amygdala Neurons During Acquisition and Extinction of Conditioned Fear, Using Hebbian Learning." In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-15078.

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Abstract:
The amygdaloid complex located within the medial temporal lobe plays an important role in the acquisition and expression of learned fear associations (Quirk et al. 2003) and contains three main components: the lateral nucleus (LA), the basal nucleus (BLA), and the central nucleus (CE) (Faber and Sah, 2002). The lateral nucleus of the amygdala (LA) is widely accepted to be a key site of plastic synaptic events that contributes to fear learning (Pare, Quirk, LeDoux, 2004). There are two main types of neurons within the LA and the BLA: principal pyramidal-like cells which form projection neurons and are glutamatergic and local circuit GABAergic interneurons (Faber and Sah, 2002). In auditory fear conditioning, convergence of tone [conditioned stimulus (CS)] and foot-shock [unconditioned stimulus (US)] inputs potentiates the synaptic transmission containing CS information from the thalamus and cortex to LA, which leads to larger responses in LA in the presentation of subsequent tones only. The increasing LA responses disinhibit the CE neurons via the intercalated (ITC) cells, eliciting fear responses via excessive projections to brain stem and hypothalamic sites (Pare, Quirk, LeDoux, 2004). As a result, rats learn to freeze to a tone that predicts a foot-shock. Once acquired, conditioned fear associations are not always expressed and repeated presentation of the tone CS in the absence of US causes conditioned fear responses to rapidly diminish, a phenomenon termed fear extinction (Quirk et al. 2003). Extinction does not erase the CS-US association, instead it forms a new memory that inhibits conditioned response (Quirk et al. 2003)
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