ライフサイエンスコーパス: GABA(A) receptor

1 d by clonazepam, a positive modulator of the GABAA receptor.

2 y via a pentameric chloride ion channel, the GABAA receptor.

3 G residues during agonist activation of the GABAA receptor.

4 g domains through which propofol acts on the GABAA receptor.

5 such as hetero-oligomeric alpha1beta2gamma2 GABAA receptors.

6 dation process remains poorly understood for GABAA receptors.

7 ric activation of synaptic and extrasynaptic GABAA receptors.

8 ines the hyperpolarizing action of GABA) and GABAA receptors.

9 etic with putative actions on the inhibitory GABAA receptors.

10 likely mediated by delta subunit-containing GABAA receptors.

11 r understand the physiology of extrasynaptic GABAA receptors.

12 t the oscillations depended on both AMPA and GABAA receptors.

13 h recruitment of extrasynaptic high-affinity GABAA receptors.

14 ble of photolabelling their binding sites on GABAA receptors.

15 r are accounted for by its interactions with GABAA receptors.

16 loC) to the reversal potential of endogenous GABAA receptors.

17 bition mediated by alpha5 subunit-containing GABAA receptors.

18 oactive steroids potentiate a wider-range of GABAA receptors.

19 els, in particular, by enhancing activity of GABAA receptors.

20 ts, abolished by pharmacological blockade of GABAA receptors.

21 r type 1, oxytocin, ionotropic glutamate and GABAA receptors.

22 modulator of both synaptic and extrasynaptic GABAA receptors.

23 synaptic trapping of glycine (GlyR) but not GABAA receptors.

24 ical structure acting as a PAM at particular GABAA receptors.

25 uld be compensated for by an upregulation of GABAA receptors.

26 ty for brain gamma-aminobutyric acid type A (GABAA) receptors.

27 arizing vs. hyperpolarizing) of postsynaptic GABAA receptor actions.

28 Excitation of GABA neurons was mediated by GABAA receptor activation and involved stress-induced fu

29 synaptic scaling; conversely, alterations in GABAA receptor activation due to action-potential-indepe

30 urround light responses depend on endogenous GABAA receptor activation.

31 pathomimetics, pancreatic lipase inhibitors, GABAA receptor activators, a serotonin 2C receptor agoni

32 GABAA receptor agonism and antagonism had opposite effec

33 ynaptic responsiveness to local puffs of the GABAA receptor agonist isoguvacine.

34 ns into specific parietal circuits using the GABAA receptor agonist muscimol and validated the lesion

35 gm, we examined the effects of injecting the GABAA receptor agonist muscimol or the GABAA receptor an

36 r phenotype in C57BL/6J mice by infusing the GABAA receptor agonist, 4,5,6,7-tetrahydroisoxazolo-[5,4

37 n rats by microinjection of small amounts of GABAA-receptor agonists into an upper brainstem region n

38 ecting brain-state switching when exposed to GABAA-receptor agonists.

39 ediol, are neuroactive steroids and positive GABAA receptor allosteric modulators.

40 The GABAA receptor alpha subunit beta1 strand runs anti-para

41 GABAA receptor alpha1 and gamma2L subunits were co-expre

42 onocular cortex, cortical inhibition via the GABAA receptor alpha1 subunit restricts cross-modal plas

43 These findings implicate movement of the GABAA receptor alpha1 subunit's beta1 strand during agon

44 low concentrations was absent in slices from GABAA receptor alpha1(H101R)mutant mice.

45 However, no expression of GABAA receptor alpha2 subunit was detected.

46 region-specific conditional knockouts of the GABAA receptor alpha2 subunit, we demonstrate that inhib

47 alpha5 have revealed that alpha2-containing GABAA receptors (alpha2-GABAARs) are required for diazep

48 e dentate gyrus or CA3 via alpha2-containing GABAA receptors (alpha2GABAARs) is required to suppress

49 Here we show that GABAA receptor alpha3 (Gabra3), normally exclusively exp

50 mory by modulating alpha5-subunit containing GABAA receptors (alpha5-GABAARs).

51 and anesthetic agent that can both activate GABA(A) receptors and potentiate receptor activation eli

52 luences ligand-gated channels, including the GABAA receptor and others.

53 Zn(2+) has been shown to inhibit synaptic GABAA receptors and alter the hippocampal network excita

54 omplexes affect surface targeting of AMPA or GABAA receptors and synaptic transmission.

55 cated that they were mediated by distinctive GABAA receptors and that in coculture with neurons, the

56 the postsynaptic clustering of gephyrin and GABAA receptors and the strength of inhibitory, but not

57 neuronal ion channels, including subunits of GABAA receptors and voltage-gated calcium channels.

58 antibodies against NMDAR, LGI1, CASPR2, the GABAA receptor, and the AMPA receptor using live cell-ba

59 se stability through opposing endocytosis of GABAA receptors, and requires a newly described interact

60 -treated rats and this effect was blocked by GABAA receptor antagonism.

61 g the GABAA receptor agonist muscimol or the GABAA receptor antagonist bicuculline into the IC or NBM

62 ent was fully blocked by Zn(2+), akin to the GABAA receptor antagonist gabazine.

63 Treatment of control mice with a GABAA receptor antagonist or deletion of the chloride-ac

64 inephrine or serotonin, was prevented by the GABAA receptor antagonist picrotoxin.

65 epilepsy following repeated exposure to the GABAA receptor antagonist, flurothyl, in which mice deve

66 Administration of either bicuculline, a GABAA receptor antagonist, or CGP 35348, a GABAB recepto

67 rgic transmission using local application of GABAA receptor antagonists.

68 The effects of steroids on the GABA(A) receptor are typically determined by comparing s

69 Here we show that immobile and diffusing GABA(A) receptors are stabilized by distinct synaptic sc

70 GABAA receptors are brain inhibitory chloride ion channe

71 lated differentially by GABA release: Axonal GABAA receptors are down-regulated but dendritic recepto

72 alpha4betaxdelta GABAA receptors are extrasynaptic receptors important fo

73 y and arrangement of synaptic alphabetagamma GABAA receptors are generally accepted as 2alpha:2beta:1

74 GABAA receptors are pentameric ligand-gated channels med

75 onal development synaptic events mediated by GABAA receptors are progressively reduced in their durat

76 GABAA receptors are the primary inhibitory ion channels

77 ents mediated by high-affinity extrasynaptic GABAA receptors, are increasingly recognized as importan

78 Here, using the alpha1 subunits of GABAA receptors as a model substrate, we demonstrated th

79 Antibodies directed against GABA(A) receptor-associated protein, and the glycine-alp

80 newly described interaction with GABARAP, a GABAA receptor-associated protein.

81 scaffold protein mediating the anchoring of GABAA receptors at inhibitory synapses.

82 Blocking GABAA receptors attenuated stimulus-related inhibition,

83 GABAA-receptor-based interneuron circuitry is essential

84 onists at the benzodiazepine-binding site of GABAA receptors (BDZs) enhance synaptic inhibition throu

85 tions in the gamma-aminobutyric acid type A (GABAA ) receptor beta3 subunit gene GABRB3 and one in th

86 for three de novo missense mutations in the GABAA receptor beta3 subunit gene (GABRB3) identified in

87 inked genes, including GABRB3, which encodes GABAA receptor beta3 subunits and is among the maternal

88 zed the effects of these GABRG2 mutations on GABAA receptor biogenesis and channel function.

89 ecular mechanisms that might link defects in GABAA receptor biophysics and biogenesis to patients wit

90 In long-term bioluminescence recordings, GABAA receptor blockade desynchronized the Fbxl3(+/+) bu

91 receptor, oxytocin, ionotropic glutamate or GABAA receptors but instead involves a close relationshi

92 s anesthetic, is a positive modulator of the GABAA receptor, but the mechanistic details, including t

93 Zn(2+) inhibits synaptic GABAA receptors, but its interaction is less well apprec

94 on of the GABA signaling and blockage of the GABAA receptor by the specific inhibitors both significa

95 the EC50 for activation of the GABA type A (GABAA) receptor by the transmitter GABA and basal activi

96 mately the synaptic accumulation of AMPA and GABAA receptors, by interacting with key components of b

97 GABAA receptors can be directly activated and potentiate

98 be related to the extent of the reduction of GABAA receptor channel function and the differential dom

99 ns from the TMN evoked tonic (extrasynaptic) GABAA receptor Cl(-) currents onto medium spiny neurons

100 apses primarily on dendritic spines, whereas GABAA receptors cluster at inhibitory synapses mainly on

101 s during development suggests differences in GABAA receptor composition.

102 Importantly, axonal and dendritic GABAA receptors comprise distinct subunit compositions t

103 onal gray matter increases were explained by GABAA receptor concentration in addition to T1 relaxatio

104 rogate marker of water content, but not with GABAA receptor concentration, a surrogate of neuronal in

105 ontent, and not to any substantial degree by GABAA receptor concentration, an indirect marker of neur

106 ay matter increases were partly explained by GABAA receptor concentration, indicating some form of ne

107 viding voxel-wise absolute quantification of GABAA receptor concentration.

108 with wild-type alpha1beta2gamma2L receptors, GABAA receptors containing a mutant gamma2 subunit had r

109 GABAA receptors containing alpha5-subunits (GABAAR-alpha

110 GABAA receptors containing subunit alpha1, showing the s

111 a, DCUK-OEt acted primarily on extrasynaptic GABAA receptors containing the alpha1 subunit and genera

112 and are modulated by agonists that activate GABAA receptors containing the delta subunit.

113 ulation of tonically activated synaptic-type GABAA receptors contributes to the clinical actions of s

114 d exclusively by enhancement of granule cell GABAA receptor currents, which only occurs in DBA/2J mic

115 BAergic activity at delta subunit-containing GABA(A) receptors (delta-GABA(A)Rs).

116 cell volume homeostasis and Cl(-)-permeable GABAA receptor-dependent membrane excitability.

117 intenance of gamma-aminobutyric acid type A (GABAA) receptors dictates their function in controlling

118 ervation is particularly interesting because GABAA receptor disturbances, leading to altered behavior

119 e show that synaptic-type alpha1beta2gamma2L GABAA receptors expressed in HEK293 cells respond with l

120 By using recombinant GABAA receptors expressed in HEK293 cells, and native GA

121 asal activity employing concatemeric ternary GABAA receptors expressed in Xenopus oocytes.

122 and D1 receptor activation result in minimal GABAA receptor expression and activity and greatly dimin

123 rated light-sensitive versions of the entire GABA(A) receptor family.

124 membrane protein, even wild type subunits of GABAA receptors fold and assemble inefficiently in the e

125 cement of synaptic transmission (mediated by GABAA receptors) followed by a long lasting (>500 ms) in

126 steric modulator of gamma-aminobutyric acid (GABAA) receptors, for the treatment of post-partum depre

127 GABA(A) receptors form Cl(-) permeable channels that med

128 of gamma-aminobutyric acid type A receptor (GABA(A)) receptor function.

129 e brain during CO2 compensation could change GABAA receptor function and account for the behavioural

130 determined the impact of GABRB mutations on GABAA receptor function and biogenesis.

131 All five de novo GABRB mutations impaired GABAA receptor function by rearranging conserved structu

132 The role of the beta1 strand in GABAA receptor function is unclear.

133 play a role in ethanol-induced sedation and GABAA receptor function, but does not regulate excessive

134 l amygdala neurons, deletion of Tlr4 altered GABAA receptor function, but not GABA release.

135 crease of fEPSP is induced by a reduction in GABAA receptor function.

136 y residues that are critical for maintaining GABAA receptor function.

137 anisms by which EOEE-linked mutations affect GABAA receptor function.

138 n, which is a scaffold protein that recruits GABAA receptors (GABAA Rs) at the postsynapse.

139 We recently located the anaesthetic sites on GABAA receptors (GABAA Rs) by photolabelling with an ana

140 toneurons by complete blockade of spiking or GABAA receptor (GABAAR) activation for 2 d in vivo Here,

141 ctional modulators of heterologous expressed GABAA receptor (GABAAR) isoforms (synaptic alpha1beta3ga

142 GABAA receptor (GABAAR) pentamers are assembled from a p

143 he interaction between oxytocin receptor and GABAA receptor (GABAAR), remains to be elucidated.

144 we report a mechanism of KCC2 regulation by GABAA receptor (GABAAR)-mediated transmission in mature

145 e regulation of cognition and emotion is the GABAA receptor (GABAAR).

146 experience depolarization upon activation of GABAA receptors (GABAAR) because their intracellular chl

147 types (alpha1, alpha2, alpha3 and alpha5) of GABAA receptors (GABAAR).

148 ition in the brain is mediated by ionotropic GABAA receptors (GABAARs) and metabotropic GABAB recepto

149 diates fast synaptic inhibition via synaptic GABAA receptors (GABAARs) and persistent tonic inhibitio

150 efficacy of neuronal inhibition mediated by GABAA receptors (GABAARs) containing beta3 subunits are

151 odulator at human alpha1,2,3,5beta2,3gamma2S GABAA receptors (GABAARs) expressed in Xenopus oocytes,

152 synaptic GABA receptors, there is a group of GABAA receptors (GABAARs) that is located extrasynaptica

153 n the brain is mediated mostly by ionotropic GABAA receptors (GABAARs), but their essential component

154 GABAA receptors (GABAARs), the main postsynaptic recepto

155 expression of extrasynaptic alpha4betadelta GABAA receptors (GABARs).

156 ng with vesicular amino acid transporter and GABA(A)-receptor gamma2 subunit immunoreactivities.

157 Mice with a knock-in F77I mutation in the GABAA receptor gamma2 subunit gene are zolpidem-insensit

158 lationship between these phenotypes, we used GABAA receptor gamma2 subunit heterozygous (gamma2(+/-))

159 pairing inhibitory neurotransmission, mutant GABAA receptor gamma2(Q390X) subunits accumulated and ag

160 s in the inhibitory gamma-aminobutyric acid (GABAA) receptor gamma2 subunit gene, GABRG2 (OMIM 137164

161 The gamma-aminobutyric acid (GABAA) receptor gamma2 subunit gene, GABRG2, is abundant

162 onal importance of residues in loop G of the GABAA receptor has not been investigated.

163 hat selective inactivation of GABAB, but not GABA(A), receptors impairs firing rate homeostasis by di

164 force for the chloride-permeable ionotropic GABAA receptor in mature neurons.

165 is thought to be altered current across the GABAA receptor in neuronal cells due to changes in ion g

166 duces its anesthetic effect, largely via the GABAA receptor in the CNS, and also reduces the N-formyl

167 ylation enables effects of this chaperone on GABAA receptors in addition to nAChRs.

168 Surprisingly, we observed PSCs mediated by GABAA receptors in addition to nicotinic acetylcholine r

169 face expression of alpha2 subunit-containing GABAA receptors in immature developing neurons, but not

170 s the function of synaptic and extrasynaptic GABAA receptors in physiologic and pathologic conditions

171 ale for targeting synaptic and extrasynaptic GABAA receptors in the development of therapies for pati

172 This differs from GABAA receptors in the dorsal horn, where different rece

173 Selective potentiation of GABAA receptors in the frontal cortex by systemic zolpid

174 Using these mice, GABAA receptors in the frontal motor neocortex and hypot

175 ion of neurosteroid-sensitive, extrasynaptic GABAA receptors in the hippocampus has direct implicatio

176 data on the distribution and composition of GABAA receptors in the human amygdala are lacking.

177 irregularity; (iii) conversely, blockade of GABAA receptors in the KF of healthy rats mimicked the R

178 2+) of neurosteroid-sensitive, extrasynaptic GABAA receptors in the mouse hippocampus dentate gyrus,

179 BAA receptors, the nanoscale distribution of GABAA receptors in the postsynaptic area is a crucial de

180 ively low-affinity gamma2 subunit-containing GABAA receptors in the thalamus, which can contribute to

181 e constitutive exocytic vesicles of AMPA and GABAA receptors in vitro and in vivo, we demonstrate tha

182 RIC-3 on muscle excitability are mediated by GABAA receptor inhibition.

183 R)mutation renders alpha1-subunit containing GABAA receptors insensitive towards benzodiazepines.

184 tracellular applications of p4, a blocker of GABA(A) receptor internalization.

185 munoreactivity for the alpha2 subunit of the GABAA receptor is higher in layers 2/superficial 3 of th

186 the subunit arrangement of alpha4beta2delta GABAA receptors is not strongly predefined but is mostly

187 larizing inhibition mediated by type A GABA (GABAA) receptors is dependent on chloride extrusion by t

188 phabetagamma2 receptors, which are the major GABAA receptor isoforms in the brain.

189 ype profiles, depending on the extrasynaptic GABAA receptor isoforms targeted.

190 ences in the distribution and composition of GABAA receptors may account for distinct effects and sid

191 In the developing brain, however, GABAA receptors mediate excitatory actions due to an inc

192 ehensive optogenetic toolkit for controlling GABA(A) receptor-mediated inhibition in the brain.

193 GABA(A) receptor-mediated IPSCs evoked by electrical or

194 om layer V pyramidal cells, and monosynaptic GABA(A) receptor-mediated IPSCs were elicited.

195 th determined the direction and magnitude of GABAA receptor-mediated current amplitudes and was obser

196 ociation between KCC2 transport strength and GABAA receptor-mediated current amplitudes was investiga

197 e elicited by lower GABA concentrations than GABAA receptor-mediated enhancement of EPSCs, suggesting

198 GABAergic inhibitory transmission, we evoked GABAA receptor-mediated monosynaptic IPSPs in deep cereb

199 Potassium elevations associated to GABAA receptor-mediated population events were confirmed

200 s mechanosensory dysfunction through loss of GABAA receptor-mediated presynaptic inhibition of inputs

201 or enabling inhibitory neuronal responses to GABAA receptor-mediated signaling.

202 /Cl(-) cotransporter KCC2 and a depolarizing GABAA receptor-mediated synaptic component following LTP

203 We found that hypoxia caused a loss of GABAA receptor-mediated synaptic input to NG2 cells, ext

204 such as 4-PIOL, may be useful for modulating GABAA receptor-mediated tonic currents, but the directio

205 ntial mechanism for modulating extrasynaptic GABAA receptor-mediated tonic currents.

206 sporter KCC2 (SLC12A5) tunes the efficacy of GABAA receptor-mediated transmission by regulating the i

207 only a local and limited effect on the rho1 GABAA receptor model system.

208 cued by treatment with a positive allosteric GABAA receptor modulator.

209 GABAA receptors must be inactive during novel tasting to

210 Moreover, depressive-like phenotypes of GABAA receptor mutant mice can be reversed by treatment

211 eptors expressed in HEK293 cells, and native GABAA receptors of cerebellar granule cells, hippocampal

212 n of dendritic IPSCs isolated after blocking GABAa receptor on the soma.

213 The homeostatic increase in GABAA receptors on bipolar cell dendrites is pathway-spe

214 tes increases the expression and activity of GABAA receptors on the dendrites of the cells and that s

215 ntial vanilloid (TRPV1) receptor, glutamate, GABAA receptors, or a combination of 5-HT1B/1D receptors

216 Further, GABAA receptor pharmacology determined an excitatory eff

217 To address this hypothesis, GABAA receptor pharmacology was used to locally inhibit

218 complete development of a mature inhibitory GABAA receptor phenotype and faster production of electr

219 intervention with alpha2/3 subtype-selective GABAA receptor positive allosteric modulators during the

220 Zolpidem, a GABAA receptor-positive modulator, is the gold-standard

221 recent modeling study of the beta3 homomeric GABA(A) receptor postulated a high-affinity propofol bin

222 While synaptic inhibition was mediated by GABAA receptors, potentiation involved astrocyte GABAB r

223 naling by treating aged apoE4-KI mice with a GABAA receptor potentiator pentobarbital (PB) before and

224 ling by treating aged apoE4-KI mice with the GABAA receptor potentiator pentobarbital (PB) for 4 week

225 uced by local M1 modulation of D1, AMPA, and GABAA receptors, providing preclinical support for the n

226 erologously expressed rat alpha1beta2gamma2L GABA(A) receptors, ranging from essentially inert to hig

227 Blocking GABAA receptors reduces orientation selectivity of the i

228 These results reveal that GABAA receptor regulation in oligodendrocytes is driven

229 in1A/B-VAMP2 complexes, whereas insertion of GABAA receptors relies on SNAP23-syntaxin1A/B-VAMP2 comp

230 tion, mediated by synaptic and extrasynaptic GABAA receptors, respectively, in physiological and path

231 Synaptic GABAA receptors respond to synaptically released GABA an

232 Cerebellar granule cell GABAA receptor responses to alcohol vary as a function o

233 netic differences in cerebellar granule cell GABAA receptor responses to recreational concentrations

234 s, we inactivated the gamma2 subunit gene of GABAA receptors selectively in these neurons (SSTCre:gam

235 characterized two animal toxins that enhance GABAA receptor sensitivity to agonist, thereby establish

236 GABAA receptors shape synaptic transmission by modulatin

237 ntly decreases the hyper-excitable action of GABAA receptor signaling and restores network homeostati

238 ta indicate that sex-specific adaptations in GABAA receptor signaling modulate opioid analgesia in pe

239 Modulation of the D1/GABAA receptor signaling pathway of ON-cBC dendrites by

240 Dysfunctional GABAA receptor signaling that results in modified tonic

241 Compounds that can act on GABAA receptor subtype in a selective manner, without th

242 This GABAA receptor subtype is thought to mediate sedation.

243 nzotriazine, already identified as selective GABAA receptor subtype ligands endowed with anxiolytic-l

244 Continuing our research on GABAA receptor subtype ligands, here is reported the syn

245 Here, we examine the GABAA receptor subtype selectivity of the weak partial a

246 However, the contribution of GABAA receptor subtypes to anxiolysis is still controver

247 expression levels of different extrasynaptic GABAA receptor subtypes, and on the ambient GABA levels.

248 actions on different native and recombinant GABAA receptor subtypes.

249 n which the "photoswitch-ready" version of a GABA(A) receptor subunit genomically replaces its wild-t

250 The postsynaptic gamma2-GABA(A)-receptor subunit and the presynaptic vesicular i

251 artial agonist is heavily dependent upon the GABAA receptor subunit composition underpinning tonic in

252 g on the cell type studied, their respective GABAA receptor subunit compositions, and critically, on

253 hree distinct interneuron types have similar GABAA receptor subunit content.

254 Differences in GABAA receptor subunit expression between the human and

255 Mutations in GABAA receptor subunit genes are frequently associated w

256 s mediating synaptic transmission, including GABAA receptor subunit genes.

257 leading to propofol-selective binding within GABAA receptor subunit interfaces, with stable hydrogen

258 and for targeted-ABPP and observed a lack of GABAA receptor subunit protection.

259 estigation demonstrates striking interfacial GABAA receptor subunit selectivity in the native milieu,

260 s provide important insight into the role of GABAA receptor subunit under- or overexpression in disea

261 Further, expression of an important GABAA receptor subunit, GABAAR alpha1, was significantly

262 gulated in the low pH treatment, including a GABAA receptor subunit.

263 s and the complementary genetically modified GABA(A) receptor subunits.

264 amic principal neurons were found to express GABAA receptor subunits alpha1 , alpha3 , beta2/3 , gamm

265 Here, the expression of GABAA receptor subunits alpha1, alpha2, alpha3, alpha5,

266 regional staining intensity for all positive GABAA receptor subunits from the dorsolateral pole to ve

267 ere performed, and subcellular expression of GABAA receptor subunits was analyzed semiquantitatively.

268 g the unbiased capture of five alpha or beta GABAA receptor subunits.

269 rneurons showed relatively low expression of GABAA receptor subunits.

270 Simulated docking of DCUK-OEt at the GABAA receptor suggested that its binding site may be at

271 s more sensitive to GABA than enhancement by GABAA receptors, suggesting GABAB receptors may be activ

272 tion phenotype, and targeting the cerebellar GABAA receptor system may be a clinically viable therape

273 s suggest that dopamine may directly inhibit GABAA receptors that are both immediately adjacent to do

274 However, DPA potently antagonizes GABAA receptors that contain alpha1 and beta2 subunits b

275 that, in addition to the number of synaptic GABAA receptors, the nanoscale distribution of GABAA rec

276 sic and tonic responses mediated by neuronal GABAA receptors through both presynaptic and postsynapti

277 potentiation of the human alpha1beta2gamma2L GABAA receptor to demonstrate that: 1) curvilinear isobo

278 suggests that for some women, failure of the GABAA receptor to regulate overall GABA-ergic tone in th

279 the Cb-mediated recruitment of gephyrin and GABAA receptors to developing inhibitory postsynapses an

280 The gamma2 subunits have a critical role in GABAA receptor trafficking and clustering at synapses.

281 Yet, blockade of the GABA(A) receptors transforms GDPs to epileptiform discha

282 properties of recombinant alpha1beta2gamma2L GABAA receptors transiently expressed in HEK293T cells.

283 Previous studies have shown that GABAA receptors typically enhance vesicle release while

284 tsynapses and is required for clustering the GABA(A) receptor UNC-49.

285 electrophysiological studies on recombinant GABAA receptors under a wide range of agonist and/or ane

286 he potassium-chloride cotransporter KCC2 and GABAA receptors, undergo remarkable fluctuations within

287 ively modulate the activity of extrasynaptic GABAA receptors underlying tonic inhibition is likely to

288 icating perhaps increased neuronal matter or GABAA receptor upregulation and inflammatory edema.

289 ensitivity of these responses to blockade of GABAA receptors using bath-applied SR95531.

290 DCUK-OEt modulation of alpha1beta2gamma2 GABAA receptors was not blocked by flumazenil.

291 Whereas the activation of GABAA receptors was responsible for the direct inhibitio

292 s a selective modulator of alpha3-containing GABAA receptors, was shown to be anxiolytic.

293 ntral benzodiazepine site located within the GABAA receptor, we quantified and mapped neuronal damage

294 Potential structural perturbations in mutant GABAA receptors were explored using structural modeling.

295 roteins because Nav1.2 channels, but not AIS GABAA receptors, were also endocytosed.

296 activated non-alpha-containing (beta3gamma2) GABAA receptors, whereas gabazine suppressed spontaneous

297 ling the constitutive exocytosis of AMPA and GABAA receptors, which are critical for the regulation o

298 clarifies a Grp94-mediated ERAD pathway for GABAA receptors, which provides a novel way to finely tu

299 mediated by type A gamma-aminobutyric acid (GABAA) receptors, which are Cl(-)-permeable, ligand-gate

300 mma2, alpha5beta3gamma2 and alpha1beta3delta GABAA receptors, while having no significant PAM effect