ライフサイエンスコーパス: GABA(B) receptor

1 ms) inhibition of transmission (mediated by GABAB receptors).

2 tracellular coiled-coil heterodimer of human GABAB receptor.

3 panied by a strong reduction of cell surface GABAB receptors.

4 lecular targets tested, including opioid and GABAB receptors.

5 total as well as cell surface expression of GABAB receptors.

6 n Cav2.2 channels and transfected with human GABAB receptors.

7 dopamine neurons, preferentially activating GABAB receptors.

8 ch can be suppressed by reducing presynaptic GABAB receptors.

9 K+ basket cell terminals through presynaptic GABAB receptors.

10 ment with R-baclofen, a selective agonist of GABAB receptors.

11 of MIB2 and Lys-63-linked ubiquitination of GABAB receptors.

12 le sites is the lysosomal sorting signal for GABAB receptors.

13 expression of total as well as cell surface GABAB receptors.

14 llum, which co-express presynaptic GABAA and GABAB receptors.

15 ubiquitination and lysosomal degradation of GABAB receptors.

16 the fold-related metabotropic glutamate and GABAB receptors.

17 unit-containing nAChRs, are mediated through GABAB receptors.

18 ChRs, are mediated through the activation of GABAB receptors.

19 a (SNr) lose tonic presynaptic inhibition by GABAB receptors.

20 led to elicit detectable effects mediated by GABA(B) receptors.

21 ing that baclofen was acting on postsynaptic GABA(B) receptors.

22 synapses were not modulated by postsynaptic GABA(B) receptors.

23 ambient GABA concentration can also activate GABA(B) receptors.

24 ABAergic interneurons targeting postsynaptic GABA(B) receptors.

25 rat medial entorhinal cortex (mEC) involves GABA(B) receptors.

26 n in part through activation of metabotropic GABA(B) receptors.

27 additional role in the surface stability of GABA(B) receptors.

28 GABA(A) beta3 subunit and only occasionally GABA(B) receptors.

29 y on bipolar cell terminals, most likely via GABA(B) receptors.

30 ve to agonists of cannabinoid, mu-opioid, or GABA(B) receptors.

31 into GABA, which then activates presynaptic GABA(B) receptors.

32 or subunits beta2, delta, and pi, as well as GABA(B) receptors.

33 alance the inhibitory effects of presynaptic GABA(B) receptors.

34 ry synaptic currents mediated by GABA(A) and GABA(B) receptors.

35 ttenuated by neural activity and presynaptic GABA(B) receptors.

36 A result from the activation of metabotropic GABA(B) receptors.

37 ly investigating interactions between SP and GABA(B) receptors.

38 that contain a potentially enormous pool of GABA(B) receptors.

39 utable to an indirect action via presynaptic GABA(B) receptors.

40 ted glutamate release from ORN terminals via GABA(B) receptors.

41 y showed colocalisation of the antibody with GABA(B) receptors.

42 beta(2)AR), and the gamma-aminobutyric acid (GABA(B)) receptor.

43 ay involving gamma-aminobutyric acid type B (GABA(B)) receptor.

44 e neurons and do they act via the GABA(A) or GABA(B) receptor?

45 It functions as an obligatory heterodimer of GABAB receptor 1 (GBR1) and GABAB receptor 2 (GBR2) subu

46 y heterodimer of GABAB receptor 1 (GBR1) and GABAB receptor 2 (GBR2) subunits.

47 tion of morphine-induced CPP indicating that GABA(B) receptor actions are independent of the primary

48 Here, we examined the effects of GABA(B) receptor activation on neuronal excitability in

49 eutic opportunities to prevent the excessive GABA(B) receptor activation that appears necessary for t

50 GABAB receptor activation selectively suppresses N-type

51 ing potassium (KIR) conductance activated by GABA(B) receptors adds substantial robustness to network

52 roaches, we report novel interaction between GABAB receptor agents and CXCR4 and demonstrate alloster

53 The GABA(B) receptor agonist baclofen (20 mum) enhanced GABA

54 The GABA(B) receptor agonist baclofen facilitates the extinc

55 of VDCCs nor their inhibition by either the GABA(B) receptor agonist baclofen or intracellular guano

56 mitter release from POMC neurons, as did the GABA(B) receptor agonist baclofen.

57 Application of baclofen, a specific GABA(B) receptor agonist, inhibited significantly neuron

58 The GABAB receptor agonist baclofen also inhibited inward cu

59 ong-term ( approximately 5 years) use of the GABAb receptor agonist baclofen by SCI patients reduced

60 The orthosteric GABAB receptor agonist baclofen has been shown to suppre

61 sitivity of SOM-IPSCs, but not PV-IPSCs to a GABAb receptor agonist baclofen.

62 Baclofen is a GABAB receptor agonist commonly used to relief spasticit

63 The selective GABAB receptor agonist R-baclofen previously reversed so

64 e prevention, we examined whether baclofen-a GABAB receptor agonist that reduces mesolimbic dopamine

65 rminals can be readily modulated, opioid and GABA(B) receptor agonists were applied.

66 quantify the relative binding affinities of GABA(B) receptor agonists, antagonists and the effect of

67 ect of LH reversible inactivation by GABAA + GABAB receptor agonists (muscimol + baclofen) on this ef

68 versible inactivation of CeA or BLA by GABAA+GABAB receptor agonists (muscimol+baclofen, 0.03+0.3 nmo

69 We explored whether metabotropic GABA(B) receptors also participate in this feedback path

70 Here we provide evidence that GABAB receptors also associate with hetero-oligomers of

71 e potentiating influence of Girk1, using the GABA(B) receptor and Girk1/Girk2 heteromer as a model sy

72 Presynaptic GABA(B) receptors and functional depletion of synaptic v

73 of slow inhibitory transmission mediated by GABA(B) receptors and G protein-gated inwardly rectifyin

74 a decrease in slow inhibition, mediated by a GABAB receptor and a potassium channel.

75 These effects are mediated by GABAB receptors and change in the Cl(-) driving force.

76 the fraction of Lys-63-linked ubiquitinated GABAB receptors and enhanced the expression of total as

77 olecular and functional repertoire of native GABAB receptors and modulates physiologically induced K(

78 his receptor in heterologous systems lacking GABAB receptors and performed competition binding experi

79 y diminished Lys-63-linked ubiquitination of GABAB receptors and prevented their lysosomal degradatio

80 es are believed to result from it activating GABAB receptors and subsequently inhibiting CaV2.2 volta

81 hinery determines the number of cell surface GABAB receptors and thereby GABAB receptor-mediated neur

82 s were critically dependent on activation of GABAB receptors and, together, appeared to temporally se

83 assium currents that could be blocked by the GABA(B) receptor antagonist CGP 35348 and the G protein

84 2 s, and were fully blocked by the selective GABA(B) receptor antagonist CGP 52432.

85 sion of excitatory events was blocked by the GABA(B) receptor antagonist CGP 54626.

86 This enhancement was blocked by the GABA(B) receptor antagonist CGP 55845 and intracellular

87 Treatment with the GABA(B) receptor antagonist CGP55845 restored memory of

88 In the indirect pathway, the GABA(B) receptor antagonist reduces EPSC amplitude in an

89 In the direct pathway, the GABA(B) receptor antagonist reduces EPSC amplitude, indi

90 B-induced respiratory depression, a specific GABA(B) receptor antagonist, (2S)-(+)-5,5-dimethyl-2-mor

91 lu2/3 receptor antagonist, LY341495, and the GABA(B) receptor antagonist, CGP52432, which was shown t

92 CGP55845, a potent GABA(B) receptor antagonist, was employed to determine t

93 g, a synthetic fluorophore and a fluorescent GABA(B) receptor antagonist.

94 re no longer detectable in the presence of a GABAb receptor antagonist CGP52432.

95 CK+ basket cells even in the presence of the GABAB receptor antagonist CGP55845 (2 mum).

96 The GABAB receptor antagonist CGP55845 (3 mum) increased the

97 The GABAB receptor antagonist saclofen (200 mum) occluded ef

98 a GABAA receptor antagonist, or CGP 35348, a GABAB receptor antagonist, blocked the antinociceptive a

99 was rescued by intra-VTA administration of a GABAB receptor antagonist, demonstrating that reversal o

100 In hippocampal slices, treatment with the GABA(B) receptor antagonists CGP55845 or CGP52432 enhanc

101 performance through treatment with selective GABA(B) receptor antagonists motivates studies to furthe

102 ts in DS by defining the effect of selective GABA(B) receptor antagonists on behavior and synaptic pl

103 c and heterospecific vocalizations), whereas GABAB receptor antagonists [10 mum saclofen; 10-50 mum C

104 sults provide the first demonstration of how GABA(B) receptors are activated by endogenous GABA relea

105 DOWN state transitions, whilst postsynaptic GABA(B) receptors are essential for the afferent termina

106 chemistry demonstrated that both GABA(A) and GABA(B) receptors are expressed in the taste bud.

107 e is no direct demonstration that functional GABA(B) receptors are needed for inhibition of the Ca(v)

108 GABA(B) receptors are the G-protein coupled receptors (G

109 GABAA and GABAB receptors are co-expressed at many presynaptic ter

110 Cell surface GABAB receptors are constitutively internalized and eith

111 Metabotropic GABAB receptors are crucial for controlling the excitabi

112 GABAB receptors are emerging therapeutic targets for the

113 We found that GABAB receptors are expressed in cortico-bulbar axons th

114 GABAB receptors are G-protein-coupled receptors that med

115 GABAB receptors are heterodimeric G protein-coupled rece

116 actors regulating cell surface expression of GABAB receptors are poorly characterized.

117 the membrane of mouse dopamine neurons when GABAB receptors are stimulated.

118 GABAB receptors are the G-protein coupled receptors for

119 e development of compounds that activate the GABA(B) receptor as agonists or positive allosteric modu

120 GABA(B) receptors assemble from principle and auxiliary

121 ntation and metabolic labeling, we show that GABA(B) receptors associate with KCTD12 while they resid

122 A receptors, potentiation involved astrocyte GABAB receptors, astrocytic glutamate release, and presy

123 aired recordings, we reveal that presynaptic GABA(B) receptors at interneuron-pyramidal connections r

124 characterization of beta(1)-/beta(2)ARs and GABA(B) receptors at single-molecule resolution.

125 support that the up-regulation of functional GABA(B) receptors at the neuronal plasma membrane is an

126 irst description of a pediatric patient with GABAB receptor autoantibodies.

127 gamma-Aminobutyric acid type B (GABAB) receptor autoantibodies were identified in the se

128 ds the clinical phenotype and indicates that GABAB receptor autoimmunity should be considered in case

129 ata support a model in which the fraction of GABAB receptors available for plasma membrane traffickin

130 a potent mechanism regulating the number of GABAB receptors available for signaling and is expected

131 degradation actively controls the number of GABAB receptors available for signaling.

132 This study demonstrates that activation of GABAB receptors biases the excitation/inhibition balance

133 in the presence of adenosine A1 receptor and GABAB receptor blockade.

134 the slow sustained IPSPs were blocked by the GABAB receptor blocker CGP-54626.

135 ing ATPase activity prevented degradation of GABAB receptors but not the removal of Lys(48)-linked ub

136 tro as positive allosteric modulators of the GABAB receptor by potentiating GTPgammaS stimulation ind

137 trol during strong activation of presynaptic GABAB receptors by (+/-)baclofen (10 mum), GABA (2 mm) o

138 gulation of CHOP down-regulates cell surface GABAB receptors by preventing their trafficking from the

139 ctivity-dependent proteasomal degradation of GABAB receptors by the ERAD machinery is a potent mechan

140 Mammalian GABAB receptors can functionally substitute for GBB-1 in

141 amplitude and kinetics of synaptic inputs by GABAB receptors can improve precision of ITD computation

142 Here we report that GABAB receptors can physically associate with the potass

143 nist reduces EPSC amplitude, indicating that GABA(B) receptors cause enhanced glutamate release from

144 igomerization, but increased the mobility of GABA(B) receptor complexes.

145 Native GABA(B) receptors comprise principle and auxiliary subun

146 urring in brain ischemia that down-regulates GABAB receptors, considerably increased the expression o

147 tors, these results suggest that presynaptic GABA(B) receptors contribute to spontaneous DOWN state t

148 ted inhibitory synapses of Fmr1 KO mice in a GABAB receptor-dependent manner.

149 ith GABA(B) agonist application, presynaptic GABA(B) receptors desensitized, suggesting that resistan

150 ry synapses co-express presynaptic GABAA and GABAB receptors, despite their opposing actions on synap

151 g with recently shown receptor-architectonic GABAB receptor distribution in ACC, whereas Gln distribu

152 Overall, GABA(B) receptors do contribute to feedback regulation o

153 Our data indicate that postsynaptic GABA(B) receptors enhance the function of extrasynaptic

154 rat brain slices, activation of postsynaptic GABA(B) receptors enhances the magnitude of the tonic GA

155 culating hemolymph and binds to metabotropic GABAB receptors expressed on blood progenitors within th

156 Efficient knockdown of GABA(B) receptor expression at mRNA and protein levels w

157 degradation contributes to the regulation of GABAB receptor expression levels.

158 subsets of bipolar cell output regulated by GABA(B) receptor feedback (direct, indirect and null), i

159 It is increasingly appreciated that the GABAB receptor forms part of larger signaling complexes,

160 removing ionotropic GABA(A) or metabotropic GABA(B) receptors from histidine decarboxylase-expressin

161 Genetic deletion of GABAB receptors from dopamine neurons in adult mice did

162 GABA(B) receptor functions as a heterodimeric assembly o

163 Somatodendritic Girk currents evoked by the GABA(B) receptor (GABA(B)R) agonist baclofen were dimini

164 Pharmacological GABA(B) receptor (GABA(B)R) blockade or genetic deletion

165 hat Girk/K(IR)3 channels mediate most of the GABA(B) receptor (GABA(B)R)-dependent inhibition of laye

166 ransporter GAT-1 and in both subunits of the GABA(B) receptor (GABA(B)R).

167 Although primarily studied at the cell body, GABA(B) receptors (GABA(B)Rs) are abundant at spines and

168 ry entrainment, but the role of metabotropic GABA(B) receptors (GABA(B)Rs) in mediating slow presynap

169 In rat hippocampal CA1 axons, GABA(B) receptors (GABA(B)Rs) inhibit presynaptic Ca(2+)

170 GABA(B) receptors (GABA(B)Rs) mediate slow inhibitory ef

171 tussis toxin-sensitive Gi/o proteins via the GABAB receptor (GABA(B)R) and potently suppresses pain i

172 ound that genetic deletion of Nxph1 impaired GABAB receptor (GABA(B)R)-dependent short-term depressio

173 ptors, suggesting an increase in presynaptic GABAB receptor (GABAB R) signalling.

174 GABAB receptors (GABAB Rs) suppress voltage-gated calciu

175 nels mediate the direct inhibitory effect of GABAB receptor (GABABR) and D2 DA receptor (D2R) activat

176 o psychostimulants decreases the size of the GABAB receptor (GABABR)-activated GIRK currents (IBaclof

177 asticity changes depended on the strength of GABAB receptor (GABABR)-mediated presynaptic inhibition

178 GABAb receptor (GABAbR)-mediated suppression of glutamat

179 Inhibitory GABAB receptors (GABABRs) can down-regulate most excitat

180 GABAB receptors (GABABRs) exert powerful pre- and postsy

181 phology and interacts with the C terminus of GABAB receptors (GABABRs) to control their cell surface

182 itory signaling in the brain is mediated via GABAB receptors (GABABRs), but the molecular function of

183 c GABAA receptors (GABAARs) and metabotropic GABAB receptors (GABABRs).

184 aptic inhibition is mediated by metabotropic GABAB receptors (GABABRs).

185 Using conditional astrocyte-specific GABAB receptor (Gabbr1) knockout mice, we confirmed the

186 mediated by tonic activation of presynaptic GABAb receptors gated by the spontaneous activity of som

187 evity effect is mediated by the metabotropic GABAB receptor GBB-1, but not ionotropic GABAA receptors

188 Malfunction of GABA(B) receptor has been implicated in several neurolog

189 beneficial effects by acting as agonists of GABAB receptors has caused confusion over whether blocka

190 g the reinforcing properties of alcohol, and GABAB receptors have been proposed as a potential target

191 odies to the gamma-aminobutyric acid type B (GABAB) receptor have recently been identified as a cause

192 atories, we found that chronic activation of GABAB receptors improved performance on a series of cogn

193 Here we examined a role for GABA(B) receptors in cognitive deficits in DS by definin

194 and facilitated their functional coupling to GABA(B) receptors in neurons.

195 surface trafficking, and internalization of GABA(B) receptors in the presence of the KCTD12 subunit.

196 y, our findings suggest that GABA(A) but not GABA(B) receptors in the tLH act to suppress feeding beh

197 Our findings support a causal role of GABAB receptors in alcohol reinforcement and relapse to

198 spiking activity required the activation of GABAB receptors in CA3 PCs.

199 nhanced total and cell surface expression of GABAB receptors, indicating the constitutive degradation

200 Agonists for mu-opioid, nociceptin, and GABA(B) receptors induced postsynaptic currents that des

201 ligomers impart unique kinetic properties to GABAB receptor-induced Kir3 currents in heterologous cel

202 tors typically enhance vesicle release while GABAB receptors inhibit release.

203 The metabotropic GABA(B) receptor is a G protein-coupled receptor central

204 These findings indicate that the GABA(B) receptor is positioned to presynaptically modula

205 of GABA(A) receptor function by postsynaptic GABA(B) receptors is a newly identified mechanism that w

206 ly shown that signaling through postsynaptic GABA(B) receptors is significantly increased in the dent

207 Metabotropic GABAB receptor is a G protein-coupled receptor that medi

208 The GABAB receptor is also a GPCR that mediates metabotropic

209 ndicate that down-regulation of cell surface GABAB receptors is caused by the interaction of the rece

210 Inhibition of synaptic transmission by GABAB receptors is more sensitive to GABA than enhanceme

211 Vc1.1 and RgIA was significantly reduced in GABA(B) receptor knockdown DRG neurons.

212 We identified the GABAB receptor-like family member GrlB as the major GABA

213 that in vivo modulation of synaptic input by GABAB receptors may act to preserve ITD selectivity acro

214 n enhancement by GABAA receptors, suggesting GABAB receptors may be activated by ambient GABA or rele

215 or-mediated enhancement of EPSCs, suggesting GABAB receptors may be selectively activated by ambient

216 GABA(B) receptors mediate slow inhibitory neurotransmiss

217 Thus, OF causes opposing changes in GABAb receptor mediated suppression of GABA release from

218 GABA(B) receptor-mediated inhibition in the EC was media

219 of neuronal excitability in the EC underlies GABA(B) receptor-mediated inhibition of spatial learning

220 ocampal neurons reduces the magnitude of the GABA(B) receptor-mediated K(+) current response.

221 ing potassium channel, and moreover inhibits GABA(B) receptor-mediated transmission through an intera

222 3 pyramidal neurons by silencing widespread, GABA(B) receptor-mediated, monosynaptic inhibition.

223 We also find that GABAB receptor-mediated inhibition can be elicited by lo

224 The magnitude of GABAB receptor-mediated inhibition essentially depends o

225 ) neurons in layer 5, activating a source of GABAB receptor-mediated inhibition.

226 GABAB receptor-mediated inhibitory synapse defects are c

227 of cell surface GABAB receptors and thereby GABAB receptor-mediated neuronal inhibition.

228 receptors (GPCRs) (adenosine A(1) receptors, GABA(B) receptors, metabotropic glutamate receptors, and

229 A, acting through both presynaptic GABAA and GABAB receptors, modulate the amplitude and short-term p

230 This form of GABA(B) receptor modulation has widespread implications

231 Here we examine GABA(B) receptor modulation in layer 2/3 pyramidal neuro

232 tial-dependent release probability, or mGluR/GABA(B) receptor modulation of GABA release.

233 Together, these results confirm that GABA(B) receptors must be activated for the modulation o

234 GABA(B) receptors on histaminergic neurons were dispensa

235 ition of 5-HT neuron activity by presynaptic GABA(B) receptors on non-5-HT neurons in the DRN is one

236 Loss of GABA(B) receptors on primary afferent neurons may contri

237 e release through differential activation of GABAb receptors on glutamatergic inputs to neurons and i

238 interneurons to increase tonic inhibition at GABAB receptors on presynaptic corticostriatal terminals

239 he first synapse of the olfactory system via GABAB receptors on sensory terminals.

240 e of GABA innervation through both GABAA and GABAB receptors on subthalamic principal neurons.

241 Antagonism of GABA(B) receptors or dopamine D2 receptors partially rev

242 salamander slice preparation, we found that GABA(B) receptor pathways regulate bipolar cell release

243 Metabotropic GABA(B) receptors play a fundamental role in modulating

244 We tested the effects of ADX71441, a novel GABAB receptor positive allosteric modulator, on alcohol

245 -induced alcohol seeking were blocked by the GABAB receptor positive allosteric modulator.

246 Jointly, these observations indicate that GABAB receptor positive allosteric modulators merit bein

247 beta(1)ARs (monomers/dimers) and highest for GABA(B) receptors (prevalently dimers/tetramers of heter

248 During repetitive stimuli, activation of GABAB receptors reduced the amount of depression observe

249 olian gerbils, we confirm that activation of GABAB receptors reduces the amplitude of excitatory and

250 in the auditory cortex, and that presynaptic GABA(B) receptors regulate this development.

251 to further evaluate the hypothesis that the GABAB receptor represents a promising pharmacological ta

252 ere, we show that proteasomal degradation of GABAB receptors requires the interaction of the GABAB2 C

253 vity diminished the interaction of Rtp6 with GABAB receptors resulting in increased total as well as

254 dent hippocampus, we show that activation of GABAB receptors results in a decrease in KCC2 function,

255 d level of cell surface receptors diminished GABAB receptor signaling and, thus, neuronal inhibition.

256 tination sites increased receptor levels and GABAB receptor signaling in neurons.

257 change in paired-pulse ratio--and depend on GABAB receptor signaling.

258 IP as a key modulator of peripherally evoked GABAB-receptors signaling.

259 ts are mediated predominately by presynaptic GABAB receptor signalling in the TA pathway of Fmr1 KO m

260 semisynthetic fusion protein containing the GABA(B) receptor, SNAP- and CLIP-tag, a synthetic fluoro

261 ce dramatically sensitizes GIRK responses to GABAB receptor stimulation and markedly slows channel de

262 oton glutamate uncaging, we then reveal that GABA(B) receptors strongly inhibit NMDA receptor calcium

263 We studied GABAB receptor subunit 1 (GABAB1) splicing in alcoholic

264 e are short splicing variants in addition to GABAB receptor subunit GABAB1a, the longest known major

265 s needed functional expression of both human GABA(B) receptor subunits.

266 its alpha1 , alpha3 , beta2/3 , gamma2 , and GABAB receptor subunits R1 and R2.

267 ice was also more sensitive to inhibition of GABAB receptors, suggesting an increase in presynaptic G

268 The presynaptic GABA(B) receptors suppress Ca(2+) channel activity and i

269 Thus, stimulation of GABAB receptors suppresses an outward current, increasin

270 ata reveal a unique activation mechanism for GABA(B) receptor that involves the formation of a novel

271 structural asymmetry in the active state of GABA(B) receptor that is unique to the GABAergic system.

272 Corticostriatal terminals have presynaptic GABA(B) receptors that limit glutamate release, but how

273 eins 8, 12, and 16 are auxiliary subunits of GABAB receptors that differentially regulate G-protein s

274 eins 8, 12, and 16 are auxiliary subunits of GABAB receptors that differentially regulate G-protein s

275 Whereas the EC expresses a high density of GABA(B) receptors, the functions of these receptors in t

276 and postsynaptic trafficking itineraries on GABA(B) receptors, thereby contributing to their physiol

277 e in respiratory rate, indicating agonism at GABA(B) receptors to be primarily responsible for GHB-in

278 findings are evidence for a contribution of GABA(B) receptors to changes in hippocampal-based cognit

279 pothesis that GABA works through GABA(A) and GABA(B) receptors to influence the development of the PV

280 r in mouse taste buds, acting on GABA(A) and GABA(B) receptors to suppress transmitter (ATP) secretio

281 itory effects are mediated by signaling from GABAB receptor to the G protein-gated Inwardly-rectifyin

282 orward inhibition mediated by both GABAA and GABAB receptors to control the efficacy and temporal rul

283 t multiple sites by MIB2 controls sorting of GABAB receptors to lysosomes for degradation under physi

284 The signal that sorts GABAB receptors to lysosomes is currently unknown.

285 Although the mechanisms of GABAB receptor trafficking are studied to some extent, i

286 The gamma-aminobutyric acid type B (GABAB) receptor undergoes splicing and is an alcoholism

287 el currents after transient knockdown of the GABA(B) receptor using RNA interference.

288 Pharmacological blockade of GABA(B) receptors using the antagonist CGP55845 prolonge

289 ously showed that proteasomal degradation of GABAB receptors via the endoplasmic reticulum (ER)-assoc

290 dulation of GABA(A) currents by postsynaptic GABA(B) receptors was not observed in CA1 pyramidal cell

291 oxin and was abolished when both GABA(A) and GABA(B) receptors were blocked.

292 rently freely diffusing on the cell surface, GABA(B) receptors were prevalently organized into ordere

293 GABAB receptors were shown to associate with homo-oligom

294 stablished, the contribution of metabotropic GABAB receptors, which control excitatory neurotransmiss

295 Furthermore, activation of GABAB receptors, which reduces presynaptic calcium throu

296 mediated by gamma-aminobutyric acid type B (GABAB) receptors, which are heterodimeric G-protein-coup

297 recent report of the X-ray structure of the GABA(B) receptor with bound agonists and antagonists pro

298 ing ERAD function, and by the interaction of GABAB receptors with the essential ERAD components Hrd1

299 ains of high-frequency stimulation GABAA and GABAB receptors work together (rather than oppose one an

300 trains of stimulation, presynaptic GABAA and GABAB receptors work together to reduce short-term facil