ライフサイエンスコーパス: GABA(B) receptor

1 ltured neurons (e.g., antibodies against the GABAb receptor).

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

3 tracellular coiled-coil heterodimer of human GABAB receptor.

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

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

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

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

8 ubiquitination and lysosomal degradation of GABAB receptors.

9 the fold-related metabotropic glutamate and GABAB receptors.

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

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

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

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

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

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

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

17 lecular targets tested, including opioid and GABAB receptors.

18 dopamine neurons, preferentially activating GABAB receptors.

19 ch can be suppressed by reducing presynaptic 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 A inhibited DA release predominantly through GABA(B) receptors.

33 n mEPSCs, which were mediated by presynaptic GABA(B) receptors.

34 of heterodimeric and homodimeric full-length GABA(B) receptors.

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

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

37 yte signaling via gamma-aminobutyric acid B (GABA(B)) receptors.

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

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

40 The human GABA(B) receptor-a member of the class C family of G-pro

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

42 GABAB receptor activation selectively suppresses N-type

43 abinoid CB1 receptor-mediated suppression of GABA(B) receptor activity allows substance P to induce a

44 Only within a narrow range does prolonging GABA(B) receptor activity promote channel opening and in

45 pendence of T-type calcium channel gating on GABA(B) receptor activity regulates network oscillations

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

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

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

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

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

51 astric distension that could be rescued with GABA(B) receptor agonist.

52 The GABAB receptor agonist baclofen also inhibited inward cu

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

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

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

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

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

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

59 nally, we used local infusion of GABA(A) and GABA(B) receptor agonists (muscimol + baclofen) to show

60 Application of either GABA(A) or GABA(B) receptor agonists attenuated the colonic afferen

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

62 promoted by 4-aminopyridine and inhibited by GABA(B) receptor agonists, and appears far more sensitiv

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

64 as attenuated in the presence of GABA(A) and GABA(B) receptor agonists, the VMR was only consistently

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

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

67 f GABA(A) and GABA(B) receptors together, or GABA(B) receptors alone, significantly enhanced DA relea

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

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

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

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

72 he molecular details of KCTD binding to both GABA(B) receptors and G-protein betagamma subunits.

73 s crosstalk between postsynaptic GABA(A) and GABA(B) receptors and identifies the signaling pathways

74 These LNs inhibit PNs via GABA(B) receptors and mediate subtractive gain control.

75 A can inhibit DA release through GABA(A) and GABA(B) receptors and that these actions are not mediate

76 We show that GABA(B)-receptor and insulin-receptor play important rol

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

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

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

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

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

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

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

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

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

86 2 s, and were fully blocked by the selective GABA(B) receptor antagonist CGP 52432.

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

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

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

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

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

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

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

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

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

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

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

98 Conversely, GABA(A) and GABA(B) receptor antagonists increased the stretch respo

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

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

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

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

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

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

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

106 hotolytic uncaging of RuBi-GABA we show that GABA(B) receptors are tonically active and enhance extra

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

108 Cell surface GABAB receptors are constitutively internalized and eith

109 Metabotropic GABAB receptors are crucial for controlling the excitabi

110 GABAB receptors are emerging therapeutic targets for the

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

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

113 GABAB receptors are heterodimeric G protein-coupled rece

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

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

116 GABAB receptors are the G-protein coupled receptors for

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

118 GABA(B) receptors assemble from principle and auxiliary

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

120 a fundamentally novel approach for targeting GABA(B) receptor-associated neuropsychiatric disorders.

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

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

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

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

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

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

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

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

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

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

131 the muSPOT technology, we first defined the GABA(B) receptor-binding epitope mediating the KCTD inte

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

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

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

135 Stimulation of the metabotropic GABA(B) receptor by gamma-aminobutyric acid (GABA) resul

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 present a near full-length structure of the GABA(B) receptor, captured in an inactive state by cryo-

144 ased inhibitor that interferes with the KCTD/GABA(B) receptor complex and efficiently isolates endoge

145 us, we provide a template for modulating the GABA(B) receptor complex, revealing a fundamentally nove

146 This is particularly relevant to the GABA(B) receptor complex, which plays a prominent role i

147 ing a key protein-protein interaction of the GABA(B) receptor complex-the interaction with KCTD prote

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

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

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

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

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

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

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

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

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

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

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

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

160 n OSN release probability and a reduction in GABA(B) receptor expression in the conditioned glomerulu

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

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

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

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

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

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

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

168 es principal neuron excitability by reducing GABA(B) receptor (GABA(B)R)-mediated activation of G-pro

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

170 x(5-24)]NPY also reduced tonic activation of GABA(B) receptors (GABA(B)R), which increased PN excitab

171 Inhibitory G protein signaling mediated by GABA(B) receptors (GABA(B)Rs) and D(2) DA receptors (D(2

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

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

174 dulation of this microcircuit by presynaptic GABA(B) receptors (GABA(B)Rs) in the rodent hippocampus.

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

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

177 tors (mGluRs) and gamma-aminobutyric acid B (GABA(B)) receptors (GABA(B)Rs) most prominently.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

194 re heterodimerization for function(2-6), the GABA(B) receptor has two subunits, GABA(B1) and GABA(B2)

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

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

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

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

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

200 Here, we found that genetic ablation of GABA(B) receptors in medial prefrontal cortex astrocytes

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

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

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

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

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

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

207 Here, we found that GABA(A) and GABA(B) receptors inhibit DA release without requiring c

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

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

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

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

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

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

214 The GABAB receptor is also a GPCR that mediates metabotropic

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

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

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

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

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

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

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

222 GABA(B) receptors mediate slow inhibitory neurotransmiss

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

224 after the critical period, it only restored GABA(B) receptor-mediated IPSP amplitudes.

225 s, we recorded the amplitudes of GABA(A) and GABA(B) receptor-mediated IPSPs in auditory cortical and

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

227 3 pyramidal neurons by silencing widespread, GABA(B) receptor-mediated, monosynaptic inhibition.

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

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

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

231 GABAB receptor-mediated inhibitory synapse defects are c

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

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

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

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

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

237 ion of dopamine D1 or D2 receptors, GABAA or GABAB receptors, NMDA receptors, P2Y1 ATP receptors, met

238 GABA(B) receptors on histaminergic neurons were dispensa

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

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

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

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

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

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

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

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

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

254 emonstrate that striatal astrocytes, through GABA(B) receptor signaling, regulate behaviors including

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 GABA(B)-receptor signalling is tightly regulated by auxi

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

261 triatal GABA operating through predominantly GABA(B) receptors.SIGNIFICANCE STATEMENT The principal i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

283 Furthermore, antagonists of GABA(A) and GABA(B) receptors together, or GABA(B) receptors alone,

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

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

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

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

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

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

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

291 GABAB receptors were shown to associate with homo-oligom

292 e exhibited normal presynaptic inhibition by GABA(B) receptors, which inhibit VGCCs, but defective pr

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

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

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

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

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

298 as reduced by GABA or agonists of GABA(A) or GABA(B) receptors, with effects prevented by selective G

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