ライフサイエンスコーパス: GlyR

1 GlyR activation accounted for 15% of interneuron IPSC am

2 GlyR are found in the spinal cord and brain stem, and mo

3 GlyR are involved in motor coordination, respiratory rhy

4 GlyR Cl(-) channels are expressed on ASM and regulate sm

5 GlyR subtypes have differing caffeine sensitivity.

6 GlyR-Ab was detected in one patient with TM.

7 GlyRs are members of the pentameric ligand-gated ion cha

8 GlyRs containing the alpha2 subunit are highly expressed

9 GlyRs expressed by hECNs were activated by glycine with

10 GlyRs not only regulate the excitability of motor and af

11 VGKC-complex, LGI1, CASPR2 and contactin-2, GlyR, D1R, D2R, AMPAR, GABA(B)R and glutamic acid decarb

12 ta GlyR, which suggests that the alphaChb+a- GlyR reconstitutes structural components and recapitulat

13 he beta+/alpha- interface in the alphaChb+a- GlyR were also found in the heteromeric alphabeta GlyR,

14 interfaces in a homomeric GlyR (alphaChb+a- GlyR), we were able to functionally characterize the alp

15 finite CJD had NSA-abs, including NMDAR-abs, GlyR-abs, LGI1-abs, or CASPR2-abs.

16 as inhibitory receptors, presynaptic-acting GlyRs (preGlyRs) can also facilitate glutamate release u

17 and other endogenous molecules can activate GlyRs.

18 The deltaL2 mutations did not affect GlyR or GABA(A)R sensitivity, respectively, to Zn(2+) or

19 After GlyR beta-loop binding, the stability of the E domain in

20 the only antagonist, strychnine, blocks all GlyR subunit combinations.

21 lass of tricyclic sulfonamides as allosteric GlyR potentiators.

22 subunit interfaces from the homomeric alpha GlyR, subunit interfaces from the heteromeric alphabeta

23 to the alpha+/alpha- interface in the alpha GlyR.

24 al modification could indeed modulate alpha1 GlyR behavior.

25 Aspartate-97, located at the alpha1 GlyR interface, is a conserved residue in the cys-loop r

26 also replaced the M3-M4 linker of the alpha1 GlyR with much shorter peptides and found that none of t

27 model of the N-terminal domain of the alpha1 GlyR, we hypothesized that an arginine-119 residue was f

28 icroscopy structures of the zebrafish alpha1 GlyR with strychnine, glycine, or glycine and ivermectin

29 es in mice bearing point mutations in alpha1 GlyRs that are responsible for a hereditary startle-hype

30 stry indicated that the expression of alpha1 GlyRs in nervous tissues and spinal cord neurons (SCNs)

31 Thus, presynaptic alpha1 GlyRs emerge as a potential therapeutic target for domin

32 subtypes and are dominated by the alpha1beta GlyR.

33 hird transmembrane domain of purified alpha3 GlyR.

34 e conclude that functional alpha2 and alpha3 GlyRs are present in various regions of the forebrain an

35 pressing human alpha1, rat alpha2 and alpha3 GlyRs.

36 ous regions of the forebrain and that alpha3 GlyRs specifically participate in tonic inhibition in th

37 Our findings suggest that the alpha3 GlyRs mediate glycinergic cannabinoid-induced suppressio

38 effect is absent in mice lacking the alpha3 GlyRs.

39 with cannabinoid potentiation of the alpha3 GlyRs.

40 However, because the alpha3beta GlyR is more than 3-fold less sensitive to glycine than

41 d inhibition was observed for P36A at alpha7-GlyR.

42 ne domain of alpha1 glycine receptor (alpha7-GlyR).

43 it interfaces from the heteromeric alphabeta GlyR have not been characterized unambiguously because o

44 were also found in the heteromeric alphabeta GlyR, which suggests that the alphaChb+a- GlyR reconstit

45 lpha- interface in the heteromeric alphabeta GlyR.

46 e to functionally characterize the alphabeta GlyR beta+/alpha- interfaces.

47 intersubunit electrostatic interaction among GlyR subunits thus contributes to the stabilization of t

48 Here, we analyzed GlyR currents in several regions of the adolescent mouse

49 MDAR 13/48 (27%), VGKC-complex 7/48(15%) and GlyR 1/48(2%).

50 Ion selectivity of CFTR, ANO1 and GlyR is critically affected by the electric permittivity

51 ermeability (P HC O3/ Cl ) of CFTR, ANO1 and GlyR.

52 ming the previous result, two had CASPR2 and GlyR antibodies and one had CASPR2 and NMDAR antibodies;

53 aneous glycinergic postsynaptic currents and GlyR immunolabeling revealed that A8 cells express GlyRs

54 The GABAAR and GlyR pore blocker picrotoxin prevented desensitization,

55 Molecular interaction between Gbetagamma and GlyR could be used as a target for pharmacological modif

56 tive relationship exists between insulin and GlyR, because insulin enhances the glycine-activated cur

57 the presence of antibodies to AQP4, MOG, and GlyR using cell-based assays.

58 MOG in 10 patients, AQP4 in 6 patients, and GlyR in 7 patients (concurrent with MOG in 3 and concurr

59 dicating that the crosstalk between KARs and GlyRs relies on the SUMOylation status of PKC.

60 In Glra2(-/Y) animals, GlyR tonic currents were preserved; however, the amplitu

61 ar clustering and pharmacological profile as GlyRs on MNTB principal cells.

62 ining synaptic heteromeric alpha1(Q177K)beta GlyRs had decreased current amplitudes with significantl

63 in synaptic integration of alpha1(Q177K)beta GlyRs.

64 and capsaicin, delays the maturation of both GlyR subunits and glycinergic inhibition, maintaining do

65 per physiological postsynaptic inhibition by GlyR in vivo.

66 own about the molecular basis of cannabinoid-GlyR interactions.

67 ctivation of kainate receptors (KARs) causes GlyR endocytosis in a calcium- and protein kinase C (PKC

68 ne, an agonist of glycine receptor chloride (GlyR Cl(-)) channels, was found to relax contracted ASM,

69 In contrast, GlyR IPSC and NMDAR-EPSC decay times were unchanged.

70 These findings are the first to define GlyR subunit-specific control of visual function and Gly

71 hese results, we threaded the WT and deltaL2 GlyR sequences onto the x-ray structure of the bacterial

72 Here we show two functionally different GlyRs populations in the rat medial nucleus of trapezoid

73 R beta+/alpha- interface, which could direct GlyR beta+/alpha- interface-specific drug design, but al

74 cuss recently emerging functions of distinct GlyR isoforms.

75 Tested against the EC(50) of each GlyR subtype, the order of caffeine potency (IC(50)) is:

76 The endogenous GlyR activity was strongly enhanced by inhibition of the

77 Peptide D12-116 markedly enhanced GlyR currents at low micromolar concentrations but had n

78 To examine GlyRs in ALS motoneurons, we bred G93A-SOD1 mice to Hb9-

79 located on all hcrt/orx cells and excitatory GlyRs located on presynaptic terminals contacting some h

80 mmunolabeling revealed that A8 cells express GlyRs containing the alpha2 subunit.

81 We describe an extracellular GlyR alpha1 subunit mutation (Q177K) in a novel mouse st

82 tonic conductance mediated by extrasynaptic GlyRs, which dominates DR inhibition.

83 These findings identify extrasynaptic GlyRs as critical regulators of DR excitability and a no

84 by two GlyR pools: inhibitory extrasynaptic GlyRs located on all hcrt/orx cells and excitatory GlyRs

85 Finally, GlyR tone varied inversely with extracellular fluid toni

86 In addition to being the first GlyR model threaded on GLIC, the juxtaposition of the tw

87 e amide moiety of asparagine was crucial for GlyR activation.

88 op D/beta2-3 is an important determinant for GlyR trafficking and functionality, whereas alterations

89 SUMOylation-dependent regulatory pathway for GlyR endocytosis, which may have important physiological

90 -complex, one of which was also positive for GlyR antibodies.

91 xcitability associated with gain-of-function GlyR expression in glutamatergic neurons resulted in rec

92 network excitability due to gain-of-function GlyR expression in parvalbumin-positive interneurons res

93 del, targeted expression of gain-of-function GlyR in terminals of glutamatergic cells or in parvalbum

94 which led us to question whether functional GlyR Cl(-) channels are expressed in ASM.

95 ts provide the first evidence for functional GlyRs in identified hcrt/orx circuits and suggest that t

96 here are at least two subtypes of functional GlyRs in the PFC neurons of young rats, and their physio

97 f the neurotransmitter receptor for glycine (GlyR) that is found in hippocampectomies from patients w

98 sites, thereby anchoring inhibitory glycine (GlyR) and subsets of gamma-aminobutyric acid type A (GAB

99 n dynamics and synaptic trapping of glycine (GlyR) but not GABAA receptors.

100 tif in the large intracellular loop of GlyR (GlyR-IL), was able to inhibit the ethanol-elicited poten

101 controls with multiple sclerosis, 5 (8%) had GlyR antibodies.

102 Hence, GlyRs constitute promising targets for the development o

103 -resistant subtype the alphabeta heteromeric GlyR, was also present.

104 t/orx neurons contain alpha/beta-heteromeric GlyRs that lack alpha2-subunits, whereas alpha2-subunits

105 synaptic, presumably alphabeta heteromeric, GlyRs only after priming with PGE2.

106 Ligand-gated heteropentameric GlyRs form chloride ion channels that contain the alpha(

107 uting beta+/alpha- interfaces in a homomeric GlyR (alphaChb+a- GlyR), we were able to functionally ch

108 ), which selectively blocked alpha homomeric GlyRs.

109 they are mediated by extrasynaptic homomeric GlyRs.

110 However, GlyR activation was found to account for <3% of the PC i

111 study suggests that selective alterations in GlyR function contribute to inhibitory insufficiency in

112 Similar changes in GlyR cluster properties were found in spinal cultures fr

113 blocking action on the effect of ethanol in GlyR.

114 its disruption represents a critical step in GlyR activation.

115 en the equivalent positions were examined in GlyRs, the M2 S18'I substitution significantly altered t

116 can profoundly affect ethanol sensitivity in GlyRs and GABA(A)Rs.

117 RNA-seq indicates GlyRs are likely to be composed of alpha2 and beta subun

118 on of PKC is involved in the kainate-induced GlyR endocytosis and thus plays an important role in the

119 Zn(2)(+) can either potentiate or inhibit GlyR activity depending on its concentration, while Cu(2

120 Although an inhibitory GlyR tone is widely observed in the brain, it remains un

121 s structural element is vital for inhibitory GlyR function, signaling, and synaptic clustering.SIGNIF

122 This inhibitory GlyR tone was eliminated by pharmacological blockade of

123 Inhibitory GlyRs are also found throughout the brain, where GlyR al

124 of chronic pain and other diseases involving GlyR dysfunction.

125 This form of LTP (GlyR LTP) results from an increase in the number and/or

126 fy novel peptides that specifically modulate GlyR function.

127 Increased expression of the mutant GlyR alpha1(Q177K) subunit in vivo was not sufficient to

128 eactivation of the agonist current at mutant GlyRs.

129 We expressed mutant GlyRs in HEK293T cells, and electrophysiological analyse

130 yRbeta that coimmunoprecipitates with native GlyRs from brainstem extracts.

131 A nonfunctional GlyR subunit, truncated at the intracellular TM3-4 loop

132 NHE3), an electroneutral ion channel, and of GlyR, an inactive Cl(-) channel, do not cause CFAs, demo

133 erization of the receptor and development of GlyR-related therapeutics.

134 CGRP(+) and IB4(+) terminals were devoid of GlyR alpha1-subunit and gephyrin.

135 urrent may result from the downregulation of GlyR mRNA expression in motoneurons.

136 and glutamate receptors, with no evidence of GlyR-mediated PSCs.

137 A fragment of GlyR-IL without the basic amino acids did not interact w

138 NA expression levels and immunoreactivity of GlyR subunits, as well as ethanol sensitivity.

139 f a motif in the large intracellular loop of GlyR (GlyR-IL), was able to inhibit the ethanol-elicited

140 highlight the sensitive allosteric nature of GlyR.

141 ganglion cells do not express a plethora of GlyR subtypes and are dominated by the alpha1beta GlyR.

142 RQH(C7), can inhibit ethanol potentiation of GlyR currents.

143 hus establish that selective potentiation of GlyR function is a promising strategy against chronic in

144 dicate that ethanol mediated potentiation of GlyR is in part by Gbetagamma activation.

145 betagamma or inhibit ethanol potentiation of GlyR.

146 We investigated the presence of GlyR subunits in nAc and their modulation by ethanol in

147 We conclude that a proportion of GlyR alpha1 mutants can be transported to the plasma mem

148 otoneurons, indicating that the reduction of GlyR current may result from the downregulation of GlyR

149 erstanding of the function and regulation of GlyR.

150 ould contribute to understanding the role of GlyR alpha1 in the reward system and might help to devel

151 of GlyR beta-subunit produces segregation of GlyR subtypes involved in two different mechanisms of mo

152 ining region alters the anion selectivity of GlyR.

153 The significance of GlyR antibodies in the setting of ON is unclear and dese

154 s using the high-resolution NMR structure of GlyR TM23 in trifluoroethanol as the starting template.

155 +) binds to E192 and H215 in each subunit of GlyR with a 40 muM apparent dissociation constant, consi

156 e results suggest that specific targeting of GlyR beta-subunit produces segregation of GlyR subtypes

157 Our results show ubiquitous expression of GlyRs that mediate large-amplitude currents in response

158 cts could be explained by unique features of GlyRs that are activated by pooling of glycine across sy

159 While the prevalent adult forms of GlyRs are heteromers, previous reports suggested functio

160 found that a lack of synaptic integration of GlyRs, together with disrupted receptor function, is res

161 and they form the predominant population of GlyRs in the postnatal and adult human brain, brainstem

162 Here, we investigated the presence of GlyRs in accumbal dopamine receptor medium spiny neurons

163 siological and pharmacological properties of GlyRs in mature PFC neurons have not been well studied.

164 , we sought to better understand the role of GlyRs in the facilitation of excitatory neurotransmitter

165 localization mechanism for a minor subset of GlyRs.

166 , we mutated Loop 2 in the alpha1 subunit of GlyRs and in the gamma subunit of alpha1beta2gamma2GABA(

167 ty were observed across multiple subunits of GlyRs and GABA(A)Rs.

168 ic explanation for the effects of ethanol on GlyR-based on changes in Loop 2 structure.

169 The effects of TSP-1 on GlyRs were dependent on the activation of excitatory rec

170 and impaired hyperpolarizing GABAAR- and/or GlyR-mediated currents have been implicated in epilepsy,

171 isolated ON had antibodies to MOG, AQP4, or GlyR.

172 o human Cys-loop receptors such as GABAAR or GlyR.

173 s sensitive to glycine than any of the other GlyR subtypes, this receptor is most effectively blocked

174 For example, the determination of pentameric GlyR structures bound to glycine and strychnine have con

175 nd that five Cu(2)(+) can be coordinated per GlyR.

176 rons by viral miRNA expression, postsynaptic GlyR clusters were significantly reduced in both size an

177 onstrated a decrease of surface postsynaptic GlyR on G93A-SOD1 motoneurons.

178 Postsynaptic GlyRs on hcrt/orx cells remained functional during both

179 yR antagonist strychnine blocks postsynaptic GlyRs under all conditions, occluding RDE.

180 enous and endogenous cannabinoids potentiate GlyRs via a hydrogen bonding-like interaction.

181 CBD selectively rescues impaired presynaptic GlyR activity and diminished glycine release in the brai

182 ittle is known about the role of presynaptic GlyRs, likely alpha homomers, in diseases.

183 than are heteromers, suggesting presynaptic GlyRs as a primary target.

184 The R131A GlyR mutation, which reduces strychnine antagonism witho

185 a indicate disturbances in glycine receptor (GlyR) alpha1 biogenesis.

186 ive mutations in the human glycine receptor (GlyR) alpha1 gene (GLRA1) are the major cause of this di

187 (GLRA1) of the inhibitory glycine receptor (GlyR) and the cognate presynaptic glycine transporter (S

188 A) receptor (GABA(A)R) and glycine receptor (GlyR) are described.

189 The glycine receptor (GlyR) exists either in homomeric alpha or heteromeric al

190 Glycine receptor (GlyR) gating is initiated by agonist binding at interfac

191 The glycine receptor (GlyR) is a member of the Cys-loop superfamily of ligand-

192 The glycine receptor (GlyR) is a pentameric ligand-gated ion channel (pLGIC) m

193 The strychnine-sensitive glycine receptor (GlyR) mediates inhibitory synaptic transmission in the s

194 ovide inhibitory input via glycine receptor (GlyR) subunit alpha1 to OFF cone bipolar cells and to ON

195 In contrast, the role of glycine receptor (GlyR) subunit-specific inhibition is less clear because

196 encode the alpha1 and beta glycine receptor (GlyR) subunits, are the major cause.

197 ock-in (KI) mouse having a glycine receptor (GlyR) with phenotypical silent mutations at KK385/386AA,

198 such as CFTR, ANO1 and the glycine receptor (GlyR), by changing pore size.

199 in-1(ANO1/TMEM16A) and the glycine receptor (GlyR), revealed that the ion selectivity of anion channe

200 hances the activity of the glycine receptor (GlyR), thus enhancing inhibitory neurotransmission, lead

201 tate receptor (NMDAR), the glycine receptor (GlyR), voltage-gated potassium channel (VGKC)-complex an

202 ncipal output neurons, via glycine receptor (GlyR)-enriched synapses, virtually devoid of the main GA

203 ll patch-clamp recordings, glycine receptor (GlyR)-mediated currents in spinal motoneurons from these

204 R and the homomeric alpha1 glycine receptor (GlyR).

205 (2)(+) in the human alpha1-glycine receptor (GlyR).

206 Glycine receptors (GlyR) are inhibitory Cys-loop ion channels that contribu

207 Strychnine-sensitive glycine receptors (GlyR) play a major role in the excitability of CNS neuro

208 that ethanol can modulate glycine receptors (GlyR), in part, through Gbetagamma interaction with basi

209 islet beta-cells express glycine receptors (GlyR), notably the GlyRalpha1 subunit, and the glycine t

210 esser extent, by synaptic glycine receptors (GlyR).

211 competitive antagonist of glycine receptors (GlyRs) accelerated IPSC decay.

212 ct ethanol sensitivity in glycine receptors (GlyRs) and gamma-aminobutyric acid type A receptors (GAB

213 lation of homomeric human glycine receptors (GlyRs) and nematode glutamate-gated chloride channels (G

214 Inhibitory glycine receptors (GlyRs) are composed of homologous alpha- (alpha1-4) and

215 Glycine receptors (GlyRs) are found in most areas of the brain, and their d

216 Glycine receptors (GlyRs) are inhibitory ligand-gated ion channels expresse

217 us studies suggested that glycine receptors (GlyRs) are involved in the regulation of accumbal dopami

218 Glycine receptors (GlyRs) are ligand-gated chloride channels that mediate i

219 Glycine receptors (GlyRs) are major mediators of inhibition in the spinal c

220 Glycine receptors (GlyRs) are potentiated by ethanol and they have been imp

221 Glycine receptors (GlyRs) are structurally related to GABAA receptors and h

222 Although postsynaptic glycine receptors (GlyRs) as alphabeta heteromers attract considerable rese

223 eceptors (GABA(B)Rs), and glycine receptors (GlyRs) can be identified in patients and are associated

224 activation of heteromeric glycine receptors (GlyRs) composed primarily of alpha1 and beta subunits.

225 The properties of glycine receptors (GlyRs) depend upon their subunit composition.

226 and strychnine-sensitive glycine receptors (GlyRs) expressed by excitatory cortical neurons derived

227 ing defects of inhibitory glycine receptors (GlyRs) have been linked to human hyperekplexia/startle d

228 easing that of inhibitory glycine receptors (GlyRs) in synapses.

229 Glycine receptors (GlyRs) mediate inhibitory neurotransmission in spinal co

230 Strychnine-sensitive glycine receptors (GlyRs) mediate synaptic inhibition in the spinal cord, b

231 cellular loop 2 region of glycine receptors (GlyRs) or gamma-aminobutyric acid type A receptors (GABA

232 regulated endocytosis of glycine receptors (GlyRs) play a critical function in balancing neuronal ex

233 receptors (GABA(A)Rs) and glycine receptors (GlyRs) play a role in control of dorsal horn neuron exci

234 of a specific subtype of glycine receptors (GlyRs) that contain alpha3 subunits.

235 nnabinoids can potentiate glycine receptors (GlyRs), an important target for nociceptive regulation a

236 -loop GABAA (GABAARs) and glycine receptors (GlyRs), which both mediate fast inhibitory synaptic tran

237 ) permeable extrasynaptic glycine receptors (GlyRs).

238 d receptors (GABAARs) and glycine receptors (GlyRs).

239 ng by activating neuronal glycine receptors (GlyRs).

240 ntly mature alpha(1)/beta glycine receptors (GlyRs).

241 n allosterically modulate glycine receptors (GlyRs).

242 antagonist at ionotropic glycine receptors (GlyRs).

243 troducing the N46K mutation into recombinant GlyR alpha1 homomeric receptors, expressed in HEK cells,

244 sitization decay time constants, and reduced GlyR clustering and synaptic strength.

245 C (PKC)-dependent manner, leading to reduced GlyR-mediated synaptic activity in cultured spinal cord

246 ), a nonpsychoactive cannabinoid, can rescue GlyR functional deficiency and exaggerated acoustic and

247 6 rat hippocampal slices, we detected robust GlyR activity as a tonic current and as single-channel e

248 Surprisingly, small GlyR clusters were also found at PC synapses onto princi

249 ptic currents (IPSCs) and induce spontaneous GlyR activation.

250 the oligomerization, folding and stability, GlyR beta-loop binding, and phosphorylation of three gep

251 d synaptic clustering.SIGNIFICANCE STATEMENT GlyR dysfunction underlies neuromotor deficits in startl

252 MOG) or the glycine receptor alpha1 subunit (GlyR) is unclear.

253 es of the distribution of GABA(A)R-subunits, GlyR alpha1-subunit and their anchoring protein, gephyri

254 ng and/or cytoskeletal anchoring of synaptic GlyRs.

255 We found that GlyR alpha1 subunits are expressed at higher levels than

256 Our study shows that GlyR alpha1 in nAc is a new target for development of no

257 pses on dorsal horn neurons, suggesting that GlyR LTP is triggered during inflammatory peripheral inj

258 The GlyR antagonist strychnine blocks postsynaptic GlyRs und

259 The GlyR beta8-beta9 loop is therefore an essential regulato

260 The GlyR Cl(-) channel antagonist strychnine significantly b

261 uctural and functional information about the GlyR beta+/alpha- interface, which could direct GlyR bet

262 osteric modulator acting specifically at the GlyR has been identified, hindering both experimental ch

263 strychnine may bind to similar sites at the GlyR.

264 main in Geph-C3 is less stable and binds the GlyR beta-loop with one order of magnitude lower affinit

265 R) antagonist strychnine and mimicked by the GlyR agonist alanine.

266 ion of the X-linked gene GLRA2, encoding the GlyR alpha2 subunit, in a boy with autism.

267 disruption reveals an important role for the GlyR alpha1 subunit beta8-beta9 loop in initiating rearr

268 These structures illuminate the GlyR mechanism and define a rubric to interpret structur

269 vestigated the N46K missense mutation in the GlyR alpha1 subunit gene found in the ethylnitrosourea (

270 e (N) with lysine (K), at position 46 in the GlyR alpha1 subunit induced hyperekplexia following a re

271 Recordings from mice deficient in the GlyR alpha3 subunit (Glra3(-/-)) revealed a lack of toni

272 rst evidence to link a molecular site in the GlyR with the sedative effects produced by intoxicating

273 zed in the large extracellular domain of the GlyR alpha1 have reduced cell surface expression with a

274 in the extracellular beta8-beta9 loop of the GlyR alpha1 subunit.

275 between transmembrane regions 3 and 4 of the GlyR alpha3 subunit.

276 frameshift within the coding regions of the GlyR beta subunit.

277 4, inhibited the ethanol potentiation of the GlyR in both evoked currents and synaptic transmission i

278 Also, the potentiation of the GlyR-mediated tonic current by ethanol suggests that the

279 We found that the GlyR alpha1 subunit is preferentially expressed in nAc a

280 rfered with the binding of Gbetagamma to the GlyR and consequently inhibited the ethanol-induced pote

281 ticity of glycinergic synapses by tuning the GlyR diffusion trap.

282 By contrast, we report that unusually the GlyR antagonist strychnine reveals a large tonic conduct

283 glycine was blocked by pretreatment with the GlyR Cl(-) channel antagonist strychnine.

284 The GlyRs expressed as alpha1 homomers either in HEK-293 cel

285 ne the colocalization of GlyRbeta with these GlyR subunits in the mouse retina, >90% of the GlyRalpha

286 activity and connectivity primarily through GlyR-mediated synaptic transmission.

287 ubunit (Glra3(-/-)) revealed a lack of tonic GlyR currents in the striatum and the PFC.

288 ments within the extracellular-transmembrane GlyR interface and that this structural element is vital

289 developed hcrt/orx cells is regulated by two GlyR pools: inhibitory extrasynaptic GlyRs located on al

290 s are also found throughout the brain, where GlyR alpha2 and alpha3 subunit expression exceeds that o

291 mutation represents a new mechanism by which GlyR dysfunction induces startle disease.

292 This represents a new mechanism by which GlyR dysfunction induces startle disease.

293 yperekplexia disease and other diseases with GlyR deficiency.

294 Gbetagamma interaction with GlyR is an important determinant in ethanol potentiation

295 0 [range, 0-14]; P = .08), and patients with GlyR antibodies alone (n = 3) (median visual score, 0 [r

296 Among the 3 patients with GlyR antibodies alone, 1 patient had monophasic ON, 1 ha

297 The 3 patients with GlyR antibodies concurrent with MOG antibodies had recur

298 = .10).The median age of the 7 patients with GlyR antibodies was 27 (range, 11-38) years; 5 (71%) of

299 ical profile that favors an interaction with GlyRs that have been primed by peripheral inflammation.

300 s similar to those of maximally activated WT GlyR.