ライフサイエンスコーパス: baclofen

1 ffective when the training was combined with baclofen.

2 but not PV-IPSCs to a GABAb receptor agonist baclofen.

3 idative phosphorylation, and withdrawal from baclofen.

4 cantly blocked feeding elicited by NAC shell baclofen.

5 +) channel blocker facilitated the effect of baclofen.

6 transmission, studied with the GABAB agonist baclofen.

7 the application of diazepam or low doses of baclofen.

8 from that of the GABA(B)R agonists GABA and baclofen.

9 , 4-AP only partially blocked the actions of baclofen.

10 tagonist, CGP 35348, reversed the effects of baclofen.

11 nflammation of the colon were not altered by baclofen.

12 lease probability was reduced with Cd(2+) or baclofen.

13 g after SCI and restored by long-term use of baclofen.

14 f magnitude greater than the pharmaceutical, baclofen.

15 ying clinical effect of inrathecally infused baclofen.

16 ve agonist THIP (10 mum) were potentiated by baclofen.

17 neurons, as did the GABA(B) receptor agonist baclofen.

18 he gamma aminobutyric acid (GABA(B)) agonist baclofen (0-ng, 25-ng, or 50-ng total infusion; Experime

19 ion training (experiment 1) or muscimol plus baclofen (0.1 and 1.0 mM) or vehicle infusions into the

20 ministration of the GABA(B) receptor agonist baclofen (0.1-10 microg/50 microL) on evoked responses o

21 Baclofen (0.5-5 microM) eliminated the increase in sIPSC

22 A by GABAA+GABAB receptor agonists (muscimol+baclofen, 0.03+0.3 nmol) on cue-induced methamphetamine

23 e hyperpolarized by both the GABA(B) agonist baclofen (1 microM) and the kappa-opioid receptor agonis

24 Systemic administration of R-(+)-baclofen (1.25 mg/kg, i.p.) did not alter total distance

25 inistration of the GABA(B) receptor agonist, baclofen (10 mg/kg, i.p.), significantly reduced Fos exp

26 ort-term synaptic depression appeared during baclofen (10 mum) application when initial Pr was greate

27 ation of presynaptic GABAB receptors by (+/-)baclofen (10 mum), GABA (2 mm) or by GABA uptake inhibit

28 ts, GABA (2 mm), muscimol (10-100 microM) or baclofen (10-100 microM), in the presence of TTX, each o

29 Rats were subsequently administered baclofen (2 mg/kg i.p. or vehicle) immediately after eac

30 In a separate experiment, systemic baclofen (2.5 mg/kg) decreased the amphetamine-induced i

31 u hybridization histochemistry revealed that baclofen (2.5 mg/kg, i.p.) decreased the ability of amph

32 Baclofen (20 microM), an agonist for the G-protein-coupl

33 The GABA(B) receptor agonist baclofen (20 mum) enhanced GABA(A) currents.

34 Muscimol (25 ng) and baclofen (200 microg) each significantly and equi-effect

35 sessed for food intake following vehicle and baclofen (200 ng) in each site.

36 intakes were assessed following vehicle and baclofen (200 ng) in each site.

37 rgic neurons to the GABA(B) receptor agonist baclofen 24 hr after treatment.

38 (diazepam, 6 of 6 patients treated, and oral baclofen, 3 of 3 treated) and immunotherapy (intravenous

39 y attenuated after 7 micromol/kg intravenous baclofen (-37% +/- 10%; N = 5).

40 (-)-Baclofen (5-10 microM) caused a small (28 +/- 11 %) inhi

41 The GABA(B) receptor agonist (-)-baclofen (5-10 microM) depressed an atropine-sensitive s

42 fully reversed the depressant effects of (-)-baclofen (5-10 microM) such that in the combined presenc

43 methanesulfonate (U-50,488H; 1 microM), and baclofen (50 microM) inhibited Ca2+ currents, whereas th

44 dent participants were randomized to receive baclofen (60 mg/d; 20 mg t.i.d.) or placebo.

45 DAMGO (93%) or the GABA(B) receptor agonist baclofen (83%) with a membrane hyperpolarization or an o

46 In Experiment 2, we tested the influence of baclofen (a GABABR agonist) and diazepam (a classical be

47 Administration of baclofen, a GABA(B) agonist known to attenuate piriform

48 Baclofen, a GABAB receptor agonist, activated G-protein

49 Baclofen, a gamma-aminobutyric acid receptor(B) agonist,

50 observed following chronic treatment with R-baclofen, a selective agonist of GABAB receptors.

51 The protective effect of baclofen, a selective GABA(B) receptor agonist, on the i

52 f GHB, and the effect of GHB was mimicked by baclofen, a selective GABAB receptor agonist, whereas th

53 Application of baclofen, a specific GABA(B) receptor agonist, inhibited

54 e in relapse prevention, we examined whether baclofen-a GABAB receptor agonist that reduces mesolimbi

55 In the absence of TTX, baclofen activated an outward K+ current that hyperpolar

56 A GABA(B)R agonist, baclofen, activated Akt and stimulated neutrophil-direct

57 ocaine exposure both synaptically evoked and baclofen-activated GABA(B)R-GIRK currents were significa

58 Thus, baclofen administered in conjunction with extinction tra

59 Baclofen administration in the VTA and NAC shell was pre

60 Baclofen administration in the VTA or NACs was also prec

61 to investigate the effects of chronic oral R-baclofen administration in two independently generated m

62 Selective GABA(A) (muscimol) and GABA(B) (baclofen) agonists administered into the nucleus accumbe

63 ither GABAA (e.g., muscimol) or GABAB (e.g., baclofen) agonists into either the shell region of the n

64 Baclofen also blocked the amphetamine-induced rise in SG

65 The GABAB receptor agonist baclofen also inhibited inward currents induced by CIM02

66 RGS6(-/-) mice administered baclofen also showed exaggerated motor coordination defi

67 Baclofen also significantly decreases dorsal horn CGRP i

68 Baclofen alters this history dependence by causing no in

69 tin, and a compounded topical gel containing baclofen, amitriptyline HCL, and ketamine, these agents

70 ol mice, whereas there was no difference for baclofen, an agonist at GABA(B) receptors.

71 f these reactions to the formal syntheses of baclofen and (+)-monomorine was demonstrated.

72 aclofen treatment by either coapplication of baclofen and adenosine, or intracellular infusion of the

73 y examined the effect of the GABA(B) agonist baclofen and alpha-conotoxins Vc1.1 and RgIA on calcium

74 M) such that in the combined presence of (-)-baclofen and CGP 55845A the EPSP(M) was 134 +/- 21 % of

75 However, baclofen and CP55940 did not act identically, because on

76 odulation interventions, such as intrathecal baclofen and deep brain stimulation, are promising optio

77 ysed units from subjects who were not taking baclofen and fastest for units from the uninjured.

78 s from spinal cord injured subjects who take baclofen and have done so for a median of 7 years, 25 pa

79 Baclofen and morphine also dose-dependently ameliorated

80 nd that inhibition of LSr neurons with local baclofen and muscimol microinjection (0.3/0.03 nmol) blo

81 In contrast, combined subthreshold doses of baclofen and muscimol produced a significant synergistic

82 In the resting condition, a dose of baclofen and muscimol that blocked a behaviorally induce

83 on of the dlCPu with GABA receptor agonists (baclofen and muscimol) immediately prior to reinstatemen

84 ation, through infusion of the GABA agonists baclofen and muscimol, on place acquisition and reversal

85 Baclofen and somatostatin, agonists of Gi-coupled recept

86 The GABAB antagonist baclofen and the metabotropic glutamate receptor antagon

87 4-chlorobenzenepropanoic acid hydrochloride (baclofen) and GABA are increased at the constitutively a

88 that directly modulates GABAergic signaling (baclofen) and one agent that indirectly modifies NMDAR-m

89 toxin A), intrathecally administered drugs (baclofen), and surgery (neurectomy, rhizotomy) has becom

90 ness of both rostral and caudal MVN cells to baclofen, and a marked upregulation of the responsivenes

91 neurotransmitter release by neuropeptide Y, baclofen, and adenosine as revealed by [Zn]t closely res

92 gs of dopamine neurons showed that dopamine, baclofen, and orphanin FQ (OFQ) cause varying degrees of

93 Systemic muscimol or baclofen are antipruritic against both histamine-depende

94 Ondansetron, naltrexone, topiramate, and baclofen are examples.

95 terneuronal circuits, which are sensitive to baclofen, are part of the subcortical premotoneuronal ne

96 nsitivity of Abeta-fibre-evoked responses to baclofen, as well as an increased sensitivity of post-di

97 Application of baclofen at a high dose (10 mg/kg i.p.) reduced the powe

98 Baclofen (at doses from 10(-9) to 10(-3) M) failed to di

99 ied agonists (NMDA, clonidine, muscimol, and baclofen) at several types of receptors [NMDA, alpha2-ad

100 e vSub with GABA receptor agonists (muscimol+baclofen) before the context-induced relapse tests and p

101 Finally, baclofen blocked the frequency-dependent depression of E

102 , pretreatment with GABA(B) receptor agonist baclofen blocked the rewarding effects of morphine as me

103 oncentration of the GABA(B) receptor agonist baclofen blocks ethanol but not flunitrazepam or pentoba

104 Also, GABA and the GABA(B) agonist baclofen both elicited increases of the inwardly rectify

105 nist (SB242084) or a GABAB receptor agonist (baclofen), but not a GABAA receptor channel blocker (pen

106 ent response to the GABA(B) receptor agonist baclofen, but not DAMGO.

107 e NAC shell, and reduced feeding elicited by baclofen, but not muscimol in the VTA.

108 y 5 years) use of the GABAb receptor agonist baclofen by SCI patients reduced MEP size during precisi

109 However, the GABA(B)R agonist baclofen can also promote excitability and seizure gener

110 ioid (DAMGO), delta opioid (DPDPE), GABA(B) (baclofen), cannabinoid CB(1) (WIN 55,212-2), muscarinic

111 The selective GABA(B) agonist (R)-baclofen caused a similar response with an EC(50) of 7.1

112 Muscimol and baclofen caused reversible, dose-related inhibition of t

113 the amplitude of granule-cell-evoked IPSCs, baclofen causes a change from paired-pulse depression to

114 s mitral cell glutamate release only weakly, baclofen causes a marked reduction in the amplitude of g

115 effects of ethanol, oxotremorine, nicotine, baclofen, clonidine, and the cannabinoid receptor agonis

116 At 5.0 mg/kg, baclofen completely blocked both total distance traveled

117 activity, because the GABAB receptor agonist baclofen continued to elicit these currents in the mutan

118 t study extended this work by determining if baclofen could enhance the extinction of methamphetamine

119 However, long-term (~6 years) use of baclofen decreased active long-interval intracortical in

120 triatum using the GABA agonists muscimol and baclofen decreased context-induced reinstatement.

121 Intra-VTA methylnaloxonium or baclofen decreased ethanol-induced CPP, whereas intra-NA

122 The GABA(B) receptor agonist baclofen decreased the rate of cell movement in a dose-d

123 on-heightening effect of the GABA(B) agonist baclofen depended on the activation of 5-HT neurons in t

124 (R)-Baclofen depressed the amplitude of evoked excitatory po

125 At 2.5 mg/kg, baclofen did not alter spontaneous motor activity or tot

126 Baclofen disrupted retrieval behavior without affecting

127 The antispastic drug baclofen dose-dependently decreased the flexion response

128 This baclofen effect was occluded by a previous block of N-ty

129 The GABA(B)R agonist baclofen elicited an outward current in all neurons with

130 of mouse models of ASD, we tested both the R-baclofen enantiomer and the less potent S-baclofen enant

131 R-baclofen enantiomer and the less potent S-baclofen enantiomer in two inbred strains of mice that d

132 Baclofen enhanced the paired-pulse ratio and coefficient

133 , or a linked gene, influences SB242084- and baclofen-enhanced convulsions.

134 Baclofen evoked prominent barium-sensitive outward curre

135 ated with equivalent, dramatic reductions in baclofen-evoked current in CA1 neurons.

136 The impact of GIRK subunit ablation on baclofen-evoked current was consistent with observations

137 all of the barium-sensitive component of the baclofen-evoked current was eliminated with the ablation

138 icient dorsal root ganglia neurons had lower baclofen-evoked inhibition of high-voltage-activated cal

139 y-old pups given naloxone (Experiment 1A) or baclofen (Experiment 1B) before ethanol administration w

140 anol levels were not affected by naloxone or baclofen (Experiment 2).

141 The GABA(B) receptor agonist baclofen facilitates the extinction of morphine-induced

142 ngs converge with the prior demonstration of baclofen facilitating the extinction of morphine-induced

143 have relatively specific treatments, such as baclofen for periodic alternating nystagmus, and reposit

144 to the bathing medium or mimicked by adding baclofen (GABA(B) receptor agonist; 100 microM) to norma

145 Systemic baclofen, gabapentin, tramadol, and morphine dose-depend

146 tency of agonists was: GABA = SKF97541 > (R)-Baclofen > 3-APPA.

147 Baclofen had no effect on water or sugar water intake wh

148 The GABAB agonist baclofen has been shown to alter ethanol intake in human

149 The orthosteric GABAB receptor agonist baclofen has been shown to suppress operant self-adminis

150 Here we show that baclofen has concentration-dependent effects on the hipp

151 Diphenhydramine, Ecstasy, and baclofen have recently been implicated as the etiology o

152 In the presence of tetrodotoxin (TTX), baclofen hyperpolarized (DeltaVmax = 5.6 mV, EC50 = 2.3

153 To evaluate R-baclofen in a broader range of mouse models of ASD, we t

154 The present study assessed the effects of baclofen in a variation on a new mouse model of binge-li

155 ing responses elicited by either muscimol or baclofen in either the VTA and NAC shell following pretr

156 These findings encourage investigations of R-baclofen in other preclinical model systems.

157 d sensitivity of post-discharge responses to baclofen in spinal nerve ligated rats.

158 educed feeding elicited by muscimol, but not baclofen in the NAC shell, and reduced feeding elicited

159 eved by presession injection of muscimol and baclofen) in a novel two-reward choice task.

160 g effects (opioid antagonists decreasing and baclofen increasing food intake).

161 ignificantly blocked feeding elicited by VTA baclofen, indicating a robust and bidirectional GABA-B/G

162 ed but did not block feeding elicited by VTA baclofen, indicating a unidirectional interaction GABA-B

163 Baclofen-induced feeding elicited from the NAC was signi

164 d naltrexone, but not saclofen pretreatment, baclofen-induced feeding elicited from the nucleus accum

165 Baclofen-induced feeding elicited from the VTA was signi

166 in the VTA, and correspondingly, whether VTA baclofen-induced feeding was dose-dependently blocked by

167 uculline, into the VTA, and then whether VTA baclofen-induced feeding was dose-dependently blocked by

168 low NACs NBNI dose significantly reduced VTA baclofen-induced feeding, indicating a bidirectional kap

169 ondingly, NACs NTX significantly reduced VTA baclofen-induced feeding, indicating a robust and bidire

170 uced feeding, NACs BFNA failed to affect VTA baclofen-induced feeding, indicating a unidirectional mu

171 duced feeding, NACs NTI failed to affect VTA baclofen-induced feeding, indicating a weak unidirection

172 high, but not low VTA BFNA dose reduced NACs baclofen-induced feeding, NACs BFNA failed to affect VTA

173 hereas VTA NTI only transiently reduced NACs baclofen-induced feeding, NACs NTI failed to affect VTA

174 Whereas VTA NBNI at both doses reduced NACs baclofen-induced feeding, the high, but not low NACs NBN

175 VTA NTX significantly reduced NACs baclofen-induced feeding.

176 ficant delay in the deactivation kinetics of baclofen-induced GIRK channel currents.

177 tic mechanism because ephedrine also reduced baclofen-induced hyperpolarization by 28%.

178 -induced hyperpolarization and inhibition of baclofen-induced hyperpolarization were abolished when s

179 ne (1-10 microM) and SR95531 (10 microM) and baclofen-induced responses were sensitive to 2-hydroxy-s

180 found to be effective in vivo, potentiating baclofen-induced sedation/hypnosis in DBA mice when admi

181 As reported previously, baclofen inhibited an N-type channel current and this ac

182 young animals, the GABA(B) receptor agonist, baclofen, inhibited the amplitude of evoked EPSCs and IP

183 n of GABA(B) receptors further, we show that baclofen inhibits high-voltage-activated calcium current

184 Like VTA baclofen injection, injection of dopamine receptor antag

185 Muscimol+baclofen injections into CeA but not BLA decreased cue-i

186 Muscimol+baclofen injections into dmPFC, vmPFC, or OFC during lat

187 itionally, renewal was blocked by muscimol + baclofen injections into LH.

188 nursing behavior, and control injections of baclofen into the region dorsal to VTA were ineffective.

189 blocked by injection of the GABA(B) agonist baclofen into the VTA.

190 Injections of muscimol + baclofen into ventral mPFC in one hemisphere and D(1)-fa

191 Unilateral injections of muscimol + baclofen into ventral mPFC or SCH 23390 into the accumbe

192 (A) agonist, muscimol, or a GABA(B) agonist, baclofen, into the SCN region significantly reduced ligh

193 lthough at a high concentration (10 microM), baclofen invariably resulted in hyperpolarization, at lo

194 Baclofen is a GABAB receptor agonist commonly used to re

195 Baclofen is a promising tool to explore whether medial p

196 this effect is that the apparent affinity of baclofen is strongly reduced during physiologically rele

197 vels may require more extensive therapy when baclofen is used chronically.

198 uding midazolam, flurazepam, avermectin Ba1, baclofen, isoguvacine, and propofol, at 1 or 10 muM, pro

199 the GABA(B) receptor by the specific agonist baclofen leads to a marked translocation and accumulatio

200 Unexpectedly, at a lower dose (1 mg/kg), baclofen markedly increased gamma activity accompanied b

201 Our findings suggest that R-baclofen may have clinical utility for some of the core

202 In contrast, baclofen may have depressed the activity of all VTA proj

203 These results suggest that baclofen may inhibit the earliest type of drug cue-induc

204 spinal cord injured subjects who do not take baclofen (median: 10 years) and 45 units from uninjured

205 ther feeding elicited by the GABA-B agonist, baclofen microinjected into the NACs was dose-dependentl

206 ther feeding elicited by the GABA-B agonist, baclofen, microinjected into the NAC shell was dose-depe

207 Conversely, CeA inhibition by muscimol/baclofen microinjections prevented acquisition of cocain

208 replicate the initial efficacy findings for baclofen, modafinil, tiagabine, and topiramate.

209 , placebo-controlled clinical trials, namely baclofen, modafinil, tiagabine, and topiramate.

210 Next, we tested the hypothesis that baclofen modulates LES motor tone via GBR expressed by v

211 oltage-gated Ca(2+) channels as a target for baclofen modulation.

212 vation of OFC neurons with the GABA agonists baclofen + muscimol decreased cue-induced heroin seeking

213 Furthermore, similar to U0126, baclofen+muscimol-induced (B+M; 106.8/5.7 ng/0.5 mul/hem

214 L) region of the medial prefrontal cortex by baclofen/muscimol (B/M) during testing attenuates renewa

215 est this hypothesis, GABA receptor agonists (baclofen/muscimol) were microinjected into the anterior

216 l dorsal striatum was infused with saline or baclofen/muscimol, to temporarily inactivate the region.

217 ing with reversible inactivation techniques (baclofen/muscimol: 1.0/.1 mmol/L, .3 muL/side).

218 the increased feeding elicited by NAC shell baclofen, NAC shell bicuculline reduced but did not bloc

219 Neither baclofen nor a cannabinoid receptor agonist, CP55940, af

220 Baclofen normalized baseline gamma power without corresp

221 nificantly blocked the inhibitory effects of baclofen on evoked neuronal responses in control rats.

222 However, the inhibitory effect of baclofen on GABAergic and glycinergic spontaneous IPSCs

223 The effects of VTA baclofen on maternal behavior are similar to the effects

224 e the effects of the selective GABAB agonist baclofen on SON and PVN magnocellular neurones and to de

225 The short-term benefits of baclofen on spasticity (e.g. management of muscle spasms

226 paradigm were used to examine the effects of baclofen on subliminal cocaine (vs neutral) cues.

227 We examined the effects of baclofen on the relationship between an fEPSP during the

228 GABAA agonist muscimol and the GABAB agonist baclofen on tonically active medial vestibular nucleus (

229 The effects of baclofen on voluntary motor output are limited and not y

230 his may contribute to the limited effects of baclofen on voluntary motor output in subjects with moto

231 GABAA + GABAB receptor agonists (muscimol + baclofen) on this effect.

232 y analogous to known GABAB agonists, such as baclofen or 3-aminopropyl phosphinic acid, are presented

233 nt when release probability was lowered with baclofen or Cd(2+).

234 ition by either the GABA(B) receptor agonist baclofen or intracellular guanosine 5'-O-(3-thio)triphos

235 Baclofen or saline was microinjected into the anterior o

236 tion induced by the GABA(B) receptor agonist baclofen or the adenosine A1 receptor agonist 2-chloroad

237 can be modulated by means of GABA B agonist (baclofen) or opioid antagonist (naloxone) treatments.

238 duced transmitter release (caused by Cd(2+), baclofen, or reduced stimulus intensity) with whole-cell

239 Baclofen pretreatment blocked the induction of Fos in op

240 Intraventricular baclofen pretreatment in rats subjected to a stroke mode

241 The selective GABAB receptor agonist R-baclofen previously reversed social deficits and reduced

242 The GABAB agonist baclofen produced a significantly greater reduction in d

243 S-baclofen produced minimal effects at the same doses.

244 Baclofen produced similar magnitudes of increased food i

245 Baclofen produced similar magnitudes of increased food i

246 e biologically active compounds, such as (R)-baclofen, (R)-rolipram, (S)-curcumene, (S)-dehydrocurcum

247 combinations of GABA-A (muscimol) or GABA-B (baclofen) receptor agonists 15 to 20 minutes prior to in

248 Baclofen reduced binge-like ethanol intake when microinj

249 Baclofen reduced cell movement by up to 56% compared wit

250 P55940 did not act identically, because only baclofen reduced facilitation and affected bouton releas

251 Comparatively, baclofen reduced pattern separation between odor categor

252 However, baclofen reduced the frequency of KCl-induced mEPSCs; an

253 In addition, baclofen reduced the frequency of miniature IPSCs but no

254 Baclofen reduced the frequency of spontaneous inhibitory

255 We find that the selective GABA(B) agonist baclofen reduces mitral cell recurrent inhibition mediat

256 yric acid B metabotropic receptors (GBRs) by baclofen reduces the incidence of transient lower esopha

257 st cases tested, the effects of muscimol and baclofen remained similar when synaptic transmission was

258 ophysiology of FXS as the GABABR agonist (R)-baclofen rescued the imbalances between excitatory and i

259 gender difference in the effects of E(2) on baclofen responses, there was no gender difference in 5-

260 addition, activation of GABA(B) receptors by baclofen restored the galanin effect under low Ca (2+) c

261 compounds with a per se nonsedative dose of baclofen resulted in shorter onset and longer duration o

262 We also assessed the effect of muscimol+baclofen reversible inactivation of vmPFC, dmPFC, and OF

263 rease in mIPSC frequency, it failed to block baclofen's reduction of mIPSC frequency.

264 ation of their response to both muscimol and baclofen, seen as a rightward shift and a decrease in sl

265 Together, these results demonstrate that baclofen selectively maintains use-dependent modulation

266 observations indicate that there may be two baclofen-sensitive metabotropic GABA receptors with oppo

267 In all groups of rats, spinal baclofen significantly reduced Abeta-, Adelta- and C-fib

268 Naloxone and baclofen significantly reduced the stimulating effect of

269 In contrast, baclofen specifically increased the N100 amplitude.

270 by noxious stimulation of the colon, and (2) baclofen specifically reduces Fos expression in the supe

271 Baclofen, stimulated neutrophil chemotaxis and tubulin r

272 , the expression of GABA(B(1)) subunits, and baclofen-stimulated [35S]GTPgammaS binding, a measure of

273 functional GABA(B) receptors, as measured by baclofen-stimulated [35S]GTPgammaS binding, in the spina

274 stent with GABA(B) receptor desensitization, baclofen-stimulated GTPgammaS binding was reduced, and t

275 the presence of N(6)-cyclopentyladenosine or baclofen, suggesting that repetitive stimulation does no

276 al GABA(B) circuits may be less sensitive to baclofen than spinal GABAB circuits.

277 With paralysis and baclofen, the median motor unit tetanic forces were sign

278 y of the GABA(B) agonist and muscle relaxant baclofen, there have been substantial advancements in th

279 the potency of the GABA(B) receptor agonist baclofen to activate G protein-coupled inwardly rectifyi

280 ly the potency of the GABAB receptor agonist baclofen to activate G-protein-coupled, inwardly rectify

281 educed reflex facilitation in subjects using baclofen to control spastic behaviours.

282 sing the GABA(B) receptor (GABA(B)R) agonist baclofen to engage presynaptic inhibition and field EPSP

283 We observed that baclofen-treated participants displayed significantly le

284 Short-term (4-24 h) baclofen treatment also significantly desensitized the i

285 amplitude could be partially restored after baclofen treatment by either coapplication of baclofen a

286 R-baclofen treatment reversed social approach deficits in

287 naptic inhibition was unaffected by agonist (baclofen) treatment for up to 48 h, and was desensitized

288 The aim of our study was to evaluate whether baclofen use and paralysis due to cervical spinal cord i

289 Greater motor unit weakness with long-term baclofen use and paralysis will make the whole muscle we

290 ity), but the long-term effects of sustained baclofen use on skeletal muscle properties are unclear.

291 with rest but there was no effect of SCI or baclofen use.

292 on of N-type calcium channels in response to baclofen, Vc1.1 and RgIA was significantly reduced in GA

293 In contrast to GABA and baclofen, Vc1.1 changes Cav2.2 channel kinetics by incre

294 g the GTP analog GDP-beta-s, indicating that baclofen was acting on postsynaptic GABA(B) receptors.

295 alcium, whereas the GABA(B) receptor agonist baclofen was ineffective, suggesting that chloride-media

296 (Aminomethyl)-4-chlorobenzenepropanoic acid (baclofen) was an effective agonist for the GABA-evoked e

297 The effects of (R)-baclofen were blocked by the GABA(B) antagonist CGP 5243

298 d by the GABA(B) receptor (GABA(B)R) agonist baclofen were diminished in a dose-dependent manner in m

299 GABA-B receptors, the effects of muscimol or baclofen were studied.

300 ignant syndrome, malignant hyperthermia, and baclofen withdrawal.