ライフサイエンスコーパス: GABA

1 GABA and glycine corelease is particularly common in the

2 GABA and the antimalarial drug artemether, which acts on

3 GABA caused concentration-dependent increases in fluores

4 GABA is the primary inhibitory neurotransmitter in human

5 GABA levels were negatively correlated with the same neu

6 GABA or glutamate receptor antagonists did not block the

7 GABA synthesis is controlled by enzymes derived from two

8 GABA-, THIP- and propofol-evoked currents mediated by al

9 GABA-ergic interneurons provide diverse inhibitions that

10 GABA-mediated neurotransmission and fast-spiking (FS) GA

11 GABA-mediated spontaneous IPSCs (sIPSCs) in POMC neurons

12 GABA-mediated tonic current was enhanced by dopamine or

13 the perisomatic neuropil of CG neurons; (2) GABA is restricted to a specific terminal type, which di

14 In line with this, we show that gabazine, a GABA-A receptor antagonist, is antihyperalgesic in prime

15 piomelanocortin (POMC)-positive neurons in a GABA-dependent manner, which then leads to appetite stim

16 ynaptic levels after 48 h blockade of type A GABA receptor (GABAA R)-mediated inhibition with bicucul

17 A), FMRF-amide, and gamma-aminobutyric acid (GABA) immunoreactivity in the central nervous system (CN

18 elevated levels of gamma-aminobutyric acid (GABA) in the medial prefrontal cortex (mPFC) have been r

19 gamma-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the

20 idges detectable by gamma-aminobutyric acid (GABA) membrane transporter 1 immunoreactivity is lower,

21 e zona incerta (ZI) gamma-aminobutyric acid (GABA) neurons or their axonal projections to paraventric

22 ic inhibition of LH gamma-aminobutyric acid (GABA) neurons restricted to cue presentation disrupts th

23 5-HT2CR expressing gamma-aminobutyric acid (GABA) neurons, but not 5-HT2CR expressing dopamine (DA)

24 mmunopositive for a gamma-aminobutyric acid (GABA) receptor subunit (GABAA Ralpha1 ), and that a syna

25 nists of ionotropic gamma-aminobutyric acid (GABA) receptors.

26 PGC1alpha-mediated gamma-aminobutyric acid (GABA) secretion from muscle.

27 d concentrations of gamma-aminobutyric acid (GABA) that are normalized by antidepressant therapies.

28 antibodies against gamma-aminobutyric acid (GABA) to identify GABAergic interneurons and non-GABAerg

29 te) and inhibitory (gamma aminobutyric acid (GABA)) neurotransmitter circuits in anxiety disorders, t

30 gated by glutamate, gamma-aminobutyric acid (GABA), and acetylcholine, also have associated proteins,

31 d probes implicated gamma-aminobutyric acid (GABA), dopamine and serotonin neurotransmitter systems.

32 smitters-glutamate, gamma-aminobutyric acid (GABA), dopamine, serotonin, acetylcholine and opioids-an

33 n channels gated by gamma-aminobutyric acid (GABA), glutamate, histamine, or changes in pH, and three

34 gamma-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in the mamm

35 ilic bioisostere of gamma-aminobutyric acid (GABA), various late-stage diversifications, and by mimic

36 RAPs, in particular gamma-aminobutyric acid (GABA)-A-receptor-associated protein-like 2 (Gabarapl2; a

37 f dopamine (DA)- or gamma aminobutyric acid (GABA)-expressing neurons, with corresponding changes in

38 tively localized to gamma-aminobutyric acid (GABA)ergic and glycinergic postsynapses.

39 glutamatergic, and gamma-aminobutyric acid (GABA)ergic neurons) across its different regions (medial

40 ns, specifically in gamma-aminobutyric acid (GABA)ergic, glutamatergic, and catecholaminergic neurons

41 a next-generation gamma-amino butyric acid (GABA)-aminotransferase (AT) inhibitor, shows comparable

42 stimuli may trigger cataplexy by activating GABA cells in the CeA.SIGNIFICANCE STATEMENT Although ca

43 fluorescent cells expressed syntaxin 1A and GABA-immunoreactivity indicating they were amacrine cell

44 s containing glutamate-, acetylcholine-, and GABA-releasing neurons with connections to basal ganglia

45 three achiral amino acids Gly, beta-Ala, and GABA).

46 nd other disorders with reduced SST cell and GABA functions.

47 As DA and GABA work in concert to shape and synchronize neuronal e

48 rough temporally coordinated enkephalin- and GABA-mediated presynaptic inhibition of somatosensory ne

49 R neurons recruit both GABA and GABA-A receptors to their axon terminals in the EB, and

50 subpopulation containing both glutamate and GABA (SuM(vgat/vglut2)) and another also expressing nitr

51 compartmentalized corelease of glutamate and GABA and its differential plasticity from a single pathw

52 n humans, to measure levels of glutamate and GABA in dACC.

53 rential alterations in layer 3 glutamate and GABA neurotransmission across cortical regions may contr

54 e mossy fibers (MFs) corelease glutamate and GABA onto pyramidal cells of CA3 during development, unt

55 g persisted in the presence of glutamate and GABA receptor antagonists.

56 It is well established that glutamate and GABA signal through both ionotropic and metabotropic rec

57 asked whether the corelease of glutamate and GABA was also subjected to a target-dependent compartmen

58 cs, and dual-color uncaging of glutamate and GABA, we demonstrate that plateau potentials can broaden

59 (13)C enrichment of glutamate, glutamine and GABA (gamma-aminobutyric acid).

60 Glutamate, glutamine, and GABA were measured cortically and subcortically in bilat

61 choline species, glutamate, glutathione, and GABA.

62 Glycine and GABA are both inhibitory neurotransmitters involved in f

63 neurons in the VNLL release both glycine and GABA in the ICC, but functional evidence for their corel

64 y neurotransmitters (glutamate, glycine, and GABA) in the auditory brainstem of Fmr1 knockout mice.

65 -promoting cell types include hypocretin and GABA (gamma-aminobutyric-acid)-releasing neurons of the

66 Perceptual measures and GABA were not correlated when either age group was consi

67 n, axon guidance, and signaling of Notch and GABA receptor pathways, as well as factors important for

68 h pre-embedding avidin-biotin-peroxidase and GABA with post-embedding immunogold labeling.

69 the external aldimine formed between PLP and GABA is apparently responsible for triggering the GabR-m

70 tence of time-locked, glutamate receptor and GABA receptor-mediated mono synaptic responses evoked by

71 euromodulators involved in sleep control are GABA, dopamine, acetylcholine, serotonin, and several ne

72 known roles for astrocyte processes, such as GABA and glutamate metabolism.

73 ng a monocarboxylic gamma-amino acid such as GABA should be preferred over dicarboxylic acid ligands.

74 In animal models of FXS and of ASD, GABA-B agonists have improved both brain and behavioral

75 that MG is a competitive partial agonist at GABA-A receptors.

76 Aergic synapses, as well as classical axonal GABA release, this lack of knowledge is problematic.

77 The return to baseline GABA+ concentration indicates the reversible GABA-AT res

78 ains unclear whether the association between GABA level and visual perception reflects a general infl

79 Here, the connectivity between GABA-releasing AgRP neurons and POMC neurons was examine

80 R neurons recruit both GABA and GABA-A receptors to their axon terminals in the

81 nd homocarnosine, and CPP-115 afforded brain GABA+ concentration changes comparable to or greater tha

82 ructural modification inhibits activation by GABA.

83 ings; and (3) if a CG neuron is contacted by GABA-positive terminals, virtually all perisomatic termi

84 and nicotinic neurotransmission conveyed by GABA and ACh corelease, which inhibited DA neurons.

85 , dentate PV interneurons are depolarized by GABA signaling, which is in sharp contrast to most matur

86 ast to most mature neurons hyperpolarized by GABA.

87 (2+) buffering, and its sign was inverted by GABA-A receptor activation.

88 activation of alpha1beta2gamma2 receptors by GABA and propofol.

89 ion of a large, neutral dendrimer to a caged GABA probe we introduce a "cloaking" technology that eff

90 It colocalized GABA and MIP but not AT or ORC immunoreactivity.

91 ials in granule cells function to coordinate GABA release at relatively distant dendrodendritic synap

92 nt fraction of glycinergic boutons corelease GABA in the ICC.

93 c corticospinal excitability, local cortical GABA levels, and reaction time (RT) in a group of 20 hea

94 ents with schizophrenia had reduced cortical GABA compared with healthy relatives and the combined sa

95 These results suggest that cortical GABA reduction preferentially impairs the effort-based b

96 nd depression, may be attributed to cortical GABA level reduction.

97 Here, we estimated visual cortical GABA levels and Glx (combined estimate of glutamate and

98 s of all ages were combined, visual cortical GABA levels but not Glx levels correlated with perceptua

99 Our results show increased visual cortical GABA levels, and reduced Glx levels, in older adults.

100 volved in learning and memory, such as Creb, GABA B R and Ip3k, indicating extensive involvement of D

101 We found lower CSF GABA concentration in FEP patients compared with that in

102 Moreover, lower CSF GABA levels were associated with total and general score

103 h altered subunit stoichiometry or decreased GABA-evoked whole-cell current amplitudes, but with diff

104 11.2 DS model, our results suggest a delayed GABA-switch in Lgdel (+/-) neurons, which may contribute

105 ved through the sustained dopamine-dependent GABA release from other retinal neurons.

106 how that early post-SE abnormal depolarizing GABA and p75(NTR) signaling fosters a long-lasting rearr

107 lied Delta(9)-tetrahydrocannabinol depressed GABA cell activity, therefore downstream dopamine cells

108 agonists as well as cell transplant-derived GABA are antipruritic against acute itch and in a transg

109 al CA1 stratum radiatum, and also diminishes GABA-mediated synaptic transmission in hippocampal CA1 n

110 n POMC neurons were unaffected by disturbing GABA release from AgRP neurons either by cell type-speci

111 , and a positive correlation between l-DLPFC GABA levels, but not Glx, and minimal oxygen saturation

112 e was a negative correlation between l-DLPFC GABA levels, but not Glx, and SDB severity by AHI (r = -

113 In subjects with SDB, levels of l-DLPFC GABA, but not Glx, were significantly lower than in cont

114 Elevated GABA+ concentrations returned to baseline values followi

115 ve allosteric modulators (PAMs) that enhance GABA's actions on neuronal GABAA-Rs are in clinical use.

116 5-HT1A receptors and indirectly via enhanced GABA release.

117 was substituted by diazepam, which enhances GABA function.

118 Several reports have described excitatory GABA transmission in the suprachiasmatic nucleus (SCN),

119 replication, which is enhanced by exogenous GABA application.

120 ination of a PAM and low levels of exogenous GABA further increased human islet cell replication.

121 GAD-GFP mice, as well as immunostaining for GABA, we found that a subset of neurons in the brachium

122 Immunogold labeling for GABA confirmed that the transplanted cells were GABAergi

123 neurons express major proteins necessary for GABA synthesis and release and that sensory neurons rele

124 erpolarization of the reversal potential for GABA (EGABA).

125 (GAD67) protein, the enzyme responsible for GABA synthesis in these boutons.

126 cleus, expressing vesicular transporters for GABA or glutamate (hereafter, DRN(Vgat) and DRN(VGLUT3)

127 isposed to an activity-dependent switch from GABA-mediated inhibition to excitation.

128 nsplanted MGE progenitors enhance functional GABA-mediated inhibition, reduce spontaneous seizure fre

129 ally reversed following blockade of GABAARs (GABA Type A receptors), but not GABABRs (GABA Type B rec

130 Rs (GABA Type A receptors), but not GABABRs (GABA Type B receptors).

131 We propose that greater GABA capacity in the motor cortex counteracts an intrins

132 Moreover, individuals with higher GABA concentration in the ATL showed better semantic per

133 How hippocampal GABA contributes to stopping unwanted thoughts is unknow

134 reater resting concentrations of hippocampal GABA predicted better mnemonic control.

135 s the first functional evidence to implicate GABA cells in the amygdala as regulators of cataplexy tr

136 ing placebo showed no significant changes in GABA+ concentration.

137 ions in older adults to a likely decrease in GABA (Gamma Aminobutyric Acid) concentration in visual c

138 rect evidence for an age-related decrease in GABA concentration in human visual cortex.

139 Aergic interneurons with global reduction in GABA levels in the forebrains of the Dlx1/Dlx2 double kn

140 This interindividual variability in GABA level is linked to interindividual differences in m

141 on of whether interindividual variability in GABA reflects an overall variability in visual inhibitio

142 Endocannabinoids inhibit GABA release in the RVM, but it is not known whether thi

143 generation of TLE, we permanently inhibited GABA release selectively from PV neurons of the ventral

144 ated and regulated by neighboring inhibitory GABA cells.

145 ch demonstrate a role for reduced inhibitory GABA level and function across disorders.

146 Expression of the key GABA-synthesizing enzyme GAD67 was significantly lower i

147 w that inhibition of the terminals of the LH GABA neurons in ventral-tegmental area (VTA) facilitates

148 eeking behavior, but only activation of LHA (GABA) neurons increased overall chow consumption.

149 We identified a subpopulation of LHA (GABA) neurons that coexpress the neuropeptide galanin (L

150 eurons may represent a subpopulation of LHA (GABA) neurons that mediates food reward independent of d

151 LHA (Gal) or LHA (GABA) neuronal activation both increased operant food-se

152 Additionally, LHA (Gal) or LHA (GABA) neuronal activation similarly induced locomotor ac

153 ales by using fast action potentials to link GABA release at many different synaptic contacts formed

154 s and indirectly inhibits them through local GABA neurons, but the relative magnitudes of the two mec

155 onse induced by the semantic task, the lower GABA concentration in the same region.

156 terpreted as compensatory responses to lower GABA levels in ChCs.

157 To manipulate GABA cells specifically, we developed a new mouse line t

158 nce analysis revealed a reduction in maximal GABA-evoked Popen , suggesting impaired agonist efficacy

159 We addressed this hypothesis by measuring GABA, glutamate, glutamine, and the sum of glutamine plu

160 Mechanistically, GABA depolarized the majority of sensory neuron somata,

161 cally innervating aversion-encoding midbrain GABA cells.

162 -aminobutyric acidergic (GABAergic) neurons (GABA-CB1R).

163 populations expressing the neurotransmitters GABA or glutamate within this circuit markedly reduced t

164 analyses, we conclude that MGE cells are not GABA pumps, but alleviate pain and itch through synaptic

165 Finally, blocking NMDA, but not GABA, receptors causes ATM levels to rise while ATR leve

166 fety and potential to enhance the ability of GABA, secreted from ss-cells, or exogenously administere

167 of GABAAR expressing cells in the absence of GABA and demonstrated positive allosteric modulation in

168 ated outward Cl(-) current in the absence of GABA.

169 gest that PAMs may potentiate the actions of GABA secreted by islet ss-cells on GABAA-Rs and provide

170 We found that chemogenetic activation of GABA CeA cells triggered a 253% increase in the number o

171 Activation of GABA receptors in rRPa does not mediate the cholinergic

172 ChR in rRPa does not depend on activation of GABA receptors in rRPa.

173 Antagonists of GABA or VIP signaling or action potentials did not disru

174 In addition, focal application of GABA receptor antagonists to sensory ganglia triggered o

175 he increase in BAT SNA evoked by blockade of GABA receptors in rRPa.

176 d-type and IL-31Tg mice with combinations of GABA-A (muscimol) or GABA-B (baclofen) receptor agonists

177 ation of responses to a low concentration of GABA by the drug pair of alfaxalone and propofol agree v

178 cerebrospinal fluid (CSF) concentrations of GABA were analyzed in 41 first-episode psychosis (FEP) p

179 and, paradoxically, higher concentrations of GABA.

180 of determining the functional consequence of GABA released from POMC neurons in terms of the regulati

181 We show corelease of GABA and glycine for the first time in the central nucle

182 overed that SynII affects the time course of GABA release, and that this effect is interneuron subtyp

183 f the present study documented elevations of GABA levels both in the mPFC and, for the first time, in

184 a region- and feature-dependent influence of GABA level on human visual perception.

185 a region- and feature-dependent influence of GABA level on human visual perception.

186 However, the widespread influence of GABA raises the question of whether interindividual vari

187 In vivo focal infusion of GABA or GABA reuptake inhibitor to sensory ganglia drama

188 Inhibition of GABA release from CCK neurons disinhibits parvalbumin (P

189 te that specific and sustained inhibition of GABA release from parvalbumin-expressing interneurons (m

190 ncing of PV neurons, transient inhibition of GABA release from PV neurons through the designer recept

191 The effect of LHb injection of GABA agonists was mimicked by intra-LHb muscarinic choli

192 Consistently, inoculation of GABA enhanced arboviral infection, indicating that GABA

193 selective correlations between the level of GABA and the magnitude of contextual illusion.

194 Levels of GABA and those of the combined resonances of glutamate a

195 r MEPs were associated with higher levels of GABA in M1, but not in three other cortical regions.

196 nation associations were found for levels of GABA or Glx in right or left hippocampal region.

197 OEt from other currently known modulators of GABA function (e.g., anesthetics, neurosteroids or ethan

198 n the EC50 Finally, we altered the number of GABA-binding sites by a mutation and again found that th

199 eceptor activation using the agonist pair of GABA and propofol or potentiation of responses to a low

200 be a positive allosteric modulator (PAM) of GABA currents with alpha1beta2gamma2, alpha1beta3gamma2,

201 ive allosteric modulation in the presence of GABA, whereas benzodiazepines only exhibited positive al

202 e FGR gene responsible for the production of GABA.

203 Additionally, the ratio of GABA-positive neurons to total cortical neurons in old r

204 However, the inward rectification of GABA-induced transport currents by all three deletion mu

205 te pain and itch through synaptic release of GABA.

206 rtance of considering the functional role of GABA release in addition to the peptide transmitters fro

207 ndent neural regulation of PNEC secretion of GABA in a neonatal disease model.

208 hestrating PNEC innervation and secretion of GABA.

209 that PNECs were the only cellular source of GABA in airways.

210 ays a significant role in local synthesis of GABA in synapses.

211 mouse line that enables genetic targeting of GABA cells in orexin(-/-) mice.

212 lts and found stimulation-induced effects on GABA levels, reflecting augmented local plasticity and f

213 by agonists of the Gi-coupled micro opioid, GABA-B and NPY receptors.

214 OB interneurons or locally introducing DA or GABA receptor antagonists alters kinship preference.

215 In vivo focal infusion of GABA or GABA reuptake inhibitor to sensory ganglia dramatically

216 urons producing acetylcholine, glutamate, or GABA.

217 opaminergic marker (TH), serotonin (5-HT) or GABA do not co-localize with Galphat-S-ir neurons althou

218 ce with combinations of GABA-A (muscimol) or GABA-B (baclofen) receptor agonists 15 to 20 minutes pri

219 eeded to impart full efficacy to the partial GABA agonists.

220 ve and respond with full efficacy to partial GABA agonists, to generate distinct ensembles of recepto

221 Higher hippocampal, but not prefrontal GABA, predicted stronger fronto-hippocampal coupling dur

222 (CB1) receptors known to inhibit presynaptic GABA release was significantly reduced in the RVM of CFA

223 A (PKA)-dependent enhancement of presynaptic GABA release.

224 eristics of polyphenolic components profile, GABA contents and in vitro antioxidant capacity of the f

225 magnetic resonance spectroscopy to quantify GABA levels as well as resting-state functional magnetic

226 vation of gamma-aminobutyric acid receptors (GABA-Rs) on ss-cells can promote their survival and repl

227 link between PMCA2 and glutamate receptors, GABA receptors (GABARs), and glutamate transporters that

228 issing-hand territory also exhibited reduced GABA levels, suggesting a reduction in connectional sele

229 itical periods of development, which reflect GABA circuit maturation, BDNF, and circadian Clock genes

230 For either brain region, GABA levels at 4 weeks or posttreatment did not differ b

231 show that Dlx1/Dlx2 homeobox genes regulate GABA synthesis during forebrain development through dire

232 ase isoforms (Gad1 and Gad2), which regulate GABA synthesis from the excitatory neurotransmitter glut

233 nd release and that sensory neurons released GABA in response to depolarization.

234 A mu opioid receptor antagonist restored GABA currents in D2-, but not D1-MSN synapses of cocaine

235 GABA+ concentration indicates the reversible GABA-AT resynthesis following drug washout.

236 on of blood by mosquitoes resulted in robust GABA production from glutamic acid derived from blood pr

237 sought to test the hypothesis that selective GABA agonists as well as cell transplant-derived GABA ar

238 cally, higher concentrations of sensorimotor GABA are associated with more selective cortical tuning,

239 all perisomatic terminals supplying it show GABA immunoreactivity.

240 ributing a significant source of spontaneous GABA input to POMC neurons.

241 during sematic processing and resting-state GABA concentrations in the ATL.

242 ental brain disorders.SIGNIFICANCE STATEMENT GABA is the major inhibitory neurotransmitter in the bra

243 lso generated a new mouse model for studying GABA neurons in narcoleptic mice, which could serve as a

244 Whether such GABA elevations are also present in other brain regions

245 Instead, sustained GABA input is provided by a subpopulation of wide-field

246 gic terminals); 2.38% (GABAergic terminals); GABA-CB1 -RS, 1.92% (glutamatergic terminals); 77.92% (G

247 re complex than previously thought, and that GABA may play a neuromodulatory role in the control of l

248 nhanced arboviral infection, indicating that GABA signaling facilitates the arboviral infection of mo

249 The existing consensus is that GABA regulates the initial integration of adult-born neu

250 We show that GABA cell activation only promotes cataplexy attacks ass

251 Previous research shows that GABA-mediated presynaptic inhibition has a critical role

252 s, there is evidence from avian studies that GABA may also be involved.

253 Our findings suggest that GABA level of a cortical region selectively influences p

254 These data suggest that GABA-mediated presynaptic inhibition is not critical for

255 ned with running-wheel assays suggested that GABA, pigment-dispersing factor, myoinhibitory peptides

256 ut affecting their duration, suggesting that GABA cells play a functional role in initiating but not

257 The GABA transporter GAT-1 mediates electrogenic transport o

258 The GABA-sensitive cell cluster is centered on a tegmental (

259 o identify the cell type responsible for the GABA release and the site of its modulation by dopamine.

260 (L170R) and M2-M3 loop (A305V) that form the GABA binding/channel gating coupling junction and the ch

261 To address this, we studied how the GABA levels of parietal and occipital cortices related t

262 ted and the caudal-to-rostral decline in the GABA measure was enhanced in the illness.

263 coupling of ion and substrate fluxes in the GABA transporter family.

264 , genetic or pharmacologic disruption of the GABA metabolic pathway decreased the incidence of brain

265 e decarboxylase 1 (GAD1), a regulator of the GABA neurotransmitter metabolic pathway.

266 dsRNA-mediated interruption of the GABA signaling and blockage of the GABAA receptor by the

267 a" residue in transmembrane domain 10 of the GABA transporter GAT-1 provides extra bulk, probably in

268 m:symporters, GAT-1 and other members of the GABA transporter subfamily all contain an extra amino ac

269 nship between the EC50 for activation of the GABA type A (GABAA) receptor by the transmitter GABA and

270 Prospectively, acting on the GABA-polarity switch offers a potential target for 22q11

271 o-controlled, crossover trial found that the GABA-B agonist arbaclofen improved social avoidance symp

272 e further analyzed the response of NS to the GABA receptor antagonist bicuculline.

273 dorsolateral prefrontal cortex, whereas the GABA measure showed the opposite pattern.

274 nfluence on visual perception or whether the GABA levels of different cortical regions have selective

275 nfluence of visual inhibition or whether the GABA levels of different cortical regions selectively in

276 ile of GAD1 expression and may contribute to GABA dysfunction in the PFC and hippocampus of patients

277 e rather than positive energetic coupling to GABA binding.

278 shift from glutamate-dominant excitatory to GABA-dominant inhibitory processing in early visual area

279 CPP-115-induced changes were exclusive to GABA and homocarnosine, and CPP-115 afforded brain GABA+

280 se enzyme isoforms that convert glutamate to GABA.

281 roisoxazolo[5,4-c]pyridine-3-ol) relative to GABA was impaired.

282 M levels to rise while ATR levels respond to GABA, but not NMDA, receptor blockade.

283 rons also release the amino acid transmitter GABA, which can inhibit downstream neurons.

284 A type A (GABAA) receptor by the transmitter GABA and basal activity employing concatemeric ternary G

285 ea that interactions between the transmitter GABA and the allosteric agonists propofol, pentobarbital

286 ollowing 4 weeks of antipsychotic treatment, GABA levels in patients with FEP decreased relative to b

287 leucine, methionine, phenylalanine, valine, GABA, glutamine, alanine, glycine and taurine were separ

288 cell type-specific deletion of the vesicular GABA transporter or by expression of botulinum toxin in

289 persists in the presence of blockers of VIP, GABA or neuronal firing.

290 ned excitatory plasticity in fluorescent VTA GABA cells.

291 s a novel form of synaptic plasticity in VTA GABA cells, and the synaptic remodeling that can occur a

292 of glutamatergic synaptic plasticity in VTA GABA neurons, a currently understudied cell type that is

293 GABAergic inputs from the NAc and local VTA GABA neurons were differentially modulated and activated

294 mate transcripts tended to increase, whereas GABA transcript levels tended to decrease, from caudal t

295 e source of this GABAergic input and whether GABA contributes to a specific CG function remains to be

296 increase in phenolics, flavonoids along with GABA contents.

297 ron microscopic analysis in conjunction with GABA-immunogold staining showed that (1) GAD-positive te

298 Most patients improve with GABA-enhancing drugs and intravenous immunoglobulin, but

299 tent stimulation led to body weight gain; ZI GABA neuron ablation reduced weight.

300 ected robust orexigenic potential for the ZI GABA neurons.