ライフサイエンスコーパス: GABA neuron

1 hCpG methylation was detected in GLU versus GABA neurons.

2 cessing and is composed of dopamine (DA) and GABA neurons.

3 differences in eCB synthesis between DA and GABA neurons.

4 synergistic overinhibition of nigro-thalamic GABA neurons.

5 leus (DR), which contains both serotonin and GABA neurons.

6 ng-lasting polysynaptic complex EPSCs in SNr GABA neurons.

7 1)(-)/(-)) mice for CB(1) receptors in brain GABA neurons.

8 progenitors generated similar populations of GABA neurons.

9 nucleus incertus, a population of tegmental GABA neurons.

10 but showed TRH axons terminating on or near GABA neurons.

11 by increasing synaptic inhibition from local GABA neurons.

12 rrelated with the appearance of degenerating GABA neurons.

13 ropathic pain through NR1 phosphorylation in GABA neurons.

14 creased substance P NK1-R internalization on GABA neurons.

15 some direct synaptic influence on VTA DA and GABA neurons.

16 hat is likely to excite DA cells and inhibit GABA neurons.

17 h nAChRs that desensitize less than those on GABA neurons.

18 ification of all hippocampal interneurons as GABA neurons.

19 uced below a detectable level in a subset of GABA neurons.

20 uced below a detectable level in a subset of GABA neurons.

21 ill result in a powerful inhibition of these GABA neurons.

22 processed for immunocytochemical staining of GABA neurons.

23 oradrenaline (tyrosine hydroxylase; TH), and GABA neurons.

24 fonylureas increase transmitter release from GABA neurons.

25 n the development of embryonic monoamine and GABA neurons.

26 by analysis of immunoreactive 5-HT, TH, and GABA neurons.

27 re mediated by the activation of presynaptic GABA neurons.

28 of I(h) in VTA dopamine neurons, but not in GABA neurons.

29 inhibition of DA neurons by inhibiting local GABA neurons.

30 ly biased toward synaptic contact with local GABA neurons.

31 related neurons, such as VTA dopamine and VP GABA neurons.

32 l and non-coincident inputs, to LC-NA and LC-GABA neurons.

33 he VTA, including in the locations of DA and GABA neurons.

34 ferents from other brain regions than in VTA GABA neurons.

35 ected robust orexigenic potential for the ZI GABA neurons.

36 mRNAs, markers for gamma-aminobutyric acid (GABA) neurons.

37 ession in lateral hypothalamus GABAergic (LH(GABA)) neurons.

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

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

40 we found that ablation of glutamate, but not GABA, neurons abolishes escape behavior in response to t

41 inhibition of dopamine reuptake affected SNr GABA neuron activity in a D(1)-like receptor-dependent m

42 Together, we demonstrate that VTA-GABA neuron activity preferentially attenuates the abili

43 eas targeted manipulation of LH(GABA) or CA3(GABA) neuron activity reversed memory deficits in NS-V m

44 Such phasic bursting by GABA neurons also occurred in WT mice in association wit

45 homologue of unc-47 is expressed by central GABA neurons and confers vesicular GABA transport in tra

46 in the opioid-induced inhibition of midbrain GABA neurons and consequent disinhibition of dopamine (D

47 ults revealed that social defeat engaged DRN GABA neurons and drove GABAergic sensitization that stre

48 sive disorder, implicate dendritic targeting GABA neurons and GABA synthesis, and, together, suggest

49 DA neuron activation lags behind GABA neurons and is dependent on scratching of the itchy

50 inhibit axon regeneration of both C. elegans GABA neurons and mammalian cortical neurons.

51 currents were significantly depressed in VTA GABA neurons and remained depressed for 7 days.

52 study the migrational trajectories of DA and GABA neurons and show that they occupy ventral mesenceph

53 ic, glutamatergic drive to both DRN 5-HT and GABA neurons and that this architecture was conducive to

54 mine neurons in embryonic rat brain, because GABA neurons and their receptors appear in brainstem dur

55 ith the function of gamma-aminobutyric acid (GABA) neurons and alter the brain oscillations.

56 argets of lateral hypothalamic GABAergic (LH(GABA)) neurons and that activation of this pathway in vi

57 hanism, CeA inputs preferentially target SNL GABA neurons, and CeA->SNL and SNL dopamine neurons resp

58 inhibited STN-triggered burst firing in SNr GABA neurons, and CP93129's inhibitory effect was strong

59 the magnitude of electrical coupling between GABA neurons, and GJ blockers increased the threshold fo

60 ted non-CpG sites were identified in GLU and GABA neurons, and non-CpG methylation was a better predi

61 inhibitory input onto VTA dopamine (DA) and GABA neurons, and that the GABAergic projection drives f

62 brane domains, that the gene is expressed by GABA neurons, and that the protein colocalizes with syna

63 the level of gene expression in a subset of GABA neurons, and the resulting changes in GABA neurotra

64 TRH excited LH GABA neurons, and this was also reduced by NCX inhibitor

65 >SNr projection, reduces burst firing in SNr GABA neurons, and thus may play a critical role in movem

66 r this change is present in all or only some GABA neurons, and whether long-term treatment with halop

67 of a subpopulation of perisomatic-targeting GABA neurons, and, when activated, suppresses the releas

68 Given the critical role that PV-containing GABA neurons appear to play in regulating the cognitive

69 ptic terminals on the remaining dendrites of GABA- neurons appeared not to undergo major age-related

70 isturbed but whether specific populations of GABA neurons are affected is not known.

71 These results suggest that the LH GABA neurons are critical for storing and later dissemin

72 The chandelier class of GABA neurons are of particular interest because their ax

73 e observations show that, unexpectedly, ESR1-GABA neurons are only essential for the positive feedbac

74 s were not altered, suggesting that afferent GABA neurons are the primary targets.

75 noradrenergic and gamma-amino-butyric acid (GABA) neurones are implicated in the system's regulation

76 cystokinin class of gamma-aminobutyric acid (GABA) neurons, are lower in the dorsolateral prefrontal

77 elegans, leads to increased degeneration of GABA neurons as well as reduced survival of animals foll

78 In addition, activation of SNr GABA neurons attenuated heroin-primed, but not cue-induc

79 Lesion of peri-LC GABA neurons blocked LH stimulation-induced eating, esta

80 pression is relatively unaltered in most PFC GABA neurons but is reduced below a detectable level in

81 OIG-1 is secreted from GABA neurons, but its anti-plasticity function is cell a

82 ional deletion of CB(1) receptors from brain GABA neurons, but not from several other neuronal popula

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

84 5-HT2CR expressing gamma-aminobutyric acid (GABA) neurons, but not 5-HT2CR expressing dopamine (DA)

85 eding and locomotor activity similar to LHA (GABA) neurons, but without inducing compulsive-like beha

86 s and evoked synaptic glutamate release onto GABA neurons by activation of Y1 and Y5 receptors.

87 hat the dynamic interplay between VTA DA and GABA neurons can control the initiation and termination

88 ation, whereas optogenetic activation of SNr GABA neurons caused a robust increase in heroin self-adm

89 Optogenetic activation of VTA GABA neurons caused place aversion and inhibited cocaine

90 a risky decision-making task, inhibiting VP(GABA) neurons caused them to more readily select a small

91 Here we show that SNr GABA neurons coexpress dopamine D(1) and D(5) receptor m

92 % of parvalbumin-containing septohippocampal GABA neurons colocalized the mu receptor, which at the u

93 These GABA neurons communicate with dopamine neurons, where th

94 e mesencephalon, where dopaminergic (DA) and GABA neurons constitute two major neuronal populations.

95 In addition, GABA neurons contributed no more than 20% to each projec

96 Activity of VTA-to-VP-projecting GABA neurons correlates consistently with size and palat

97 indings indicate that the discharging of VTA GABA neurons correlates with psychomotor behavior and th

98 compromised GABA-mediated inhibition of VTA GABA neurons corresponding with increased ethanol-induce

99 sensory cortical development, and thus that GABA neurons could provide an important substrate for ex

100 investigate whether these same hypothalamic GABA neurons decrease their activity postcastration in f

101 Activation of VTA-GABA neurons decreased cue-induced responding and accura

102 Our results indicate that the mechanism of GABA neuron degeneration is calcium-dependent and requir

103 ath is also consistent with our finding that GABA neuron degeneration requires the mitochondrial fiss

104 ggered complex EPSCs and burst firing in SNr GABA neurons, demonstrating the effects of endogenous 5-

105 e intimate relationship between dopamine and GABA neuron development revealed here may offer novel in

106 rect activation of GIRK channels in midbrain GABA neurons did not enhance motor activity.

107 r the selective ablation of GIRK channels in GABA neurons, diminished morphine-induced motor activity

108 Furthermore, optogenetic stimulation of VTA GABA neurons directly suppressed the activity and excita

109 Furthermore, optogenetic silencing of DRN GABA neurons disinhibited neighboring 5-HT neurons and p

110 w that in vivo optogenetic activation of VTA GABA neurons disrupts reward consummatory behavior but n

111 e (GAD) 65-positive neurons, indicating that GABA neurons do not express either transporter.

112 laterally stimulating ventral tegmental area GABA neurons dramatically reduces anticipatory licking t

113 ocal rhythmic bursting by the pGABA and pNon-GABA neurons drove rhythmic theta activity in the EEG.

114 Unlike its effect on VP(GABA) neurons, dynorphin surprisingly potentiated the in

115 Early-born gamma-aminobutyric acid (GABA) neurons (EBGNs) are major components of the hippoc

116 doses of nicotine, by stimulating DA but not GABA neurons, exaggerates these phenotypes and produces

117 Rostromedial tegmental nucleus (RMTg) GABA neurons exert a primary inhibitory drive onto midbr

118 Here, we demonstrate that mouse VTA GABA neurons express a GIRK channel formed by GIRK1 and

119 These CeA GABA neurons express dynorphin, somatostatin, and/or cor

120 We here report that both dopamine and GABA neurons express NUCB2/nesfatin-1 in the VTA.

121 gy is the dysfunction of cortical inhibitory GABA neurons expressing parvalbumin, which are essential

122 Targeted activation of mesoaccumbal GABA neurons facilitates adaptation in reward-seeking be

123 However, lesion of VTA GABA neurons failed to disrupt this effect.

124 D(1)-like receptor blockade reduced SNr GABA neuron firing frequency and increased their firing

125 e often associated with abnormalities in SNr GABA neuron firing intensity and/or pattern.

126 mine, or halothane significantly reduced VTA GABA neuron firing rate and converted their activity int

127 VTA GABA neuron firing rate decreased 53% during slow-wave s

128 and EPSC frequencies were increased in hilar GABA neurons from slices ipsilateral to the injury versu

129 model, we found that tangential migration of GABA neurons from the basal to the dorsal forebrain and

130 and functions cell-autonomously to regulate GABA neuron function.

131 ling complex and function together to affect GABA neuron function.

132 cosyltransferase activity is dispensable for GABA neuron function.

133 ogt-1 and eel-1 act in parallel to regulate GABA neuron function.

134 orter, but Prlr deletion from these dopamine/GABA neurons had no effect on feedback regulation of pro

135 ularly involving parvalbumin (PV)-expressing GABA neurons, has been proposed as a key mechanism under

136 to dopamine (DA) or gamma-aminobutyric acid (GABA) neurons have not yet been investigated.

137 This was associated with LH(GABA) neuron hyperexcitability and impaired hippocampal

138 arized GABA neurons including neuroendocrine GABA neurons identified by antidromic median eminence st

139 rter, a transcription factor that determines GABA neuron identity, a classic inhibitory GABA receptor

140 of a homogeneous population of presumed VTA GABA neurons, implicated in cortical arousal, increases

141 We show that acute inhibition of vHPC GABA neurons in adult mice results in behavioral changes

142 To solidify the importance of these VTA GABA neurons in behavioral function, we employed the neu

143 vidence is lacking for a causal role of vHPC GABA neurons in behaviors associated with schizophrenia.

144 se findings establish a causal role for vHPC GABA neurons in controlling behaviors relevant to schizo

145 togenetic stimulation and recording of these GABA neurons in mice revealed that they can discharge in

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

147 Whole-cell recording of GABA neurons in nigral slices confirmed that NOP recepto

148 altered in the majority of prefrontal cortex GABA neurons in schizophrenic subjects but is reduced be

149 MOR agonists could modulate the activity of GABA neurons in the Acb via receptors located mainly at

150 odulators reduces the activity of inhibitory GABA neurons in the ARC by multiple presynaptic and post

151 ncy within the TIDA population, the dopamine/GABA neurons in the arcuate nucleus represent a subpopul

152 These observations demonstrate that Sst-GABA neurons in the brainstem are crucial for regulating

153 The activity of the Sst-GABA neurons in the DMV is inhibited by both melanocorti

154 ggest that swim stress engages CRF inputs to GABA neurons in the dorsolateral DR that function to inh

155 We provide the first characterization of GABA neurons in the DRN that monosynaptically inhibit 5-

156 that hcrt fibers projected to both 5-HT and GABA neurons in the DRN.

157 onal PFC glutamate synapses on both 5-HT and GABA neurons in the DRN.

158 There were abnormally few GABA neurons in the hypothalamus in the mutant larvae, a

159 hippocampus of mice in which BFCNs and some GABA neurons in the medial septum had been destroyed by

160 enic mice, we demonstrate that glutamate and GABA neurons in the MnPO/OVLT reciprocally regulate wate

161 of the granule cell layer preceding that of GABA neurons in the molecular layer.

162 mu opioid receptors (MORs) are expressed in GABA neurons in the neighboring SNr than in the VTA, and

163 Immunolabeling indicates that GABA neurons in the rostromedial tegmental nucleus (RMTg

164 h-affinity sites may be on axon terminals of GABA neurons in the SN.

165 ogether, these findings suggest that MORs on GABA neurons in the SNr play more important roles in opi

166 ghly expressed in GABA neurons, with ~50% of GABA neurons in the substantia nigra pars reticulata (SN

167 Thus, a network of electrically coupled GABA neurons in the ventral brain may form the elusive n

168 resulted from ethanol-induced excitation of GABA neurons in the ventral tegmental area.

169 ely Activated by Designer Drugs (DREADDs) to GABA neurons in the VTA of wild-type rats trained to res

170 We show here that GABA neurons in the VTA, midbrain, hypothalamus, and tha

171 tion did not affect the activity of presumed GABA neurons in the VTA.

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

173 ch was taken to trace the projections of ARN GABA neurons in vivo.

174 TA dopamine or VTA gamma-amino-butyric acid (GABA) neurons in beta2(-/-) mice to double-dissociate th

175 chemogenetic activation of LHA (Gal) or LHA (GABA) neurons in mice to compare their role in feeding b

176 Gamma-aminobutyric acid (GABA) neurons in the ventral tegmental area (VTA) provid

177 a subpopulation of gamma-aminobutyric acid (GABA) neurons in the VTA increases in anticipation of BS

178 Parvalbumin (PV)-containing cortical GABA neurons include chandelier cells (PVChCs) and baske

179 y reduced the firing rate and hyperpolarized GABA neurons including neuroendocrine GABA neurons ident

180 al that can act in the brain, also inhibited GABA neurons, including identified neuroendocrine cells,

181 pulations of DA and gamma-aminobutyric acid (GABA) neurons, including those projecting to the prefron

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

183 Ca(2+) imaging from LH(GABA) neurons indicate that they are both wake and rapid

184 pulse ratio of the monosynaptic EPSCs in SNr GABA neurons, indicating a presynaptic 5-HT1B receptor-m

185 Activation of LHA (GABA) neurons induced compulsive-like locomotor behavior

186 tic stimulation of lateral hypothalamic (LH) GABA neurons induces rapid vigorous eating in sated anim

187 Furthermore, optogenetic activation of VTA GABA neurons inhibited cocaine, but not heroin, self-adm

188 lf-administration, whereas activation of SNr GABA neurons inhibited heroin reward and relapse.

189 the ventral tegmental area (VTA) and targets GABA neurons, inhibiting them and thereby disinhibiting

190 tory synaptic activity was detected in hilar GABA neurons ipsilateral to the injury after glutamate p

191 est that excitatory drive to surviving hilar GABA neurons is enhanced by convergent input from both p

192 tion in females showed that leptin action on GABA neurons is not necessary for estradiol-mediated sup

193 tered inhibition from parvalbumin-containing GABA neurons is thought to contribute to impaired gamma

194 The molecular identity of LHA (GABA) neurons is heterogeneous and largely undefined.

195 certain classes of gamma-aminobutyric acid (GABA) neurons is very complex.

196 However, GABA neurons lie intermingled with the cholinergic neuro

197 Here, we show that tVTA GABA neurons lose their capacity to disinhibit, but not

198 These findings suggest that VTA GABA neurons may be involved in the attentive processes

199 aversive effects, while beta2* nAChRs on VTA GABA neurons mediate the conditioned rewarding effects i

200 related visual information is relayed to VTA(GABA+) neurons mediating innate behavioral responses, su

201 alance between D1 and D2 receptors can alter GABA neuron migration from the basal forebrain to the ce

202 romotes and D2 receptor activation decreases GABA neuron migration from the medial and caudal ganglio

203 r dopamine receptor activation can influence GABA neuron migration is not known.

204 corroborating the in vivo data on tangential GABA neuron migration.

205 orable environment for dopamine to influence GABA neuron migration.

206 e effects of dopamine receptor activation on GABA neuron migration.

207 ogenetic circuit mapping indicated that MSDB GABA neurons monosynaptically project to cholinergic neu

208 se 67)-synthesizing cells, we identified ARC GABA neurons (n > 300) and used whole-cell recording to

209 m the inhibition of the activity of NPY/AgRP/GABA neurons (NAG) in the arcuate nucleus of the hypotha

210 Analysis of GABA neuron numbers in the cerebral wall of the dopamine

211 argets that included a preferential input to GABA neurons of both mesoaccumbens and mesoprefrontal po

212 GABA neurons of epithalamus are derived from the embryon

213 ases recovered GABA(B)R-GIRK currents in VTA GABA neurons of METH-injected mice.

214 GABA neurons of the cerebral cortex and other telencepha

215 In contrast to the local axons of GABA neurons of the cortex and hippocampus, lateral hypo

216 targets, including the serotonin (5-HT) and GABA neurons of the dorsal raphe nucleus (DRN).

217 We report that leptin targets DA and GABA neurons of the VTA, inducing phosphorylation of sig

218 GABA neurons of ventral thalamus (reticular nucleus, ven

219 nesfatin-1 hyperpolarizes dopamine, but not GABA, neurons of the VTA by inducing an outward potassiu

220 A selective loss of VTA GABA neurons on Day 14 was demonstrated through reduced

221 ract the pronounced inhibitory effect of Sst-GABA neurons on vagal pre-motor neurons in the DMV that

222 GABA+ neurons, on the other hand, may have evolved patte

223 other sub-populations of prefrontal cortical GABA neurons or abnormalities in the parvalbumin-contain

224 e chemogenetically activating either the VTA-GABA neurons or their projections to the NAc.

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

226 A) -> VLPO pathway, presynaptic inputs to LH(GABA) neurons originate from several canonical stress- a

227 We used mossy fiber bouton to GABA neuron paired recordings in the CA3 to demonstrate

228 ere, we determined whether VTA-glutamate or -GABA neurons play a role in innate defensive behavior.

229 ession of the 5-HT3R is selective within the GABA neuron population in the rat telencephalon.

230 survive transplantation, there were abundant GABA neurons present in the graft.

231 rphin-saporin (DS) to selectively lesion VTA GABA neurons prior to assessing spontaneous motor activi

232 -seeking behavior, whereas inhibition of SNr GABA neurons produced optical intracranial self-stimulat

233 We found that VTA GABA neurons project widely to forebrain and brainstem t

234 vious work has suggested that a subset of LH GABA neurons projects to the ventral tegmental area (VTA

235 ion of dorsal raphe gamma-aminobutyric acid (GABA) neurons promoted movement in negative but not posi

236 Activation of LDT(GABA) neurons promotes aversion and reduces DA release i

237 ndelier subclass of gamma-aminobutyric acid (GABA) neurons provides potent inhibitory control over py

238 Optogenetic manipulations of VTA GABA neurons rapidly modulated scratching behaviors thro

239 that this results from an action of SSRIs on GABA neurons rather than as a secondary consequence of m

240 ynaptic inputs from anterior neocortex while GABA neurons receive disproportionally higher input from

241 We found that VTA-DA (and VTA-GABA) neurons receive excitatory, inhibitory, and modula

242 rophysiological recordings, we show that VTA(GABA+) neurons receive direct excitatory inputs from the

243 Inhibition of VTA(GABA+) neurons reduced looming-evoked defensive flight b

244 TA) opioid function classically involves VTA GABA neuron regulation of VTA dopamine neurons via a mu-

245 consequences of selective activation of VTA GABA neurons remains unknown.

246 We report that VTA(GABA+) neurons respond to a looming stimulus.

247 GABA neurons responded positively to both antagonists, b

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

249 trast, activating all ventral tegmental area GABA neurons resulted in a uniform decrease in respondin

250 lts show that optogenetic stimulation of Sst-GABA neurons results in a robust inhibition of action po

251 However, examination of the proportion of GABA neurons revealed an unexpected late peak at postnat

252 n opioid reward and relapse than MORs on VTA GABA neurons.SIGNIFICANCE STATEMENT Opioid reward has lo

253 s a direct correlation between increased VTA GABA neuron slowing and increased delta wave power.

254 The GABA neuron-specific LEPR knock-out females and males sh

255 Esr1(lox/lox) line to generate animals with GABA-neuron-specific or glutamate-neuron-specific deleti

256 (B)R signaling removes an intrinsic brake on GABA neuron spiking, which may augment GABA transmission

257 essels have greater disturbances in cortical GABA neurons suggests that these cell-type distinct path

258 se onto neighboring gamma-aminobutyric acid (GABA) neurons than onto serotonin cells.

259 Given that rostral LS contains GABA neurons that are projection neurons or local intern

260 ifferent but overlapping populations of vHPC GABA neurons that express either PV or GAD65 by selectiv

261 ns in parvalbumin-positive fast-spiking (FS) GABA neurons that may cause abnormal gamma oscillations.

262 at in distinct regions of the telencephalon, GABA neurons that react to cannabinoids may also be resp

263 he input sector by activation of hippocampal GABA neurons that terminate exclusively on apical dendri

264 urons induced a direct inward current in SNr GABA neurons that was sensitive to D(1)-like blockade.

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

266 roduce LHA (Gal) neurons as a subset of LHA (GABA) neurons that lack direct innervation of the ventra

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

268 matergic SC-VTA projections synapse onto VTA(GABA+) neurons that project to the central nucleus of th

269 he threshold for electrical coupling between GABA neurons, the degree of responding for IC self-stimu

270 lthough thought to contain only dopamine and GABA neurons, the VTA also includes a recently discovere

271 dynorphin attenuated inhibitory input to VP(GABA) neurons through a postsynaptic mechanism.

272 MDD, particularly affecting SST/NPY-related GABA neurons, thus linking the neurotrophic and GABA hyp

273 tes selectively regulate excitation of local GABA neurons to drive a distinct avoidance circuit that

274 ivation of P2X receptors excited presynaptic GABA neurons to increase GABA release, which was excitat

275 uit, astrocytes facilitate excitation of VTA GABA neurons to increase inhibition of dopamine neurons,

276 ally released dopamine tonically excites SNr GABA neurons via D(1)-D(5) receptor coactivation that en

277 During exercise, muscle afferents excite NTS GABA neurons via substance P and microinjection of a sub

278 dose- and time-related selective loss of VTA GABA neurons was accomplished using this novel neurotoxi

279 postnatal day 60 and the final proportion of GABA neurons was higher in auditory cortex.

280 Excitation of GABA neurons was mediated by GABAA receptor activation a

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

282 r of undermethylated CpG sites in GLU versus GABA neurons were identified.

283 f the axon terminals of other populations of GABA neurons were not altered in the schizophrenic subje

284 Retrogradely labeled GABA neurons were not numerous, and most non-tyrosine hy

285 Immunocytochemically labelled nonpyramidal GABA neurons were present from postnatal day 1 throughou

286 In freely behaving rats, VTA GABA neurons were relatively fast firing (29 +/- 6 Hz du

287 GAD+ and GABA+ neurons were most prominently distributed in Rt.

288 was found largely on nondopaminergic (i.e., GABA) neurons, whereas NOP mRNA was located on DA neuron

289 the axon terminals of parvalbumin-containing GABA neurons, which are known to have low levels of GAD6

290 he cholinergic neurons lie intermingled with GABA neurons, which could play a similar or opposing rol

291 global activation of ventral tegmental area GABA neurons, which will activate local inhibitory circu

292 tide and marker of gamma-amino butyric acid (GABA) neurons, which specifically inhibit pyramidal neur

293 At the cellular level, the density of GABA neurons with detectable levels of GAD67 mRNA is ~30

294 suggests heterogeneity of both serotonin and GABA neurons with respect to the inputs they receive.

295 or (MOR) gene, Oprm1, is highly expressed in GABA neurons, with ~50% of GABA neurons in the substanti

296 N15 suggest that some of the early-appearing GABA neurons within the developing molecular layer of th

297 vivo the properties, activities, and role of GABA neurons within the laterodorsal tegmental and subla

298 aring population of gamma-aminobutyric acid (GABA) neurons within the developing molecular layer.

299 The absolute numbers of CR+, PV+, CB+, and GABA+ neurones within individual layers in a column of c

300 (Gal) neurons define a subpopulation of LHA (GABA) neurons without direct VTA innervation that mediat