ライフサイエンスコーパス: VTA

1 VTA optical stimulation in ChR2- mice did not restore ri

2 VTA self-activation was accompanied by increased mesolim

3 ES on mesocorticolimbic circuit activation, VTA gene expression, and morphine intake.

4 In addition, VTA mTOR signaling regulates cocaine-cue associative lea

5 Adolescent VTA neurons with dopamine-like characteristics lacked a

6 e genetic inactivation of Robo2 in the adult VTA of mice, reduced inhibitory control results in alter

7 neurons also form connections with vSNc and VTA neurons; however, although photo-excitation of LDT c

8 Ventral tegmental area (VTA) activity is critical for reward/reinforcement and i

9 Activation of the ventral tegmental area (VTA) and mesolimbic networks is essential to motivation,

10 urons project to the ventral tegmental area (VTA) and nucleus accumbens (NAc); however, direct neuroa

11 on of neurons in the ventral tegmental area (VTA) and substantia nigra (SN) has been examined at mult

12 eting efferents from ventral tegmental area (VTA) and substantia nigra pars compacta (SNc).

13 he DA neurons of the ventral tegmental area (VTA) and the suprachiasmatic nucleus (SCN).

14 amine neurons in the ventral tegmental area (VTA) are critical substrates of drug rewards.

15 amine neurons in the ventral tegmental area (VTA) are strongly implicated in cognitive and affective

16 eptor (CRF1R) in the ventral tegmental area (VTA) can modulate ethanol consumption in rodents.

17 mice and found that ventral tegmental area (VTA) Cav1.3 channels mediate cocaine-related and depress

18 ferent inputs to the ventral tegmental area (VTA) control reward-related behaviors through regulation

19 s, causing increased ventral tegmental area (VTA) DA neurons' activity and stress-related behaviors,

20 ic transmission onto ventral tegmental area (VTA) dopamine (DA) neurons is a critical component of su

21 While ventral tegmental area (VTA) dopamine (DA) neurons may mediate social reward, a

22 er FAs are sensed by ventral tegmental area (VTA) dopamine (DA) neurons to control food-motivated beh

23 synaptic strength in ventral tegmental area (VTA) dopamine (DA) neurons.

24 tients and mice with ventral tegmental area (VTA) dopamine depletion had attenuated delta activity (1

25 During oestrus, ventral tegmental area (VTA) dopamine neuron activity is enhanced and drives pos

26 dramatically higher ventral tegmental area (VTA) dopamine neuron firing and burst activity.

27 spontaneously active ventral tegmental area (VTA) dopamine neurons (ie, reduced dopamine neuron popul

28 AMPAR/NMDAR ratio in ventral tegmental area (VTA) dopamine neurons in midbrain slices ex vivo.

29 stress both activate ventral tegmental area (VTA) dopamine neurons, increasing downstream extracellul

30 of GluA1 subunits in ventral tegmental area (VTA) dopamine neurons, which subsequently enhance the mo

31 This contrasts with ventral tegmental area (VTA) dopamine neurons, whose glutamate afferents react r

32 The ventral tegmental area (VTA) dopamine system is important for reward, motivation

33 amine neurons in the ventral tegmental area (VTA) encode reward prediction errors and can drive reinf

34 e LH GABA neurons in ventral-tegmental area (VTA) facilitates learning about reward-paired cues.

35 y delete mTOR in the ventral tegmental area (VTA) in adult male mTOR(loxP/loxP) mice, we investigated

36 (DA) neurons in the ventral tegmental area (VTA) is widely accepted.

37 transmission in the ventral tegmental area (VTA) may contribute to the increased motivational valenc

38 (DA) neurons in the ventral tegmental area (VTA) mediate the positive reinforcing effects of nicotin

39 Dopaminergic ventral tegmental area (VTA) neurons are critically involved in a variety of beh

40 ission from midbrain ventral tegmental area (VTA) neurons underlies behavioral processes related to m

41 m emanating from the ventral tegmental area (VTA) plays a key role in regulating reward-seeking behav

42 OR) localized in the ventral tegmental area (VTA) plays a key role in the reinforcing and addictive p

43 OR) localized in the ventral tegmental area (VTA) plays a key role in the reinforcing and addictive p

44 alamic area (LHA) to ventral tegmental area (VTA) projection is an important neural pathway involved

45 t interface with the ventral tegmental area (VTA) to form a socially engaged reward circuit.

46 minergic inputs from ventral tegmental area (VTA) to striatum encode reward prediction errors and rei

47 ubstantia nigra, and ventral tegmental area (VTA) where they regulate firing patterns critical for mo

48 urons in the lateral ventral tegmental area (VTA) while mice performed classical conditioning tasks.

49 itu in slices of rat ventral tegmental area (VTA) with MAPK activation and two additional cell signal

50 ynapses in the adult ventral tegmental area (VTA), a brain region important for the production of the

51 (OXT) release in the ventral tegmental area (VTA), a key node of the brain's reward circuitry, is nec

52 compacta (SNpc) and ventral tegmental area (VTA), and compared these findings with cholinergic inter

53 onist nor-BNI in the ventral tegmental area (VTA), but not the infralimbic prefrontal cortex (PFC) or

54 thalamus (LH) to the ventral tegmental area (VTA), containing both GABAergic and glutamatergic compon

55 y with volume of the ventral tegmental area (VTA), habenula, periaqueductal gray, cerebellum, hypotha

56 (SP) neurons in the ventral tegmental area (VTA), subsequently increasing SP release onto dopaminerg

57 antia nigra (SN) and ventral tegmental area (VTA), supporting an important function of tau in maintai

58 amine neurons in the ventral tegmental area (VTA), that may also influence drug reward.

59 isual stimuli in the ventral tegmental area (VTA), the origin of the mesolimbic dopaminergic reward s

60 rons of the midbrain ventral tegmental area (VTA), where Cbln1 deletions impair sociability and weake

61 from the LHA to the ventral tegmental area (VTA), which may affect dopamine signaling and motivation

62 ensely innervate the ventral tegmental area (VTA), with modulation of food reward and consumption; ye

63 tions that prime the ventral tegmental area (VTA)-a brain reward region-to be in a depression-like st

64 ergic neurons in the ventral tegmental area (VTA).

65 avior, including the ventral tegmental area (VTA).

66 t innervation of the ventral tegmental area (VTA).

67 nd motivation in the ventral tegmental area (VTA).

68 those located in the ventral tegmental area (VTA).

69 nsmission within the ventral tegmental area (VTA).

70 egulated Lepr in the ventral tegmental area (VTA).

71 circuits within the ventral tegmental area (VTA).

72 amine neurons of the ventral tegmental area (VTA).

73 in DA neurons of the ventral tegmental area (VTA).

74 ns projecting to the ventral tegmental area (VTA)/rostromedial tegmental nucleus (RMTg) regions were

75 te loss of the bilateral vertebral arteries (VTAs) that extend along the ventrolateral sides of the s

76 ed to placebo, participants showed bilateral VTA hypoactivation to high-calorie food stimuli.

77 cits in temporal control of action caused by VTA dopamine depletion.

78 Thus, OTR expression by VTA neurons implicates that OT regulation of reward circ

79 spring that are differentially influenced by VTA leptin antagonism.

80 action potential properties of ClockDelta19 VTA dopamine neurons potentially through network effects

81 otor behavior to understand how differential VTA connectivity and transmitter release in these LHA ne

82 motor behavior is also based on differential VTA innervation.

83 eking actions, risk of punishment diminishes VTA-driven neural synchrony between the two regions.

84 s also modulate food reward, but lack direct VTA innervation.

85 t mediates food reward independent of direct VTA innervation.

86 ehaviors, which we propose to require direct VTA innervation.

87 ulation of LHA (GABA) neurons without direct VTA innervation that mediate noncompulsive food-seeking

88 embles of putative dopamine and non-dopamine VTA neurons and mPFC neurons encode the relationship bet

89 ic increases in the activity of dopaminergic VTA-PFC fibers.

90 phasic nor tonic stimulation of dopaminergic VTA-PFC projections elicited place preference.

91 Rather, dopaminergic VTA-PFC activity can control whether mice maintain or de

92 summary, despite the fact that dopaminergic VTA-PFC projections exhibit phasic increases in activity

93 procedure enhances fear learning by engaging VTA synaptic plasticity.

94 Optogenetically enhancing VTA dopamine neuron burst activity in HAD mice decreases

95 ation of this pathway preferentially excites VTA dopamine neurons and is sufficient to induce behavio

96 About one-third of OTR-expressing VTA neurons did not colocalize with either DA or GLU phe

97 OTR-expressing VTA neurons project to NAc, prefrontal cortex, the exten

98 tion of subset of 5-HT2C receptor expressing VTA neurons in the modulation of appetite and food-motiv

99 xamined excitatory plasticity in fluorescent VTA GABA cells.

100 our findings uncover a fundamental role for VTA dopaminergic circuitry in the maintenance of the awa

101 r the percentage of symmetrical synapses for VTA dopaminergic vs. striatal neurons.

102 during task performance simultaneously from VTA and mPFC, two reciprocally connected regions implica

103 To determine the causal roles of VP --> VTA and VP --> STN pathways in context-induced reinstate

104 ch and show that silencing either the VP --> VTA or VP --> STN pathways is sufficient to reduce both

105 -unit extracellular recordings of identified VTA dopamine neurons.

106 Importantly, VTA formation is not affected by ablation of other CNS c

107 BABR) and D2 DA receptor (D2R) activation in VTA DA neurons.

108 e studies demonstrate that KOR activation in VTA dopamine neurons disrupts behavioral inhibition in a

109 Binge-induced changes in VTA CRF system protein and messenger RNA were also asses

110 ependent decrease in GABABR-GIRK currents in VTA DA neurons did not depend on a mechanism of dephosph

111 id-mediated long-term synaptic depression in VTA dopamine neurons.

112 e magnitudes of the two mechanisms differ in VTA and SNc.

113 nant-negative GluN1 subunit (HSV-dnGluN1) in VTA neurons to study the effect of transient NMDAR inact

114 te pellets and increased c-fos expression in VTA 5-HT2CR expressing gamma-aminobutyric acid (GABA) ne

115 ization, we detected CB2R mRNA expression in VTA DA neurons in wildtype and DAT-Cnr2 cKO heterozygous

116 f AMPA, suggesting a paradoxical increase in VTA AMPA receptor responsiveness.

117 BAergic inhibition because of an increase in VTA GABAergic neuron firing.

118 e magnitude of excitation and an increase in VTA inhibition, as a result of a shift in the type of ce

119 NMDARs mediate cocaine-induced increases in VTA GluA1 expression, but such transient NMDAR inactivat

120 balance between excitation and inhibition in VTA dopamine neurons, while PDE4 inhibition reestablishe

121 induced reduction of GABAergic inhibition in VTA dopamine neurons.

122 ion and reduction of GABAergic inhibition in VTA dopamine neurons.

123 uggest that gene and seizure interactions in VTA glutamatergic neurons impair sociability by downregu

124 inhibitory postsynaptic currents (IPSCs) in VTA dopamine neurons, and these effects were mediated by

125 d-mediated long-term depression (eCB-LTD) in VTA DA neurons.

126 juvenile-but not adult-knockdown of Otx2 in VTA mimics early life stress by increasing stress suscep

127 g and cocaine-induced synaptic plasticity in VTA dopamine neurons.

128 ifies a novel form of synaptic plasticity in VTA GABA cells, and the synaptic remodeling that can occ

129 form of glutamatergic synaptic plasticity in VTA GABA neurons, a currently understudied cell type tha

130 long-lasting transcriptional programming in VTA mediated by Otx2.

131 ociated with enhanced context sensitivity in VTA/SN.

132 ggest that restoring normal eCB signaling in VTA DA neurons could be a useful strategy for treating b

133 rons increased BOLD and CBVw fMRI signals in VTA-innervated limbic regions, including the ventral str

134 of augmented excitatory synaptic strength in VTA DA neurons and increased addiction risk after PE.SIG

135 Increased excitatory synaptic strength in VTA DA neurons is a critical cellular mechanism for addi

136 of enhanced excitatory synaptic strength in VTA DA neurons, which in turn contributes to PE-induced

137 effects on basal excitatory transmission in VTA dopamine neurons but caused an increase in GABAergic

138 unit action potential firing rate in vivo in VTA dopamine neurons, which was blocked by rolipram pret

139 c activation of, or restoration of Cbln1 in, VTA glutamatergic neurons reverses the sociability defic

140 Using chemogenetic approaches, we increase VTA activity to mechanistically link oestrous cycle-depe

141 (2-AG biosynthesis) rescues nicotine-induced VTA GABA signaling following CNE.

142 , however, participants volitionally induced VTA activation without external aids, relative to baseli

143 n reduces binge-like drinking; 2) inhibiting VTA-projecting BNST CRF neurons attenuates binge-like dr

144 r, PPTg glutamate neurons directly innervate VTA; photostimulation of this pathway preferentially exc

145 Instead, VTA dopamine directly contributes to increased vulnerabi

146 ress light-sensitive channelrhodopsin-2 into VTA glutamatergic neurons.

147 n administered systemically or directly into VTA.

148 Intra-VTA antagonism of CRF1R and activation of CRF2R resulted

149 Intra-VTA infusions of selective CRF1R and/or CRF2R compounds

150 Furthermore, intra-VTA oleate blunted the rewarding effects of high-fat/sug

151 o DA neurons and blocks the effects of intra-VTA oleate to decrease food-seeking and DA neuronal acti

152 A single intra-VTA injection of oleate, but not of the saturated FA pal

153 markedly higher locomotor responses to intra-VTA infusions of AMPA, suggesting a paradoxical increase

154 tively inhibited dopamine neurons in lateral VTA, which were unaffected by CMS.

155 eptible to the reinforcing properties of LDT-VTA stimulation.

156 Importantly, we also show that LDT-VTA optogenetic stimulation is reinforcing, and that iuG

157 about the impact of this exposure in the LDT-VTA circuit.

158 In agreement with LDT-VTA dysfunction, we show that iuGC animals present motiv

159 show that the GABAergic component of the LH-VTA pathway supports positive reinforcement and place pr

160 GABAergic inputs from the NAc and local VTA GABA neurons were differentially modulated and activ

161 al developmental cell death in the Mapt(+/-) VTA specifically increased, and the expression of microt

162 ctively inhibited dopamine neurons in medial VTA, which were most impacted by CMS.

163 us glutamate neurotransmission in modulating VTA dopamine neuron activity and behavioral reinforcemen

164 al ganglia regions that receive sparse or no VTA dopaminergic innervation, including the dorsal stria

165 ermore, optogenetic stimulation of mPOA(Nts)-VTA circuitry promotes rewarding phenotypes, social appr

166 Activation of VTA 5-HT2C receptor expressing neurons significantly red

167 In addition, activation of VTA Cav1.3 channels resulted in social behavioral defici

168 Selective activation of VTA Cav1.3 with (+/-)-BayK-8644 (BayK) enhanced cocaine

169 n of DA tone through selective activation of VTA DA neurons accelerates photoentrainment.

170 blish causation between phasic activation of VTA dopamine neurons and global fMRI signals.

171 Phasic activation of VTA dopamine neurons increased BOLD and CBVw fMRI signal

172 nowledge about whether and how activation of VTA dopamine neurons specifically influences regional or

173 ses the firing rate and bursting activity of VTA dopamine neurons, and that these increases persist f

174 racterized the cell-specific connectivity of VTA dopamine neurons, their mRNA translational profile,

175 a loss of inhibitory GABAergic constraint of VTA excitability following CNE.

176 f the midline thalamus gates mPFC control of VTA DA neuron firing by the hippocampus.

177 link oestrous cycle-dependent enhancement of VTA firing to enhanced cocaine affinity at DAT and subse

178 anges to increased intrinsic excitability of VTA DA neurons after cocaine, and explains how acute coc

179 s did not alter the baseline excitability of VTA DA neurons but significantly reduced the magnitude o

180 SK) channels; SK channels regulate firing of VTA DA neurons, but this regulation was absent after coc

181 In contrast, chemogenetic inhibition of VTA 5-HT2C receptor expressing neurons had no effect on

182 nge-like ethanol drinking, but inhibition of VTA-projecting CRF neurons from the BNST significantly r

183 Finally, AAV-shRNA-mediated knockdown of VTA GLP-1 receptors was sufficient to augment cocaine se

184 , and accordingly leads to selective loss of VTA DA neurons in the early postnatal stage.

185 cts on soma size and dendritic morphology of VTA neurons but significantly decreased dopamine release

186 In dopaminergic neurons of VTA slices, orexin A presynaptically inhibits GABAergic

187 yrosine hydroxylase-immunolabeled neurons of VTA, but did attenuate cocaine- and orexin-induced incre

188 alcium transient amplitude within neurons of VTA.

189 f heterogeneity in the basic organization of VTA dopamine neurons with regard to sex.

190 We found that photoactivation of VTA glutamatergic neurons produced robust intracranial s

191 idate findings of drug-induced plasticity of VTA DA neurons and highlight the importance of future pr

192 l cortex (ilPFC) increases the proportion of VTA DA neurons that are spontaneously active (i.e., "pop

193 GIRK channels on D2R-dependent regulation of VTA DA neuron excitability and on cocaine-induced, rewar

194 lling evidence that selective stimulation of VTA DA neurons is sufficient to induce the transition fr

195 We report that optogenetic stimulation of VTA glutamate neurons or terminals serves as a positive

196 nd survival of specific neuronal subtypes of VTA.

197 paired eCB-LTD at the excitatory synapses of VTA DA neurons primarily due to CB1 receptor downregulat

198 mygdala (BLA) and ketamine administration on VTA DA neuron activity and passivity in the modified FST

199 t only on VTA GABAergic neurons, but also on VTA glutamatergic neurons that express vesicular glutama

200 prosocial behavior through direct effects on VTA DA neurons, thus providing mechanistic insight into

201 e present study, CB1Rs are found not only on VTA GABAergic neurons, but also on VTA glutamatergic neu

202 receptor antagonist SCH-23390 before optical VTA stimulation inhibited the arousal responses and rest

203 g procedure was used to expose rats to IP or VTA amphetamine either Paired or Unpaired with an open f

204 tudied these projections and observed phasic VTA-PFC fiber photometry signals after the delivery of r

205 Furthermore, substituting phasic VTA-PFC stimulation for food rewards was not sufficient

206 ous activity of nucleus accumbens-projecting VTA (VTA-NAc) neurons is selectively higher in LAD mice.

207 s and in situ and in vivo experiments in rat VTA, we demonstrate that a significant population of the

208 re we show that at GABAergic synapses on rat VTA dopamine neurons, a single exposure to a brief cold-

209 ck the dendritic dopamine release in the rat VTA induced by local infusion of endomorphin-1, demonstr

210 We found that several VTA subdivisions share similar cellular compositions in

211 uding different parts of the striatum and SN/VTA.

212 substantia nigra/ventral tegmental area (SN/VTA) (+20%; p=0.02), ventral striatum (VST) (+14%; p<0.0

213 stantia nigra and ventral tegmental area (SN/VTA), medial temporal lobe, or subsequent memory perform

214 ffline post-learning dynamics between the SN/VTA and hippocampus, providing novel evidence for a pote

215 reased excitatory drive onto reward-specific VTA dopamine (DA) neurons.

216 ics in Th::Cre rats to selectively stimulate VTA dopamine neurons while simultaneously measuring glob

217 y marked preference for brief over sustained VTA glutamate neuron stimulation resulting in behavioura

218 that coherent theta oscillations synchronize VTA and mPFC in a bottom-up direction, effectively phase

219 Here we selectively activated TH(VTA) neurons in transgenic rats and measured resulting c

220 en those that receive little to no direct TH(VTA) input.

221 y of ventral tegmental area dopaminergic (TH(VTA)) neurons, as well as from more global maladaptation

222 Furthermore, explicit pairing of TH(VTA) neuronal activation with a forepaw stimulus of a pa

223 These data suggest that modulation of TH(VTA) neurons can impact brain dynamics across many distr

224 that selective optogenetic stimulation of TH(VTA) neurons enhanced cerebral blood volume signals in s

225 However, whether TH(VTA) activity affects large-scale brain-wide function re

226 ysomnographic recordings to demonstrate that VTA dopaminergic neurons are necessary for arousal and t

227 The VTA is necessary for reward behavior with dopamine cells

228 The VTA, however, is not a homogenous entity.

229 ity of both the anterior hippocampus and the VTA with high-level visual cortex selectively predicts m

230 tegory-selective visual cortex with both the VTA and the anterior hippocampus predicted associative m

231 nslation is controlled by p-eIF2alpha-in the VTA also prolongs cocaine-induced LTP.

232 rosine hydroxylase (pTH-Ser40) levels in the VTA and dopamine transporter expression in the NAc.

233 eceptors (CRF-R1, CRF-R2) are located in the VTA and influence dopaminergic activity.

234 .Midbrain dopaminergic neurons (mDAs) in the VTA and SNpc project to different regions and form disti

235 uffice to increase DA neuron activity in the VTA but downregulate it in SNc.

236 citation of LDT cholinergic terminals in the VTA caused positive reinforcement, LDT-to-vSNc modulatio

237 inhibition of PVN OXT axon terminals in the VTA decreased social interactions.

238 binant virus (rAAV) leptin antagonism in the VTA decreased wheel running in standard diet but not in

239 netic inhibition of local CRF neurons in the VTA did not alter binge-like ethanol drinking, but inhib

240 that overexpression of KCNQ channels in the VTA dopaminergic neurons and either local infusion or sy

241 neurons in the PVN or their terminals in the VTA enhanced prosocial behaviors.

242 the inhibitory neurotransmitter GABA in the VTA following CNE.

243 e find that targeted deletion of mTOR in the VTA had no significant effects on soma size and dendriti

244 ole of MOR-Gal1R heteromers localized in the VTA in the direct control of dopamine cell function and

245 We found that dnGluN1 expression in the VTA limited to the 3 weeks of cocaine self-administratio

246 hat enhanced glutamatergic plasticity in the VTA may contribute, at least partially, to increased add

247 Kv3.1 protein levels in the VTA of ClockDelta19 and WT mice were unaltered by acute

248 pact of the monounsaturated FA oleate in the VTA on feeding, locomotion, food reward, and DA neuronal

249 alpha7 nAChRs activation specifically in the VTA promotes stress-induced cellular and behavioral mala

250 g of the neurokinin 1 receptor (NK1R) in the VTA renders morphine non-rewarding.

251 ese results suggest that loss of mTOR in the VTA shifts the balance of excitatory and inhibitory syna

252 detect FA and that oleate has actions in the VTA to suppress DA neuronal activity and food seeking fo

253 d, almost 50% of OTR-expressing cells in the VTA were glutamate (GLU) neurons, as indicated by expres

254 he learning-evoked changes that occur in the VTA with repeated exposure to psychostimulants.

255 th dopaminergic and GABAergic neurons in the VTA, and that these projections are sensitive to estroge

256 ne increases AMPA glutamate receptors in the VTA, and this effect enhances motivation for cocaine.

257 In contrast to work in the VTA, this was due to increased NMDA receptor function wi

258 ly and indirectly inhibits DA neurons in the VTA.

259 ocaine-induced long-term potentiation in the VTA.

260 in the NAc and with up-regulated Lepr in the VTA.

261 a significant reduction of DA neurons in the VTA.

262 ed that microinjection of RO5166017 into the VTA and PrL decreased both cue- and drug priming-induced

263 he expression of fluorescent marker into the VTA of male mice that had Cre-recombinase driven by OTR

264 /hSvn-DIO-hm4D-mCherry was injected into the VTA of TH::Cre adult male rats.

265 behaving rats, isradipine injected into the VTA suppressed the acquisition of cocaine-paired context

266 f the mesocorticolimbic system: that is, the VTA, the prelimbic cortex (PrL), and infralimbic cortex

267 tivity in the inhibitory architecture of the VTA and suggest that long-range GABAergic inputs to dopa

268 (Gal1R), which modulate the activity of the VTA dopaminergic neurons.

269 smission from local GABAergic neurons of the VTA, demonstrating an important function for Robo2 in re

270 cts of binge-like ethanol consumption on the VTA CRF system were assessed following drinking-in-the-d

271 l glia is sufficient to partially rescue the VTA formation defect in vegfab mutants.

272 udy clarifies how GABAergic LH inputs to the VTA can contribute to generalized behavioral activation

273 ng these acute and persistent changes to the VTA CRF system may lead to better therapeutic interventi

274 sumption; yet, LHA (GABA) projections to the VTA exclusively modulated food consumption, not reward.

275 one expressing LHA neurons projecting to the VTA were suppressed by leptin, a peptide hormone derived

276 of two separate pathways from the LHb to the VTA, a direct and an indirect one, which may subserve di

277 ucleus of the stria terminalis (BNST) to the VTA, CRF neurons in this circuit were chemogenetically i

278 one of the most prominent projections to the VTA; however, recent studies have provided conflicting e

279 rotein and messenger RNA associated with the VTA-CRF system.

280 inue to express elevated CRF tone within the VTA and antagonism of pVTA CRF-R1 or aVTA CRF-R2 reverse

281 Here, we revealed VGluT2 neurons within the VTA and SNC of nonhuman primates and humans by simultane

282 ce of OT regulation of DA neurons within the VTA is sparse.

283 subpopulation of 5-HT2CR neurons within the VTA is sufficient to significantly reduce homeostatic fe

284 R) expressing neurons originating within the VTA, we delivered Cre-inducible adeno-associated virus t

285 Vegfr2 signaling blocks the formation of the VTAs and subsequently of the PNVP.

286 the differential afferent inputs onto these VTA DA neuron subpopulations, and consolidate findings o

287 After real-time VTA neurofeedback training, however, participants voliti

288 our data suggest that feedback inhibition to VTA DA neurons, mediated by GIRK channel activation, tem

289 ns can drive motivated behavior, and PPTg to VTA synapses may represent an important target relevant

290 l nucleus sends glutamatergic projections to VTA dopamine neurons, and that stimulation of this circu

291 nt, with an emphasis on their projections to VTA dopamine neurons.

292 le homeobox 2 (Otx2), which is restricted to VTA neurons at the postmitotic stage and selectively con

293 t that ethanol-induced activation of BNST-to-VTA CRF projections is critical in driving binge-like et

294 regulate synaptic transmission in the LHA-to-VTA neurocircuitry in an inverted "U-shape" fashion depe

295 regulatory function of leptin in the LHA-to-VTA neuronal pathway is highly sensitive to energy state

296 Unexpectedly, VTA dopamine neuron activity in high alcohol drinking (H

297 ctivity of nucleus accumbens-projecting VTA (VTA-NAc) neurons is selectively higher in LAD mice.

298 novel, overlapping mechanisms through which VTA Cav1.3 mediates cocaine-related, depressive-like and

299 um that is not traditionally associated with VTA dopamine neurotransmission.

300 of the K(+)Cl(-) co-transporter KCC2 within VTA GABAergic neurons.