ライフサイエンスコーパス: dopamine neuron

1 osine hydroxylase (TH; for identification of dopamine neurons).

2 accelerate the pacemaker activity of rodent dopamine neurons.

3 n habenula-induced feedforward inhibition of dopamine neurons.

4 d pattern of activity in different groups of dopamine neurons.

5 d activated separate receptor populations in dopamine neurons.

6 ors (GPCRs), to decrease the excitability of dopamine neurons.

7 d cocaine-induced synaptic plasticity in VTA dopamine neurons.

8 with an emphasis on their projections to VTA dopamine neurons.

9 ced reduction of GABAergic inhibition in VTA dopamine neurons.

10 ediated long-term synaptic depression in VTA dopamine neurons.

11 the striatum, as well as survival of nigral dopamine neurons.

12 ory, this RPE signal is provided by midbrain dopamine neurons.

13 or control of the activity and plasticity of dopamine neurons.

14 and reduction of GABAergic inhibition in VTA dopamine neurons.

15 +) signaling in spines and shaft synapses of dopamine neurons.

16 transporter, and affects the excitability of dopamine neurons.

17 function, normalizing the firing activity of dopamine neurons.

18 crease in inhibitory inputs onto the vPAG/DR dopamine neurons.

19 additional yet-to-be-identified subclass of dopamine neurons.

20 n the regulation of firing activity of mouse dopamine neurons.

21 ed functional subpopulations in hypothalamic dopamine neurons.

22 also been shown to alter the excitability of dopamine neurons.

23 DAT-mediated increases in firing activity of dopamine neurons.

24 ease in excitatory synaptic density onto VTA dopamine neurons.

25 re feeding behavior by "rewiring" mesolimbic dopamine neurons.

26 synaptic plasticity affects the activity of dopamine neurons.

27 ibitory pauses in subpopulations of midbrain dopamine neurons.

28 mainly due to degeneration of nigrostriatal dopamine neurons.

29 ptic regulation that control the activity of dopamine neurons.

30 PA receptor (AMPAR)/NMDAR ratios in midbrain dopamine neurons.

31 X6 to be required for development of gastric dopamine neurons.

32 decreases the normal chronic activity of the dopamine neurons.

33 bution of these receptors in living midbrain dopamine neurons.

34 and reinstated by optogenetically activating dopamine neurons.

35 5-HT2B receptors are expressed by mesolimbic dopamine neurons.

36 t extracellular recordings of identified VTA dopamine neurons.

37 als with pluripotent stem cell (PSC)-derived dopamine neurons.

38 f how intrinsic conductances shape pauses in dopamine neurons.

39 ng reduces presynaptic calcium transients in dopamine neurons, a finding consistent with reciprocal c

40 e show that at GABAergic synapses on rat VTA dopamine neurons, a single exposure to a brief cold-wate

41 This suggests that dopamine neurons access a wider variety of information t

42 These results show that dopamine neurons acquire predictive value signals from t

43 In contrast, in high reward contexts, dopamine neurons acquired a short-latency excitation to

44 lutamate neurotransmission in modulating VTA dopamine neuron activity and behavioral reinforcement.

45 Transient changes in dopamine neuron activity correlate with positive and neg

46 hes to prevent transient changes in midbrain dopamine neuron activity during the critical error-signa

47 tween hippocampal parvalbumin expression and dopamine neuron activity in F2 rats.

48 Unexpectedly, VTA dopamine neuron activity in high alcohol drinking (HAD)

49 During oestrus, ventral tegmental area (VTA) dopamine neuron activity is enhanced and drives post tra

50 d cotransmission convey discrete patterns of dopamine neuron activity to striatal neurons.

51 Specifically, ventral tegmental area of dopamine neuron activity was examined using electrophysi

52 ward-related behaviors through regulation of dopamine neuron activity.

53 ocampal hyperactivity and normalize aberrant dopamine neuron activity.

54 nula (LHb) in the CMS-induced attenuation of dopamine neuron activity.

55 showed that 5-HT2B-receptor inactivation in dopamine neurons affects their neuronal activity and inc

56 gic terminal density and modest loss of SNpc dopamine neurons after eight weeks, corresponding to rob

57 However, when dopamine neurons alone were stimulated, nAChRs had no ef

58 Here, we show that classic error-signaling dopamine neurons also respond to changes in value-neutra

59 creased bursting in vivo properties of these dopamine neurons and a concomitant increase in AMPA syna

60 rmine the full prediction error functions of dopamine neurons and compare them to each other.

61 X6 in the ENS reduced the numbers of gastric dopamine neurons and delayed gastric emptying.

62 rd prediction error, exploring the signal of dopamine neurons and describing its potential role in re

63 h causation between phasic activation of VTA dopamine neurons and global fMRI signals.

64 es neuroprotection for substantia nigra (SN) dopamine neurons and increases BDNF in the nigrostriatal

65 n of this pathway preferentially excites VTA dopamine neurons and is sufficient to induce behavioral

66 on could lead to novel strategies to protect dopamine neurons and perhaps delay the onset of Parkinso

67 sults demonstrate functionality of spines in dopamine neurons and reveal a novel modulation of spine

68 e MPTP-induced loss of substantia nigra (SN) dopamine neurons and striatal dopamine turnover in ghrel

69 gical alpha-syn conformers in human midbrain dopamine neurons and tested their contribution to the ag

70 gs represent the largest number of surviving dopamine neurons and the densest and most widespread gra

71 rs control subtype-specific mesodiencephalic dopamine neurons and their appropriate axon innervation.

72 isease is the progressive demise of midbrain dopamine neurons and their axonal projections, but the u

73 To molecularly profile mesolimbic dopamine neurons and their presynaptic inputs, we inject

74 Substantia nigra pars compacta (SNc) dopamine neurons and their targets are involved in addic

75 he contexts to examine the representation in dopamine neurons and uncover different modes of dopamine

76 n of expression of the transgene in midbrain dopamine neurons and validation of its effectiveness in

77 cleus sends glutamatergic projections to VTA dopamine neurons, and that stimulation of this circuit p

78 the firing rate and bursting activity of VTA dopamine neurons, and that these increases persist for 7

79 ibitory postsynaptic currents (IPSCs) in VTA dopamine neurons, and these effects were mediated by a p

80 ed that substantia nigra pars compacta (SNc) dopamine neurons are a key node in the circuitry that dr

81 Dopamine neurons are classically known to modulate locom

82 Midbrain dopamine neurons are crucial for many behavioral and cog

83 ve strategy for Parkinson's disease in which dopamine neurons are generated by direct conversion of a

84 The demonstration that midbrain dopamine neurons are intermixed with glutamate or glutam

85 minence suggests that only the non-GABAergic dopamine neurons are involved in the control of pituitar

86 We found that excitatory afferents to SNc dopamine neurons are sensitive to cocaine in an afferent

87 ouse line in which glutamatergic inputs onto dopamine neurons are specifically impaired, and utilized

88 Dopamine neurons are thought to encode novelty in additi

89 Dopamine neurons are thought to signal reward prediction

90 nts, changes in firing rate of nigrostriatal dopamine neurons, as well as dopamine signaling in the d

91 The involvement of each region in dopamine neuron attenuation following 5-7 weeks of CMS w

92 Conditioned by these experiences, dopamine neurons begin to fire upon the earliest present

93 f GRK3/arrestin-dependent p38alpha MAPK from dopamine neurons blocked KOR-mediated DRL disruptions.

94 In dopamine neurons, both variants can act as autoreceptors

95 Optogenetically enhancing VTA dopamine neuron burst activity in HAD mice decreases alc

96 ects on basal excitatory transmission in VTA dopamine neurons but caused an increase in GABAergic inh

97 evaluate synaptic modulation of the vPAG/DR dopamine neurons by mu opioid receptors and to (2) disse

98 Thus, whether dopamine neurons can acquire prediction signals in the a

99 resses excitatory synaptic transmission onto dopamine neurons, can abolish food approach behaviors an

100 hould assist in engineering mesodiencephalic dopamine neurons capable of regenerating appropriate con

101 Degeneration of dopamine neurons causes Parkinson's disease, whereas dys

102 se studies support the development of future dopamine neuron cell transplantation therapy-based appro

103 ons not only in dopamine release but also in dopamine neuron connectivity, cotransmission, modulation

104 tors to improve their derivation and predict dopamine neuron content after engraftment.

105 Current thought envisions dopamine neurons conveying the reinforcing effect of the

106 ed in human neuroblastoma cells and midbrain dopamine neurons derived from induced pluripotent stem c

107 lacking 5-HT2B receptors, even restricted to dopamine neurons, developed heightened cocaine-induced l

108 Ndufs4, which reduces complex I activity in dopamine neurons, did not cause a significant loss of do

109 plicated in psychiatric disorders, including dopamine neuron differentiation and innate immune respon

110 ANCE STATEMENT The frequency at which nigral dopamine neurons discharge action potentials sets baseli

111 udies demonstrate that KOR activation in VTA dopamine neurons disrupts behavioral inhibition in a GRK

112 terozygous (cHET) reduction of Gls1 in their dopamine neurons, dopamine neuron survival and transmiss

113 es that activation of ventral tegmental area dopamine neurons during sexual experience regulates cros

114 ationship between mitochondrial function and dopamine neuron dysfunction and death using C. elegans m

115 Midbrain dopamine neuron dysfunction contributes to various psych

116 New research indicates that midbrain dopamine neurons encode multiple types of error signals

117 Dopamine neurons encode the difference between actual an

118 Here we report that the deletion of CB2Rs in dopamine neurons enhances motor activities, modulates an

119 g 5-HT2B receptors totally or exclusively in dopamine neurons exhibit heightened cocaine-induced loco

120 or magnetic sorting (MAC) which give rise to dopamine neurons expressing TH and Pitx3, whilst FolR1 n

121 Dopamine neurons facilitate learning by calculating rewa

122 ices, but it has been unclear whether or how dopamine neurons factor it into their teaching signal.

123 suggest that input integration differs among dopamine neurons favoring higher sensitivity to inhibiti

124 Although all dopamine neurons fire action potentials in a pacemaker p

125 While some dopamine neurons fire single spikes at regular intervals

126 identified an unexpected property of METH on dopamine neuron firing activity.

127 atically higher ventral tegmental area (VTA) dopamine neuron firing and burst activity.

128 e discrete aversive stimuli elicit pauses in dopamine neuron firing and reductions in NAc dopamine co

129 annels play an important role in maintaining dopamine neuron firing regularity and burst firing.

130 We show that pauses in dopamine neuron firing, evoked by either stimulation of

131 increased the spontaneous spike activity of dopamine neurons followed by a progressive reduction of

132 We developed a mouse line targeting midbrain dopamine neurons for Translating Ribosome Affinity Purif

133 Moreover, we demonstrate that VTA dopamine neurons from adult rats exhibit enhanced IPSCs

134 nstitution experiments that Kenyon cells and dopamine neurons from axoaxonic reciprocal synapses.

135 s are intermixed with glutamate or glutamate-dopamine neurons from rodents to humans offers new oppor

136 Dopamine neurons from the substantia nigra pars compacta

137 These data establish SV2C as a mediator of dopamine neuron function and suggest that SV2C disruptio

138 suggest that long-range GABAergic inputs to dopamine neurons fundamentally regulate behavioral respo

139 Thus, a reduction in dopamine neuron glutamate cotransmission appears to medi

140 nd synaptic stimulation in subpopulations of dopamine neurons grouped according to their axonal proje

141 This suggests that dopamine neurons have access to a wider variety of infor

142 Midbrain dopamine neurons have been proposed to signal prediction

143 Midbrain dopamine neurons have been proposed to signal reward pre

144 Anatomic evidence suggests that some dopamine neurons have cross-hemispheric projections, but

145 , and mouse astrocytes in vivo, into induced dopamine neurons (iDANs).

146 aneously active ventral tegmental area (VTA) dopamine neurons (ie, reduced dopamine neuron population

147 Genetic deletion of GABAB receptors from dopamine neurons in adult mice did not affect general or

148 ersely, LHb activation selectively inhibited dopamine neurons in lateral VTA, which were unaffected b

149 ILPFC activation selectively inhibited dopamine neurons in medial VTA, which were most impacted

150 ial rank, together supporting a role for DRN dopamine neurons in mediating a loneliness-like state.

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

152 ted tonic firing in KORD-expressing putative dopamine neurons in midbrain.

153 probability and expected value, we asked how dopamine neurons in monkeys acquire this value signal th

154 egatively correlated with survival of nigral dopamine neurons in multiple system atrophy mice treated

155 ty of effective and selective stimulation of dopamine neurons in non-human primates and a resource th

156 adaptive coding has been linked to midbrain dopamine neurons in nonhuman primates, and evidence in s

157 of identified substantia nigra pars compacta dopamine neurons in R1441C LRRK2 transgenic rats reveal

158 tion task that brief pauses in the firing of dopamine neurons in rat ventral tegmental area at the ti

159 However, dopamine neurons in rats with ipsilateral ventral striat

160 mine and glutamatergic signaling in midbrain dopamine neurons in response to acute administration of

161 We recorded basal ganglia-projecting dopamine neurons in singing zebra finches as we controll

162 We recorded from optogenetically identified dopamine neurons in the lateral ventral tegmental area (

163 e we examined how optogenetically-identified dopamine neurons in the lateral ventral tegmental area o

164 dence on VGLUT2 are seen in ventral midbrain dopamine neurons in the mouse.

165 generative disorder characterized by loss of dopamine neurons in the substantia nigra pars compacta (

166 Dopamine neurons in the substantia nigra pars compacta a

167 toms accompanied by the preferential loss of dopamine neurons in the substantia nigra pars compacta.

168 Here, we show that, in contrast to dopamine neurons in the substantia nigra, vagal motoneur

169 dopamine in pain, the recently characterized dopamine neurons in the ventral PAG (vPAG)/dorsal raphe

170 ivational for cocaine.SIGNIFICANCE STATEMENT Dopamine neurons in the ventral tegmental area (VTA) are

171 Dopamine neurons in the ventral tegmental area (VTA) are

172 Dopamine neurons in the ventral tegmental area (VTA) are

173 Dopamine neurons in the ventral tegmental area (VTA) enc

174 Dopamine neurons in the ventral tegmental area (VTA) rec

175 ircuit, including changes in the activity of dopamine neurons in the ventral tegmental area (VTA), th

176 acity for WIN55,212-2 to stimulate firing of dopamine neurons in the ventral tegmental area and to in

177 Preventing dopamine neurons in the ventral tegmental area from firi

178 Dopamine neurons in the ventral tegmental area use gluta

179 lasticity, at least in part by disinhibiting dopamine neurons in the ventral tegmental area.

180 d this hypothesis by recording from putative dopamine neurons in the VTA of rats performing a task in

181 ient direct lineage reprogramming to induced dopamine neurons in vitro and in vivo.

182 Here, we develop a biophysical model of a dopamine neuron incorporating ion channel stochasticity

183 Building on the notion that responses of dopamine neurons increase with reward probability and ex

184 Phasic activation of VTA dopamine neurons increased BOLD and CBVw fMRI signals in

185 channels, the intrinsic excitability of VTA dopamine neurons increases.

186 s both activate ventral tegmental area (VTA) dopamine neurons, increasing downstream extracellular do

187 t-induced internalization of D2 receptors on dopamine neurons indicate a purposefully regulated local

188 substantia nigra pars compacta (SNC) contain dopamine neurons intermixed with glutamate neurons (expr

189 DCC receptor signaling in dopamine neurons is a molecular link where genetic and e

190 D2R-mediated signaling in dopamine neurons is involved in the presynaptic regulati

191 ulation of the intrinsic firing behaviors of dopamine neurons is less understood.

192 s that a approximately 30% decline of nigral dopamine neurons is necessary to cause motor symptoms in

193 hese fundamental properties, the activity of dopamine neurons is regulated and underlies the wide-ran

194 te the complexity of inputs, the output from dopamine neurons is remarkably homogeneous and robust.

195 How dopamine neurons jointly encode this information, howeve

196 ds robust inhibitory projections to midbrain dopamine neurons, leading to the hypothesis that the RMT

197 p a model where increased inhibitory tone on dopamine neurons leads to a persistent decrease in tonic

198 beta2-containing nicotinic receptors in dopamine neurons likely mediate the protective effect of

199 ved by distinct subtypes of mesodiencephalic dopamine neurons located in the substantia nigra pars co

200 athologically characterized by nigrostriatal dopamine neuron loss and the postmortem presence of Lewy

201 However, even when nigrostriatal dopamine neuron loss is severe enough to cause motor sym

202 d reduces dopamine content in the absence of dopamine neuron loss.

203 decades of research, it remains unclear how dopamine neurons make this calculation.

204 We consider targeting AMPK in dopamine neurons may recapitulate neuroprotective effect

205 Hence, ghrelin signaling through AMPK in SN dopamine neurons mediates CR's neuroprotective effects.

206 se results imply that type I excitability in dopamine neurons might be important for low firing rates

207 tion of beta2 nicotinic receptor subunits in dopamine neurons mitigates aberrant motor learning induc

208 We propose that coregulation of NAD(P)H in dopamine neuron mitochondria and ER coordinates cell red

209 n for diversity among ventral tegmental area dopamine neurons, much less is known regarding functiona

210 ype calcium current is larger in the soma of dopamine neurons of the SNc, leading to a higher charge

211 isease, characterized by the degeneration of dopamine neurons of the substantia nigra pars compacta,

212 Potentiation of excitatory inputs onto dopamine neurons of the ventral tegmental area (VTA) ind

213 ne-induced inhibitory synaptic plasticity in dopamine neurons of the ventral tegmental area (VTA).

214 ndependently modulated when driven by either dopamine neurons or cholinergic interneurons.

215 and function of dendritic spines on midbrain dopamine neurons, or the relative contribution of spine

216 Mesodiencephalic dopamine neurons play central roles in the regulation of

217 ontaneous tonic discharge activity of nigral dopamine neurons plays a fundamental role in dopaminergi

218 Moreover, only ILPFC inactivation restored dopamine neuron population activity to normal levels fol

219 tal area (VTA) dopamine neurons (ie, reduced dopamine neuron population activity) in the chronic mild

220 FC or LHb in normal rats potently suppressed dopamine neuron population activity, but in unique patte

221 of F2 and F3 MAM rats exhibited increases in dopamine neuron population activity, indicating that thi

222 control conditions, and 62-180% increases in dopamine neuron population activity.

223 ion potential properties of ClockDelta19 VTA dopamine neurons potentially through network effects.

224 found that NAc inputs synapsed directly onto dopamine neurons, preferentially activating GABAB recept

225 deletion of AMPKbeta1 and 2 subunits only in dopamine neurons prevented ghrelin-induced AMPK phosphor

226 to identify predictive markers expressed in dopamine neuron progenitors that correlate with graft ou

227 In rats, some dopamine neurons projecting to the striatum also innerva

228 nduced locomotion associated with changes in dopamine neuron reactivity.

229 The dopamine neurons receive cholinergic input via nicotinic

230 Midbrain dopamine neurons recorded in vivo pause their firing in

231 tive deletion of beta2 nicotinic subunits in dopamine neurons reduced D2R-mediated aberrant motor lea

232 , by manipulating reward size, we found that dopamine neurons reflect both the upcoming reward size a

233 Optogenetic studies have revealed that dopamine neurons release dopamine in a synaptic signal m

234 role of glutamatergic input as a whole onto dopamine neurons remains unclear.

235 Dopamine neurons respond to rewards with two components,

236 Here, we show that error-signaling rat dopamine neurons respond to the inferred, model-based va

237 he ILPFC is the primary driver of diminished dopamine neuron responses.

238 by aversive events, and expectation reduced dopamine neurons' responses to reward and punishment.

239 e odor predicted both reward and punishment, dopamine neurons' responses to that odor reflected the i

240 In contrast, Prlr deletion from all dopamine neurons resulted in profound hyperprolactinemia

241 A similar comparison between populations of dopamine neurons revealed a two times greater number of

242 behavior; most critically, it indicates that dopamine neurons selectively modulate signal reception p

243 on of 5-HT2B receptors in a subpopulation of dopamine neurons sending axons to the ventral striatum.

244 proposal that brief changes in the firing of dopamine neurons serve as full-fledged bidirectional pre

245 Midbrain dopamine neurons signal reward prediction error (RPE), o

246 Dopamine neurons signal reward prediction errors.

247 Thus, in low reward contexts, dopamine neurons signal value prediction errors (VPEs) i

248 Regional differences in dopamine neuron signaling are likely to be differentiall

249 tum attenuate habenula-induced inhibition of dopamine neurons significantly.

250 edge about whether and how activation of VTA dopamine neurons specifically influences regional or glo

251 ral responses that are notably distinct from dopamine neuron stimulation and resistant to dopamine re

252 alize neural activity in rats, we found that dopamine neuron stimulation drives striatal activity, wh

253 ist transcript was significantly enriched in dopamine neurons, suggesting tight regulation of X-linke

254 reduction of Gls1 in their dopamine neurons, dopamine neuron survival and transmission were unaffecte

255 the detrimental effect of these mutations on dopamine neuron survival.

256 not only in a signaling role at a subset of dopamine neuron synapses, but also in mediating vesicula

257 pharmacological actions targeting subsets of dopamine neuron synapses.

258 Dopamine neuron synaptic actions vary across the striatu

259 Elucidating dopamine neuron synaptic signaling offers the potential

260 riments showed also the novelty responses of dopamine neurones that decreased as learning advanced.

261 ing of excitatory synaptic transmission onto dopamine neurons that is initially offset by a transient

262 we show that SSRIs can inhibit hypothalamic dopamine neurons that normally suppress the secretion of

263 We identified dopamine neurons that uniquely coexpress the Onecut3 and

264 on of spontaneous spike activity of midbrain dopamine neurons that was followed by a progressive redu

265 enhanced the bursting activity of mesolimbic dopamine neurons that were excited by aversive stimulati

266 In addition to dopamine neurons, the ventral tegmental area (VTA) conta

267 erized the cell-specific connectivity of VTA dopamine neurons, their mRNA translational profile, and

268 We found marked homogeneity among individual dopamine neurons: their responses to both unexpected and

269 However, afferents onto SNc dopamine neurons themselves appear insensitive to drugs

270 al patterns emerge from this synthesis: that dopamine neurons themselves calculate reward prediction

271 ged micro-opioid receptors were expressed in dopamine neurons they too were internalized.

272 and critical role for positive feedback onto dopamine neurons through reciprocal connections with Ken

273 res robust information coding, allowing each dopamine neuron to contribute fully to the prediction er

274 If so, then phasic response of dopamine neurons to cues in this setting cannot be descr

275 a preparation of dissociated mouse midbrain dopamine neurons to isolate effects on intrinsic excitab

276 lateral habenula by aversive events inhibits dopamine neurons transiently, providing a neurobiologica

277 C-matching increases the survival of grafted dopamine neurons (tyrosine hydroxylase: TH+).

278 se data indicate that the features that make dopamine neurons unique are highly concordant and not a

279 Efforts to explain dopamine neuron vulnerability are hindered by the lack o

280 comparing the cue responses of serotonin and dopamine neurons, we found differences in learning rates

281 over druggable neuroprotective compounds for dopamine neurons, we have designed and synthesized a sec

282 AT's role in mediating amphetamine action in dopamine neurons, we have used novel genetic, pharmacolo

283 In low reward contexts, most dopamine neurons were exclusively inhibited by aversive

284 ase in AMPA synaptic transmission to ex vivo dopamine neurons were found in mice lacking 5-HT2B recep

285 ubunits that appear in the membrane of mouse dopamine neurons when GABAB receptors are stimulated.

286 ton microscopy to show that substantia nigra dopamine neurons, which are sensitive to stress in mitoc

287 is the normal behavior of reward processing dopamine neurons, which previously had not been tested b

288 uA1 subunits in ventral tegmental area (VTA) dopamine neurons, which subsequently enhance the motivat

289 action potential firing rate in vivo in VTA dopamine neurons, which was blocked by rolipram pretreat

290 An ASOX-mediated hyperactivity of SN dopamine neurons, which was caused by oxidative dysfunct

291 sive alpha-synucleinopathies earlier than SN dopamine neurons while exhibiting milder cell loss in PD

292 he firing patterns of monosynaptic inputs to dopamine neurons while mice performed classical conditio

293 in Th::Cre rats to selectively stimulate VTA dopamine neurons while simultaneously measuring global h

294 dopamine-dependent behaviors, but no loss of dopamine neurons, while djr-1.1 mutants showed an increa

295 nce between excitation and inhibition in VTA dopamine neurons, while PDE4 inhibition reestablishes th

296 contrasts with ventral tegmental area (VTA) dopamine neurons, whose glutamate afferents react robust

297 These data show that two viral vectors label dopamine neurons with greater than 95% specificity.

298 terogeneity in the basic organization of VTA dopamine neurons with regard to sex.

299 Approximately 50% of dopamine neurons within the arcuate nucleus were labeled

300 venly clustered on the soma and dendrites of dopamine neurons within the substantia nigra pars compac