ライフサイエンスコーパス: SNc

1 SNc and VTA dopamine neurons receive contrasting excitat

2 eriment 2, lesions that disconnected CeA and SNc prevented the acquisition of conditioned ORs but did

3 SSRIs induce SNr hyperactivity and SNc hypoactivity that can also be reversed by systemic 5

4 ive effects of PPX on striatal DA levels and SNc DA neuron survival were similar in young and aged an

5 also make pathfinding errors, while SNa and SNc axons appear normal.

6 in nerve branches (ISN, ISNb, ISNd, SNa, and SNc) in the Drosophila larva.

7 luR1a and mGluR5 immunoreactivity in SNr and SNc neurons.

8 different release mechanisms in striatum and SNc, with minimal Ca(2+) required to trigger prolonged D

9 influencing dopamine neurons of the VTA and SNc and differentially desensitizing alpha7* and non-alp

10 osphate levels were decreased in the VTA and SNc but not the prefrontal cortex after 6-OHDA lesions.

11 Here, we show that, although both VTA and SNc DA neuron activation reinforces instrumental respond

12 male and female rats, we reveal that VTA and SNc dopamine neurons generate reinforcement through sepa

13 Both VTA and SNc dopaminergic neurons innervate homogenously the lowe

14 oximately 60% and 300% higher in the VTA and SNc, respectively, after 6-OHDA lesions.

15 were nearly 80 and 85% lower in the VTA and SNc, respectively, on the lesioned side.

16 In the VTA and SNc, small populations (approximately 6-10%) of N/OFQ-co

17 e distribution of mDA neurons in the VTA and SNc.

18 uted at a higher density in both the VTA and SNc.

19 udes of the two mechanisms differ in VTA and SNc.

20 ects to the ventral tegmental area (VTA) and SNc, but neither MSt nor Area X projects to the SNr.

21 l dopaminergic activity and function both at SNc dopaminergic neurons and at a locus downstream of th

22 l data showed a positive correlation between SNc-related FC and SMN activity, whereas a negative corr

23 as a near-complete loss of GPX m-RNA in both SNc (100%, P<0.005) and SNr (88%, P<0.005).

24 immunoreactivity for group I mGluRs in both SNc and SNr neurons was mostly extrasynaptic or in the m

25 Cb-SNc projections show prominent activation for water rewa

26 During behavior, Cb-SNc projections are bilaterally activated before ambulat

27 G positive, indicating activation of the CeA-SNc pathway by the CS.

28 ylase (TH) in the substantia nigra compacta (SNc) and in two subdivisions of the ventral tegmental ar

29 bral field (RRF), substantia nigra compacta (SNc), ventral tegmental area (VTA), and ventrolateral pe

30 rea (VTA) and the substantia nigra compacta (SNc).

31 al area (VTA) and substantia nigra compacta (SNc).

32 urons in the substantia nigra pars compacta (SNc) and consequent depletion of striatal dopamine are k

33 ority of the substantia nigra pars compacta (SNc) and experiences striatal denervation.

34 rones in the substantia nigra pars compacta (SNc) and may contribute to excitotoxic cell death in Par

35 between the substantia nigra pars compacta (SNc) and striatum.

36 the midbrain substantia nigra pars compacta (SNc) and the CeA.

37 urons of the substantia nigra pars compacta (SNc) and the importance of protein aggregation in drivin

38 urons in the substantia nigra pars compacta (SNc) and the presence of intracytoplasmatic inclusions k

39 ons from the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) are involved in va

40 urons of the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) play a crucial rol

41 centers, the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA), densely innervate

42 oject to the substantia nigra pars compacta (SNc) are activated by a visual CS for food.

43 ea (VTA) and substantia nigra pars compacta (SNc) are not significantly modulated by anesthetics or t

44 ea (VTA) and substantia nigra pars compacta (SNc) convey distinct signals.

45 which in turn inhibits nigra pars compacta (SNc) DAergic neurons.

46 tions of the substantia nigra pars compacta (SNc) differentially degenerate in Parkinson's disease an

47 f the rodent substantia nigra pars compacta (SNc) display varied electrophysiological properties in v

48 acterized by substantia nigra pars compacta (SNc) dopamine (DA) neuron loss and subsequent motor defi

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

50 blished that substantia nigra pars compacta (SNc) dopamine neurons are a key node in the circuitry th

51 the loss of substantia nigra pars compacta (SNc) dopaminergic neurons in Parkinson's disease (PD).

52 t spiking in substantia nigra pars compacta (SNc) dopaminergic neurons is a key signaling event in th

53 activity of substantia nigra pars compacta (SNc) dopaminergic neurons, elevated baseline extracellul

54 he firing of substantia nigra pars compacta (SNc) dopaminergic neurons, we identified and characteriz

55 he mammalian substantia nigra pars compacta (SNc) evokes increasing activation of MLR cells with a gr

56 urons of the substantia nigra pars compacta (SNc) exhibit functional heterogeneity that likely underp

57 urons of the substantia nigra pars compacta (SNc) govern movements requires a detailed knowledge of h

58 DANs) in the substantia nigra pars compacta (SNc) have been related to movement speed, and loss of th

59 ) within the substantia nigra pars compacta (SNc) in both young and aged animals.

60 tions to the substantia nigra pars compacta (SNc) is sufficient to suppress dopamine release in the d

61 amine in the substantia nigra pars compacta (SNc) leads to increased reflex blink excitability.

62 VTA) and the substantia nigra pars compacta (SNc) mDA neurons.

63 n regulating substantia nigra pars compacta (SNc) neuron physiology in both mice and rats.

64 from that in substantia nigra pars compacta (SNc) neurons, where subthreshold calcium current plays a

65 nger in monkey than in rat SN pars compacta (SNc) neurons, whereas a moderate level of mGluR5 immunor

66 dopaminergic substantia nigra pars compacta (SNc) neurons.

67 ty among the substantia nigra pars compacta (SNc) neurons.

68 urons in the substantia nigra pars compacta (SNc) of C57bl/6J mice following MPTP administration (20

69 ctors in the substantia nigra pars compacta (SNc) on one side of the brain; the other side remained a

70 mplicated in substantia nigra pars compacta (SNc) pathology in Parkinson's disease.

71 e neurons in substantia nigra pars compacta (SNc) play such roles.

72 The substantia nigra pars compacta (SNc) projects specifically into the rostral migratory st

73 cells in the substantia nigra pars compacta (SNc) respond immediately to unexpected conditioned stimu

74 lease in the substantia nigra pars compacta (SNc) shows a limited dependence on extracellular calcium

75 ncluding the substantia nigra pars compacta (SNc) subpopulation that preferentially degenerates in Pa

76 n the monkey substantia nigra pars compacta (SNc) that retains past learned reward values stably.

77 tor into the substantia nigra pars compacta (SNc) to investigate its influence on nigrostriatal dopam

78 ea (VTA) and substantia nigra pars compacta (SNc) to that of axonal dopamine release in the dorsal st

79 ay, from the substantia nigra pars compacta (SNc) to the dorsal striatum, and on related functions re

80 AAV into the substantia nigra pars compacta (SNc) transduced both dopaminergic and non-dopaminergic n

81 orogold into substantia nigra pars compacta (SNc) were combined with larger injections of True Blue i

82 urons of the substantia nigra pars compacta (SNc) were found to exhibit sustained responses related t

83 (SC), to the substantia nigra pars compacta (SNc) where direct synaptic contacts are made with both d

84 urons in the substantia nigra pars compacta (SNc), but not in ventral tegmental area or substantia ni

85 gra pars reticulata (SNr) and pars compacta (SNc), but not the thalamus.

86 ished in the substantia nigra pars compacta (SNc), but their validity in the VTA is uncertain.

87 urons of the substantia nigra pars compacta (SNc), in addition to many other regions, including neoco

88 ea (VTA) and substantia nigra pars compacta (SNc), no clear evidence for separate structures in anamn

89 DaNs) of the substantia nigra pars compacta (SNc), resulting in the characteristic hypokinesia in pat

90 anges in the substantia nigra pars compacta (SNc), the key pathological loci.

91 that, in the substantia nigra pars compacta (SNc), the pacemaking relies more on Ca(2+) channels and

92 e neurons in substantia nigra pars compacta (SNc), whereas matrix neurons receive sensorimotor inputs

93 urons in the substantia nigra pars compacta (SNc).

94 s within the substantia nigra pars compacta (SNc).

95 urons in the substantia nigra pars compacta (SNc).

96 urons of the substantia nigra pars compacta (SNc).

97 urons in the substantia nigra pars compacta (SNc).

98 urons in the substantia nigra pars compacta (SNc).

99 in the substantia nigra (SN) pars compacta (SNc).

100 urons in the substantia nigra pars compacta (SNc).

101 urons of the substantia nigra pars compacta (SNc).

102 rones of the substantia nigra pars compacta (SNc).

103 urons in the substantia nigra pars compacta (SNc).

104 loss in the substantia nigra pars compacta (SNc).

105 urons in the substantia nigra pars compacta (SNc).

106 ea (VTA) and substantia nigra pars compacta (SNc).

107 s within the substantia nigra pars compacta (SNc).

108 logue of the substantia nigra pars compacta (SNc)/ventral tegmental area (VTA) is present in lamprey,

109 nditioning (through the striosomes), control SNc responses.

110 tic LRRK2 carriers showed globally decreased SNc volume and CNR suggesting early nigral neurodegenera

111 h H&Y stage 1 PD had significantly decreased SNc volumes.

112 e a functional distribution among excitatory SNc afferent nuclei in response to cocaine, and suggest

113 tory pathway generates CS-induced excitatory SNc dopamine bursts.

114 drial insufficiency in all DaNs, exclusively SNc neurons showed an oxidized redox-system, i.e., a low

115 VTA is a major inhibitory control center for SNc dopamine cells.

116 odulate key signaling pathways important for SNc DA neuron survival and/or proper motor control.

117 t evidence that CPu axons and terminals from SNc dopaminergic neurons can be destroyed after neurotox

118 To begin filling this gap, SNc glutamatergic synapses arising from pedunculopotine

119 n optogenetic strategy to isolate identified SNc inputs and determine whether cocaine sensitivity in

120 In SNc dopaminergic neurones from rats aged postnatal day (

121 as significantly decreased (89%, P<0.005) in SNc, and there was a near-complete loss of GPX m-RNA in

122 ing acetylation, decreased MnSOD activity in SNc dopaminergic neurons, whereas mutagenesis of lysine

123 rger Ca(2+) entry through L-type channels in SNc DA neurons than in their VTA counterparts.

124 ts form functional NMDA receptor channels in SNc dopaminergic neurones, and suggest that they may for

125 ced Ca2+ mobilization and inward currents in SNc dopamine neurons, both of which were potentiated by

126 cts may reduce the risk of excitotoxicity in SNc DA neurons and may also counteract the increased eff

127 GS) proteins, whether primarily expressed in SNc DA neurons (RGS6), striatal neurons (RGSs 4 and 9),

128 n activity in the VTA but downregulate it in SNc.

129 This might lead to a higher Ca(2+) load in SNc DA neurons and explain their higher susceptibility t

130 efore show that the constant calcium load in SNc DaNs is counterbalanced by a high mitochondrial inne

131 rs reticulata (SNr) than on those located in SNc, revealing the existence of two synaptically distinc

132 50% of maximum (t(50)) was 12-fold longer in SNc than striatum.

133 A delayed t(max) in SNc compared with striatum persisted when DA uptake was

134 ed the membrane potential of mitochondria in SNc dopaminergic neurons.

135 nds in cerebellar granule cells to 2-3 ms in SNc dopaminergic (DA) neurons.

136 for the first time, regulation of NMDARs in SNc dopaminergic neurones by changes in intracellular Ca

137 e activity-dependent regulation of NMDARs in SNc dopaminergic neurones.

138 In sharp contrast, evoked [DA](o) in SNc was nearly half-maximal in 0 mm Ca(2+) and increased

139 he mitochondrial antioxidant defense only in SNc DaNs, and thus promote the increased vulnerability o

140 By contrast, pacemaking in SNc neurons does not rely on NALCN.

141 n all areas but the SNr, and particularly in SNc (71%, P<0.001).

142 s indicate that NR2B subunits are present in SNc dopaminergic neurones.

143 required to trigger prolonged DA release in SNc.

144 variations helped us clarify this result: in SNc DA neurons, the complexity of the ABD combined with

145 The loss of Cu,Zn-SOD m-RNA in SNc in MPTP-treated marmosets and patients with PD sugge

146 The loss of GPX m-RNA in SNc in PD also suggests a localisation to dopaminergic c

147 egulators of D(2)R-Galpha (i/o) signaling in SNc DA neurons and striatal medium spiny neurons, respec

148 background sodium current is much smaller in SNc neurons than VTA neurons.

149 oxidation of matrix proteins specifically in SNc dopaminergic neurons.

150 tion of PPN axons reliably evoked spiking in SNc dopaminergic neurons.

151 perinuclear mitochondrial oxidant stress in SNc dopaminergic neurons, providing a potential basis fo

152 a maximum (t(max)) in <200 msec, whereas in SNc, [DA](o) continued to rise for 2-3 sec.

153 eristic PD hallmarks in aged mice, including SNc DA neuron loss, motor deficits, and alpha-synuclein

154 ive sensorimotor inputs and do not innervate SNc.

155 the retrograde tracer Fluoro-Gold (FG) into SNc, the rats received pairings of a visual CS with food

156 onin was correlated with higher nigral iron (SNc: r(58) = - 0.501, p < 0.001).

157 ogical properties between medial and lateral SNc neurons modulated by cholinergic neurotransmission.

158 e neurons are confined to the caudal-lateral SNc and project to the caudate tail, which encodes long-

159 ocomotion, whereas activation in the lateral SNc increased locomotion.

160 ation of cholinergic terminals in the medial SNc decreased locomotion, whereas activation in the late

161 embrane potential was maintained in MitoPark SNc DaNs.

162 he proportion of mdDA neurons with molecular SNc DA cell characteristics in these cultures.

163 s revealed the expression of Nav 1.2 by most SNc neurons and a small proportion expressing Nav 1.6.

164 RGS6, expressed in human and mouse SNc DA neurons, suppresses characteristic PD hallmarks i

165 ine whether cocaine sensitivity in the mouse SNc circuit is conferred at the level of three glutamate

166 s, calbindin-positive and calbindin-negative SNc neurons differ substantially in their calcium channe

167 l tegmental area (VTA) and substantia nigra (SNc) are crucial for this process, via engagement of a r

168 l tegmental area (VTA) and substantia nigra (SNc) encode reward prediction errors (RPEs) and are prop

169 (FR) was injected into the substantia nigra (SNc) to label dopaminergic axons and terminals in the ca

170 tions were assessed in the substantia nigra (SNc), dentate and caudate nucleus, red nucleus, putamen

171 rgic neurons (DaNs) in the substantia nigra (SNc), whereas DaNs in the neighboring ventral tegmental

172 rticular, the dopaminergic substantia nigra (SNc)-related nigrostriatal pathway is structurally and f

173 creased iron levels in the substantia nigra (SNc).

174 ctrical stimulation to the substantia nigra (SNc)/ventral tegmental area (VTA) after the random onset

175 al association cortices to SNL DANs, but not SNc DANs.

176 rrent study we found that while 88 +/- 2% of SNc neurons labelled by the neuronal marker NeuN were co

177 We find that loss of 90% of SNc dopaminergic neurons and consequent depletion of >95

178 ptor antagonism or optogenetic activation of SNc DAergic neurons reverse SSRI-induced motor deficits.

179 interact to produce the emergent activity of SNc DAs.

180 ir function, leading to accelerated aging of SNc DA neurons, particularly in the face of genetic or e

181 the burst-firing activity characteristic of SNc mDA neurons was drastically reduced in the absence o

182 urring spontaneous firing characteristics of SNc DAs.

183 Examination of SNc dopaminergic neurons ex vivo in brain slices verifie

184 c M5 increases the intrinsic excitability of SNc neurons.

185 We also found that the relative extension of SNc neuron dendrites into the SNr dictated overall GABAe

186 Aged SNCA-OVX mice exhibit reduced firing of SNc dopamine neurons in vivo measured by juxtacellular r

187 ease, the precise movement-related firing of SNc dopaminergic neurons and the resultant striatal dopa

188 These selective events augment inhibition of SNc DA neurons by SNr GABAergic neurons and also temper

189 Optogenetic inhibition of SNc DAergic neurons mimics the motor deficits due to chr

190 uggest that the excitation and inhibition of SNc dopamine neurons elicit positive and negative affect

191 s are not received, striosomal inhibition of SNc that is unopposed by excitation results in a phasic

192 The loss of SNc dopaminergic neurons affects the plasticity of stria

193 g mitochondrial oxidative stress and loss of SNc dopaminergic neurons in PD.

194 d uncoupling it results in a greater loss of SNc dopaminergic neurons.

195 3 in mice led to a clear age-related loss of SNc dopaminergic neurons.

196 Largely distinct populations of SNc and VTA dopaminergic neurons innervate Area X and su

197 drial redox status and membrane potential of SNc dopaminergic neurons from Sirt3 knockouts.

198 ining the electrophysiological properties of SNc DA neurons and their cell-to-cell variations.SIGNIFI

199 of molecular and physiological properties of SNc mDA neurons and impact on feeding behavior in adult

200 lso increased the spontaneous firing rate of SNc neurons, suggesting that activation of somatodendrit

201 her striatal neurochemistry or the rescue of SNc TH-positive neurons.

202 pecific predictive learning, and the role of SNc-DA neurons appears limited to reinforcement of instr

203 her number of L-type channels in the soma of SNc DA neurons, as well as a smaller single-channel cond

204 Thus, PPN-evoked burst spiking of SNc dopaminergic neurons in vivo may not only be extrins

205 ctivation of somatodendritic M5 receptors on SNc neurons leads to increased neuronal firing, activati

206 However, afferents onto SNc dopamine neurons themselves appear insensitive to dr

207 to deliver photostimulation into the VTA or SNc and also sought for the compartment where they recei

208 in (NpHR), or control vector into the VTA or SNc, resulting in selective expression of these opsins i

209 ater than in cell body regions of the VTA or SNc.

210 e findings reveal that activation of VTA- or SNc-DA neurons engages largely dissociable learning proc

211 of retrogradely labeled Fluorogold-positive SNc neurons.

212 l DA content, but did not rescue TH-positive SNc neurons.

213 input to the MLR originating from the primal SNc that evokes graded locomotor movements.SIGNIFICANCE

214 pamine were found to project from the primal SNc to the MLR.

215 tors of cell signaling pathways that promote SNc DA neuron survival and/or proper motor control.

216 icompartment modeling on male and female rat SNc DA neurons to determine cell-to-cell variations in A

217 functional NMDA receptors in identified rat SNc dopaminergic neurones, we have analysed the properti

218 nsity are indeed higher in the somata of rat SNc DA neurons and that this current undergoes less inac

219 Interestingly, the axon of rat SNc dopaminergic (DA) neurons displays a highly variable

220 rded and labeled dopaminergic neurons of rat SNc revealed that they received approximately 8,000 syna

221 hannels during autonomous pacemaking renders SNc DA neurons susceptible to mitochondrial toxins used

222 administration in vivo after MPTP can rescue SNc neurons.

223 ally restored striatal DA levels and rescued SNc neurons.

224 arya in the ventromedial part of the rostral SNc.

225 ng reduction of striatal dopamine terminals, SNc loss of dopamine neurons, and motor-behavior defects

226 dylmethyl]-ethylenediamine), indicating that SNc dopaminergic neurones do not contain functional NR2A

227 These results show that SNc-CeA communication is critical to mechanisms by which

228 The SNc T1w/T2w ratio had high sensitivity (0.908) and speci

229 rtex, basal forebrain, and brainstem and the SNc is widely perceived as receiving inputs mainly from

230 se immunohistochemistry, to characterize the SNc/VTA efferent and afferent connectivity, and to relat

231 locomotor frequency, but did not disrupt the SNc-evoked graded control of locomotion.

232 For the SNc, we created a weighted mean of the multiple echoes,

233 sine hydroxylase (TH)-labeled neurons in the SNc after 6-OHDA-lesions, but did block the amphetamine-

234 ant reduction of dopaminergic neurons in the SNc and dopamine (DA) and tyrosine hydroxylase (TH) leve

235 w ratio can detect PD-related changes in the SNc and may be used as a novel, parsimonious in vivo bio

236 Furthermore, VP terminals in the SNc and VTA overlap with cells that project back to Area

237 l that short-latency visual responses in the SNc are abolished by ipsilateral lesions of the SC and i

238 examine whether cholinergic signaling in the SNc controls mouse behavior, we used optogenetics in awa

239 t with activation of dopamine neurons in the SNc coupled to previously reported amplification of axon

240 n and alpha-Syn-induced neurotoxicity in the SNc in two distinct mouse models of synucleinopathy.

241 amine (6-OHDA) lesions were conducted in the SNc ipsilateral to, and 6 months after, transduction wit

242 of MnSOD was significantly increased in the SNc of PD patients.

243 proach confirmed the group difference in the SNc T1w/T2w ratio between PD and controls (p < 0.0001).

244 c acid (CPA) decreased evoked [DA](o) in the SNc, indicating a functional role for ER Ca(2+) stores i

245 eral connection, particularly evident in the SNc, involving both DA and non-DA neurons.

246 facilitate somatodendritic DA release in the SNc.

247 paminergic cell degeneration occurred in the SNc.

248 immunoreactivity compared to controls in the SNc.

249 In sagittal brain slices that isolate the SNc soma from their striatal terminals, activation of mu

250 Moreover, the SNc/VTA receives sensory information from the olfactory

251 markers for tracking the degeneration of the SNc and BF.

252 Rats received unilateral lesions of the SNc and lesions of the CeA in either the contralateral o

253 tes were found in the DAergic neurons of the SNc and neurites in the STR.

254 tly to increased GABAergic inhibition of the SNc DA neurons.

255 e outward current in dopamine neurons of the SNc from wild-type mice, but this current was completely

256 Reductions in iron content of the SNc occurred in only 3 patients, with no changes being d

257 how cholinergic inputs to subregions of the SNc regulate the excitability of DA neurons differential

258 The sensitivity and specificity of the SNc T1w/T2w ratio in discriminating between PD and contr

259 ammalian paranigral VTA, ventral tier of the SNc, interfascicular nucleus of the VTA, and supramamill

260 arger in the soma of dopamine neurons of the SNc, leading to a higher charge transfer through L-type

261 unting of TH-immunoreactive perikarya of the SNc, paranigral (PN) and interfascicular (IF) nucleus wa

262 OHDA) lesions of the dopamine neurons of the SNc, we found that microinjections of bicuculline, a GAB

263 re more highly expressed in the VTA than the SNc.

264 eports from other groups indicating that the SNc receives robust input from many of the same structur

265 tion of the arcopallium also projects to the SNc and VTA and could carry auditory information.

266 ould provide song-related information to the SNc and VTA.

267 receiving input from Area X projects to the SNc and VTA.

268 ontrol nuclei do not project directly to the SNc or VTA.

269 learning pathways from limbic cortex to the SNc, one devoted to excitatory conditioning (through the

270 l to the red nucleus and corresponded to the SNc.

271 ic mechanisms of identified afferents to the SNc.

272 activity in the SMN (hypothetically via the SNc-related nigrostriatal pathway) and SN (hypotheticall

273 and the basal ganglia connectivity with the SNc/VTA are present as part of the evaluation system, as

274 Within the SNc, RGS10 may promote DA neuron survival through the up

275 din-negative dopaminergic neurons within the SNc.

276 Therefore, SNc neurons differ substantially in their calcium channe

277 sal tier and calbindin-negative ventral tier SNc dopaminergic neurons in mice comprise functionally d

278 We found that excitatory afferents to SNc dopamine neurons are sensitive to cocaine in an affe

279 aine differentially induces modifications to SNc synapses depending on input origin.

280 on the activity of M2 neurons projecting to SNc.

281 Projections to SNc were found to originate from patch/exo-patch and mat

282 s exhibit longer aversive pauses relative to SNc neurons.

283 o exhibit longer aversive pauses relative to SNc neurons.SIGNIFICANCE STATEMENT Our study examines re

284 microscopy, we reveal the presence of a tVTA-SNc-dorsal striatum pathway.

285 Unfortunately, the mechanisms underlying SNc neurodegeneration remain unclear, and currently ther

286 A neurons whose somas are located in ventral SNc.

287 they received photostimulation into the VTA, SNc, or dorsal striatum, whereas control mice did not.

288 the functional interrelatedness of the VTA, SNc, RRF, and PAGvl.

289 njections of retrograde tracer into the VTA, SNc, RRF, or PAGvl produced labeling in many structures

290 In contrast to VTA, SNc DaNs engage calcium channels to generate action pote

291 31 +/- 11% of average control level) and VTA/SNc (79 +/- 5% of average control level).

292 ergic pathway onto the catecholaminergic VTA/SNc homologs and serotonergic raphe nuclei.

293 egmental area/substantia nigra compacta (VTA/SNc).

294 Despite this, cues predicting SC->VTA/SNc neuron activation did not reliably evoke behavior in

295 itioning paradigm, and activation of SC->VTA/SNc neurons did not support primary reinforcement or pro

296 ctions excite DA and GABA neurons in the VTA/SNc in vivo.

297 alpha7* component of the current in the VTA/SNc is not significantly desensitized by nicotine in the

298 These progressive changes in vulnerable SNc neurons were observed independently of overt protein

299 idant stress that was specific to vulnerable SNc dopaminergic neurons.

300 DLS, even during Pavlovian conditioning with SNc dopamine neuron activation, which elicited robust DL