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

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

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

6 luR1a and mGluR5 immunoreactivity in SNr and SNc neurons.

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

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

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

10 Both VTA and SNc dopaminergic neurons innervate homogenously the lowe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 dopaminergic substantia nigra pars compacta (SNc) neurons.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 In SNc dopaminergic neurones from rats aged postnatal day (

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

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

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

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

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

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

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

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

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

108 50% of maximum (t(50)) was 12-fold longer in SNc than striatum.

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

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

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

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

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

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

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

116 required to trigger prolonged DA release in SNc.

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

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

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

120 oxidation of matrix proteins specifically in SNc dopaminergic neurons.

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

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

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

124 ive sensorimotor inputs and do not innervate SNc.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 c M5 increases the intrinsic excitability of SNc neurons.

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

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

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

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

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

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

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

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

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

153 3 in mice led to a clear age-related loss of SNc dopaminergic neurons.

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

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

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

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

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

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

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

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

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

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

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

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

166 of retrogradely labeled Fluorogold-positive SNc neurons.

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

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

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

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

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

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

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

174 administration in vivo after MPTP can rescue SNc neurons.

175 ally restored striatal DA levels and rescued SNc neurons.

176 arya in the ventromedial part of the rostral SNc.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 facilitate somatodendritic DA release in the SNc.

192 paminergic cell degeneration occurred in the SNc.

193 immunoreactivity compared to controls in the SNc.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 ic mechanisms of identified afferents to the SNc.

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

215 din-negative dopaminergic neurons within the SNc.

216 Therefore, SNc neurons differ substantially in their calcium channe

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

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

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

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

221 s exhibit longer aversive pauses relative to SNc neurons.

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

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

224 A neurons whose somas are located in ventral SNc.

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

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

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

228 31 +/- 11% of average control level) and VTA/SNc (79 +/- 5% of average control level).

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

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

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

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