ライフサイエンスコーパス: GPe

1 GPe arkypallidal (arky) neurons project exclusively to t

2 GPe delta power correlated with OCD symptom severity, es

3 GPe lesions resulted in increased discharge in STN and G

4 GPe-recipient RRF(GABA) neurons, on the other hand, disp

5 Accordingly, we identify 14 SNr and 36 GPe domains and a direct cortico-SNr projection.

6 g between the parkinsonian beta rhythm and a GPe-intrinsic y rhythm.

7 c inhibition of the STN exacerbated abnormal GPe activity, and (6) exaggerated beta band activity was

8 What was distinctive about GPe Na+ channels was a prominent resurgent gating mode.

9 recorded pairs of neurons within and across GPe and SNr shifted from the pathological low-frequency

10 , synchronous inhibition of tonically active GPe-STN neurons or phasic activity of GPe-STN neurons re

11 6, comprised approximately two-thirds of all GPe neurons, and were the major GPe cell type innervatin

12 Both GPi and GPe firing frequencies differed significantly with dysto

13 for dystonia and investigate whether GPi and GPe firing rates differ between dystonia types.

14 rnal segment of the globus pallidus (GPi and GPe, respectively) in two rhesus monkeys rendered parkin

15 Finally, the MSN and GPe response groups reorganized at the outcome epoch, as

16 MSNs and GPe neurons displayed sustained average activity to cue

17 responses in decision-making scenarios, and GPe output may modulate synchrony and low-frequency osci

18 We propose that the STN and GPe constitute a central pacemaker modulated by striatal

19 w-frequency rhythmic bursting in the STN and GPe is characteristic of PD.

20 Autonomous oscillation of STN and GPe neurons underlies tonic activity and is important fo

21 tum-STN-GPe cultures, neurons in the STN and GPe spontaneously produce synchronized oscillating burst

22 o stimulation of SNr-projecting striatal and GPe neurons, including biphasic and excitatory effects,

23 Genetic ablation of this arky(GPe->DLS) circuit facilitated a shift from goal-directed

24 In contrast, arkypallidal GPe neurons originate from lateral/caudal ganglionic emi

25 FoxP2+ arkypallidal GPe neurons and subthalamic nucleus neurons were lost by

26 here was a progressive decline in autonomous GPe pacemaking, which normally serves to desynchronize a

27 However, the causal relationship between GPe neuron classes and movement remains to be establishe

28 e investigations of the relationship between GPe spiking activity and local field potential fluctuati

29 1.0-2.5, 4.5-5.5, and 7.0-9.0 msec for both GPe and GPi neurons.

30 However, unlike MSNs, neurons in both GPe response groups displayed prolonged and temporally o

31 onvey US-related information through the CeA-GPe circuit, thereby regulating learning in fear conditi

32 allidus external segment (GPe), and this CeA-GPe circuit conveys unconditioned stimulus (US)-related

33 ces the idea that the reciprocally connected GPe-STN network plays a key role in disease symptomatolo

34 lly pattern STN activity ex vivo, correlated GPe-STN activity is not normally observed in vivo.

35 Decreasing GPe and VP volumes were associated with poorer cognition

36 ools, and molecular markers to better define GPe neuron subtypes.

37 undamental biology and function of different GPe neuron classes.

38 y recorded pairs of high-frequency discharge GPe cells recorded from four monkeys during task-irrelev

39 at Npas1(+)-Nkx2.1(+) neurons are a distinct GPe neuron subclass.

40 ceive monosynaptic excitatory and disynaptic GPe-mediated inhibitory inputs from the STN.

41 imilarly, optogenetic stimulation of the DMS-GPe iMSNs reduced ethanol-containing reward-seeking, whe

42 g, whereas optogenetic inhibition of the DMS-GPe iMSNs reversed this change.

43 roaches in mice to dissect the roles of dSPN GPe collaterals in motor function.

44 etworks of sparsely coupled Type I excitable GPe neurons.SIGNIFICANCE STATEMENT Our work provides (1)

45 ver that of Lim homeobox 6 (Lhx6)-expressing GPe neurons, restores movement in dopamine-depleted mice

46 ation, (2) prototypic parvalbumin-expressing GPe neurons are excessively patterned by D2-SPNs even th

47 the activity of parvalbumin (PV)-expressing GPe neurons over that of Lim homeobox 6 (Lhx6)-expressin

48 riatum, globus pallidus interna and externa (GPe), subthalamic nucleus (STN), and substantia nigra pa

49 nit activity in the globus pallidus externa (GPe) and substantia nigra reticulata (SNr) revealed that

50 s interna (GPi) and globus pallidus externa (GPe) in children undergoing deep brain stimulation (DBS)

51 ory inputs from the globus pallidus externa (GPe) that is reciprocally connected with the STN.

52 onnections from the globus pallidus externa (GPe) to striatum are substantially stronger onto fast-sp

53 gle neurons in STN, globus pallidus externa (GPe), and substantia nigra pars reticular (SNr), and dis

54 l ganglia, the globus pallidus pars externa (GPe) has been hypothesized to mediate selective proactiv

55 a dichotomous globus pallidus pars externa (GPe) organization, and (2) an exact mean-field model tha

56 cturally homologous to the primate external (GPe) and internal (GPi) pallidal segments.

57 ained terminals in globus pallidus externus (GPe) were more abundant at 6 months and remained so out

58 ed inputs from the globus pallidus externus (GPe), a basal ganglia nucleus not previously known to pa

59 Sox6 represents a novel, defining marker for GPe neuron subtypes.

60 We found GPe PV(+) neuron-specific gene expression changes that s

61 y decreased the firing rate of low-frequency GPe neurons, but did not alter the firing of high-freque

62 We performed patch-clamp recordings from GPe neurons and found that bath application of ethanol d

63 in vivo electrophysiological recordings from GPe showed that ethanol decreased the firing of a large

64 a network containing two types of GABAergic GPe projection neuron, so-called 'prototypic' and 'arkyp

65 A first population of prototypic GABAergic GPe neurons fire antiphase to subthalamic nucleus (STN)

66 the potential contributions of two GABAergic GPe cell types to voluntary action are fated from early

67 rsal learning task, we found that changes in GPe discharge rates predicted subsequent behavioral shif

68 Conversely, rapid declines in GPe theta during low conflict conditions were related to

69 average neuronal discharge rate decreased in GPe but increased in STN and GPi.

70 The disfacilitation in GPe is then amplified in basal ganglia circuitry and gen

71 te tonic inhibition and a disfacilitation in GPe.

72 nregulated, contributing to the elevation in GPe(PV) cell excitability.

73 ctivity, which accounted for the increase in GPe labelling.

74 with autoimmunoradiography) was increased in GPe and GPi, likely reflecting increased striatal input

75 excitation followed by a weak inhibition in GPe neurons and a short-latency, very short-duration exc

76 Thus, modulations in GPe spiking activity are highest for attention-demanding

77 in the temporal firing pattern of neurons in GPe and GPi underlie the beneficial effect of HFS in the

78 This mode was significantly reduced in GPe neurons lacking functional Nav1.6 channels.

79 HFS) evoked powerful excitatory responses in GPe neurons.

80 terminants of pacemaking and fast spiking in GPe neurons are not fully understood, but voltage-depend

81 ight on the mechanisms underlying spiking in GPe neurons but also suggest that electrical stimulation

82 ored pacemaking and reduced burst spiking in GPe neurons.

83 We demonstrated that cocaine increased GPe neuron activity, which accounted for the increase in

84 s function makes it unlikely that individual GPe neurons, or even a single GPe cell type, could compu

85 Under proactive inhibition, GPe population activity occupied state-space locations f

86 organization applies to the dopamine-intact GPe.

87 tal to the operations of the dopamine-intact GPe.

88 but inhibited GABAergic transmission at iSPN-GPe projections.

89 inhibition of GABAergic transmission at iSPN-GPe synapses.

90 GABA(B) receptors modulate iSPN-GPe projections via a VGCC-dependent mechanism.

91 CB1 receptors modulate iSPN-GPe projections via a VGCC-independent mechanism.

92 Lhx6-GPe neurons, which do not express PV, are concentrated i

93 and anatomical differences suggest that Lhx6-GPe and PV-GPe neurons participate in different circuits

94 hirds of all GPe neurons, and were the major GPe cell type innervating the subthalamic nucleus (STN).

95 The median GPe firing frequency was higher in the NBIA group than i

96 number of functional GABAA receptor-mediated GPe-STN inputs.

97 three brain regions of male and female mice: GPe, striatum, and cortex.

98 lices at rates and in patterns that mimicked GPe activity in vivo.

99 HF-1 neurons, like most GPe neurons we examined, exhibited large firing rate mod

100 recorded the spiking activity of VP neurons, GPe cells (actor) and striatal cholinergic interneurons

101 tic depression caused tonic, nonsynchronized GPe-STN activity to disrupt rather than abolish autonomo

102 wing the loss of dopamine, the activities of GPe and STN neurons become more temporally offset and st

103 Phasic changes in the activity of GPe neurons during movement and their alterations in Par

104 active GPe-STN neurons or phasic activity of GPe-STN neurons reliably patterned STN activity through

105 gesting that GABA released from the axons of GPe neurons effectively activates GABA(B) receptors in t

106 urons are two distinct functional classes of GPe neurons.

107 is little consensus on the classification of GPe neurons.

108 on classes and illustrates the complexity of GPe neurons in adult mice.

109 GPe neurons reaffirm the diversification of GPe subtypes, statistical analyses strongly support the

110 hese findings warrant further exploration of GPe as a target for interventions for Parkinson's diseas

111 lication increased the spontaneous firing of GPe and GPi neurons, suggesting that GABA released from

112 r FoxP2, constituted just over one-fourth of GPe neurons, and innervated the striatum but not STN.

113 Our results suggest that a major function of GPe-projecting CeA neurons is to represent and convey US

114 Inhibition of GPe activity revealed that it contributes to two forms o

115 acemaker modulated by striatal inhibition of GPe neurons.

116 ctivation of the astrocytes or inhibition of GPe pan-neuronal activities facilitates the transition f

117 Furthermore, inhibition of GPe, contrary to STN, abolishes oscillations.

118 Notably, chronic inhibition of GPe-projecting CeA neurons with the tetanus toxin light

119 three animals with ibotenic acid lesions of GPe.

120 gical, molecular, and anatomical measures of GPe-STN transmission were compared in the STN of control

121 Modeling of GPe cells as class 2 excitability neurons with common ex

122 These models suggest that a network of GPe and subthalamic nucleus (STN) neurons computes the n

123 physiological studies of single and pairs of GPe neurons have failed to fully disclose the physiologi

124 data argue that the frequency and pattern of GPe activity profoundly influence its transmission to th

125 d its models, abnormal rates and patterns of GPe-STN network activity are linked to motor dysfunction

126 , we showed that optogenetic perturbation of GPe neuron subtypes generated unique behavioral structur

127 ct temporal activities of two populations of GPe neuron in vivo are underpinned by distinct molecular

128 Thus, two populations of GPe neuron together orchestrate activities across all ba

129 tions (f-I curves) of the two populations of GPe neurons.

130 ution and electrophysiological properties of GPe neurons reaffirm the diversification of GPe subtypes

131 nections were stimulated at the mean rate of GPe activity in vivo (33 Hz).

132 he results indicate that a mere reduction of GPe activity does not produce parkinsonism.

133 However, the role of GPe arky neurons in reward-seeking remains unknown.

134 ich harbors enriched astrocytes, the role of GPe astrocytes involved in action-selection strategies r

135 study further establishes the segregation of GPe neuron classes and illustrates the complexity of GPe

136 we confirm using optogenetic stimulation of GPe terminals within the SNr.

137 ical excitation by adjusting the strength of GPe inhibition.

138 stigation of electrophysiological studies of GPe neuron subtypes to date.

139 We also study the synchronization of GPe cells to synaptic input from the STN cell with depen

140 nel have a key role in the ethanol effect on GPe neurons, as the application of BK channel inhibitors

141 Our work predicts that ongoing GPe activity could tune the SNr operating mode, includin

142 convergence of the MSN response groups onto GPe cells.

143 nd activity was not present in the cortex or GPe-STN network.

144 driver lines that effectively capture other GPe neuron subclasses.

145 ring rate (0.78 +/- 0.136 spikes/s) in other GPe cells.

146 d the central role of the external pallidum (GPe) in abnormal beta oscillations, while showing that t

147 ernal and internal segments of the pallidum (GPe and GPi) receive heavy GABAergic innervations from t

148 nd internal segments of the globus pallidus (GPe and GPi, respectively).

149 onnected GABAergic external globus pallidus (GPe) and glutamatergic subthalamic nucleus (STN) are clo

150 onnected GABAergic external globus pallidus (GPe) and glutamatergic subthalamic nucleus (STN) neurons

151 onnected GABAergic external globus pallidus (GPe) and glutamatergic subthalamic nucleus (STN) neurons

152 onnected GABAergic external globus pallidus (GPe) and glutamatergic subthalamic nucleus (STN).

153 nucleus (STN) and external globus pallidus (GPe) are associated with the operation of the basal gang

154 the external segment of the globus pallidus (GPe) are autonomous pacemakers that are capable of susta

155 +)) neurons in the external globus pallidus (GPe) are critically involved in the motor deficits of do

156 indicate that the external globus pallidus (GPe) contains two main types of GABAergic projection cel

157 TN and inhibitory, external globus pallidus (GPe) form a feedback system that engages in synchronized

158 gic neurons in the external globus pallidus (GPe) form a local synaptic network.

159 Neurons in the external globus pallidus (GPe) generate pacemaker activity that controls basal gan

160 ulation of the DMS-external globus pallidus (GPe) iMSNs circuit alters the ethanol-containing reward

161 striatum, and the external globus pallidus (GPe) in regulating RLS-like movements, in particular pal

162 d indirect pathway external globus pallidus (GPe) inhibition of the STN are critical for normal movem

163 The external globus pallidus (GPe) is a critical node within the basal ganglia circuit

164 The external globus pallidus (GPe) is a key contributor to motor suppressing pathways

165 The external globus pallidus (GPe) is a key nucleus within basal ganglia circuits that

166 Although external globus pallidus (GPe) is critical for action selection, which harbors enr

167 nglia circuit, the external globus pallidus (GPe) is critically involved in motor control.

168 The external segment of the globus pallidus (GPe) is one of the core nuclei of the basal ganglia, pla

169 We show how external globus pallidus (GPe) neuron is sensitive to the phase of the input from

170 on of labor in the external globus pallidus (GPe) of Parkinsonian rats, showing that the distinct tem

171 composition in the external globus pallidus (GPe) undermines our ability to interrogate its precise b

172 neurons within the external globus pallidus (GPe) was not fully appreciated.

173 the external segment of the globus pallidus (GPe), a downstream structure whose computational role ha

174 al activity of the external globus pallidus (GPe), a nucleus in the basal ganglia, contributes to the

175 the external segment of the globus pallidus (GPe), neuronal populations have been defined using molec

176 ent external segment of the globus pallidus (GPe), remain unexplored.

177 using on the mouse external globus pallidus (GPe), we demonstrate that the potential contributions of

178 and the external segment of globus pallidus (GPe).

179 the external segment of the globus pallidus (GPe).

180 n the striatum and external globus pallidus (GPe).

181 the external segment of the globus pallidus (GPe).

182 the external segment of the globus pallidus (GPe).

183 the external segment of the globus pallidus (GPe)], and one neuromodulator group [striatal tonically

184 riatum (direct pathway) and globus pallidus (GPe, indirect pathway).

185 s through the globus pallidus external part (GPe), substantia nigra reticular part (SNr), thalamic nu

186 lost by 18 months but not prototypical PARV+ GPe neurons or dopaminergic nigral neurons.

187 se in the number of synaptic connections per GPe-STN axon terminal, to substantial strengthening of t

188 er of ultrastructurally defined synapses per GPe-STN axon terminal doubled with no alteration in term

189 Here, we show that GPe parvalbumin-positive (GPe(PV)) cells mediate cocaine responses by selectively

190 Here, we investigated whether the primate GPe exhibits similar functional diversity by recording s

191 lidus (GP in rodents, homolog of the primate GPe), pairs of neurons generally have uncorrelated firin

192 that exhibit activity similar to the primate GPe.

193 s knowledge gap by discovering two principal GPe neuron classes, which were identified by their nonov

194 Prototypic GPe neurons derive from the medial ganglionic eminence o

195 es, a network of arkypallidal and prototypic GPe neurons comprises a neural substrate capable of supp

196 (D2-SPNs), parvalbumin-expressing prototypic GPe (PV GPe) neurons, and STN neurons.

197 mice abnormal, temporally offset prototypic GPe and STN neuron firing results in part from increased

198 oincident D2-SPN activity, (3) autonomous PV GPe neuron firing ex vivo was upregulated, presumably th

199 ), parvalbumin-expressing prototypic GPe (PV GPe) neurons, and STN neurons.

200 l ACT, (2) abnormal phasic suppression of PV GPe neuron activity was ameliorated by optogenetic inhib

201 normally correlated and temporally offset PV GPe and STN neuron activity is generated in part by elev

202 n-expressing external globus pallidus (PV(+) GPe) neurons discharged at 2-3 times their normal rate,

203 cal differences suggest that Lhx6-GPe and PV-GPe neurons participate in different circuits with the p

204 In contrast, PV-GPe neurons are more concentrated in the lateral portion

205 stantia nigra pars compacta compared with PV-GPe neurons.

206 re we investigate population dynamics of rat GPe neurons during preparation-to-stop, stopping, and go

207 conductance changes generated from recorded GPe neuron firing patterns also became coherent with osc

208 alvia rosmarinus (rosemary) extract, reduced GPe(PV) cell excitability and impaired cocaine reward, s

209 ted CeA-to-globus pallidus external segment (GPe) circuit plays an essential role in classical fear c

210 ons to the globus pallidus external segment (GPe), and this CeA-GPe circuit conveys unconditioned sti

211 3 components of the GP-the external segment (GPe), internal segment (GPi), and ventral pallidum (VP)-

212 ing to the globus pallidus external segment (GPe).

213 d activity in the external pallidal segment (GPe) results in the abnormalities of neuronal discharge

214 imates these data were then used to simulate GPe-STN transmission.

215 Injection of simulated GPe-STN conductances revealed that synaptic depression c

216 hat individual GPe neurons, or even a single GPe cell type, could compute it.

217 itionally assumes that the feedback from STN-GPe circuit to cortex is important for maintaining the o

218 In mature organotypic cortex-striatum-STN-GPe cultures, neurons in the STN and GPe spontaneously p

219 by blocking different connections of the STN-GPe circuit.

220 tion are generated in the cortex and the STN-GPe circuits resonates at this frequency.

221 gle stimulation and during STN-BHFS, the STN-GPe excitatory response dominates over the STN-GPe-GPe r

222 e excitatory response dominates over the STN-GPe-GPe recurrent inhibition in the GPe, whereas the STN

223 rrent inhibition in the GPe, whereas the STN-GPe-GPi inhibitory response dominates over the STN-GPi e

224 DA-depletion, the spontaneous firing of Str-GPe neurons increases, and MC stimulation evokes a short

225 Corroborating our prior studies, GPe neurons can be divided into two statistically distin

226 0.6 s) of complete silence, which are termed GPe pauses.

227 We conclude that GPe exhibits several core components of a dichotomous or

228 Our results demonstrate that GPe, commonly studied in motor contexts, takes part in c

229 arning-related neural activity and show that GPe discharge rates closely matched across-trial learnin

230 Here, we show that GPe parvalbumin-positive (GPe(PV)) cells mediate cocaine

231 These results suggest that GPe may play a central role in propagating abnormal circ

232 The GPe is comprised of a heterogeneous population of neuron

233 The GPe neurons provide another major GABAergic innervation

234 ed, indicative of reduced activity along the GPe-STN pathway.

235 precisely how movement is controlled at the GPe level as a result of its cellular complexity.

236 hypotheses of how dopamine depletion at the GPe may lead to phase-amplitude coupling between the par

237 of cross-frequency coupling observed at the GPe.

238 Because the GPe powerfully regulates the frequency, pattern, and syn

239 nent of a positive feedback loop between the GPe and striatum that promotes synchronization and rhyth

240 In order to perform such computation, the GPe needs to send feedback to the STN equal to a particu

241 We suggest that common inputs decrease the GPe discharge rate and lead to a bifurcation phenomenon

242 the VP is physiologically different from the GPe and identify the transient VP neurons as a BG critic

243 ticular pallidocortical projections from the GPe to the motor cortex.

244 Furthermore, the GPe displays broad interconnectivity beyond the basal ga

245 revised framework for understanding how the GPe relates to behavior in both health and disease.

246 -sensitive responses differed greatly in the GPe ( approximately 400 ms long) and in the GPi (60 ms l

247 x1(+) lineage were similarly abundant in the GPe and displayed a heterogeneous makeup.

248 fectively activates GABA(B) receptors in the GPe and GPi and contributes significantly to the control

249 BA(B) antagonist)-sensitive responses in the GPe and GPi.

250 +/- 3% of labeled elements), whereas, in the GPe and SNr, the labeling was mainly presynaptic (71% +/

251 In vivo, most neurons in the GPe are characterized by high firing rates (50-100 spike

252 neurons and Npas1-expressing neurons in the GPe represent two nonoverlapping cell classes, amounting

253 genetically distinct cell populations in the GPe that differ molecularly, anatomically, and electroph

254 tility of cell-specific interventions in the GPe to target functionally distinct pathways, with the p

255 egions, are organized topographically in the GPe, and segregate into at least two distinct electrophy

256 activity of two neuronal populations in the GPe, elevating the activity of parvalbumin (PV)-expressi

257 In the GPe, the average sustained response was composed of two

258 the STN-GPe-GPe recurrent inhibition in the GPe, whereas the STN-GPe-GPi inhibitory response dominat

259 synchronized rhythmic burst activity in the GPe-STN loop, which may be relevant to the resting tremo

260 has sparked a resurgence in interest in the GPe.

261 are the two principal neuron classes in the GPe.

262 ion of an NBQX/CPP/gabazine mixture into the GPe.

263 and computational studies on the role of the GPe for basal ganglia dynamics in health and disease.

264 ifurcation phenomenon (pause) in some of the GPe neurons.

265 means, we investigate the projections of the GPe to the retrorubral field (RRF), a dopaminergic nucle

266 This work revises our understanding of the GPe, and provides the foundation for future studies of i

267 erminal, to substantial strengthening of the GPe-STN pathway.

268 concentrated in the lateral portions of the GPe.

269 re concentrated in the medial portion of the GPe.

270 eiled the cell and circuit complexity of the GPe.

271 he motor-suppressing "indirect-pathway," the GPe consists of a number of distinct cell types and anat

272 Relative to controls, in the HD patients the GPe showed a 54% overall volume decline, 60% neuron loss

273 In idiopathic and experimental PD, the GPe and STN exhibit hypoactivity and hyperactivity, resp

274 projections from the STN and potentially the GPe.

275 nt studies have challenged the idea that the GPe comprises a single, homogenous population of neurons

276 er, experimental studies have shown that the GPe contains at least two distinct cell types (prototypi

277 s in Parkinson's disease (PD) argue that the GPe is important in motor control.

278 To test the hypothesis that the GPe's influence is constrained by short-term synaptic de

279 e another major GABAergic innervation to the GPe itself and GPi.

280 ubset of CeA neurons send projections to the GPe, and the majority of these GPe-projecting CeA neuron

281 rmore, we show that oscillatory input to the GPe, arriving from striatum, leads to characteristic pat

282 In contrast to the GPe, STN-BHFS evoked a predominantly inhibitory response

283 he diversity of the neurons that make up the GPe.

284 the origin of the GABA(B) responses was the GPe, not the Put.

285 However, whether the GPe encodes non-motor information remains unclear.

286 rons in the cortex collateralized within the GPe, forming a closed-loop system between the two brain

287 e control via strategic adjustments to their GPe network state.

288 ctions to the GPe, and the majority of these GPe-projecting CeA neurons express the neuropeptide soma

289 In simulated dopamine-depletion, this GPe-FSI activity is necessary for the emergence of stron

290 allidal types are functionally homologous to GPe and GPi neurons, we recorded from neurons in area X

291 Applying this technology to GPe parvalbumin-expressing neurons in a mouse model of P

292 18.9 s) was also longer than pauses in tonic GPe activity in vivo.

293 asses, amounting to 55% and 27% of the total GPe neuron population, respectively.

294 al activation of STN NMDA receptors triggers GPe-STN inputs to strengthen abnormally, contributing to

295 Unitary GPe-STN synaptic connections initially generated large c

296 d by short-term synaptic depression, unitary GPe-STN inputs were stimulated in rat and mouse brain sl

297 Although phasic, unitary GPe-STN inputs powerfully pattern STN activity ex vivo,

298 Our circuit model suggests that when GPe spikes are synchronous, this pallidostriatal pathway

299 ring periods of synchronized activity within GPe.

300 omatin affected by dopamine depletion within GPe PV(+) neurons were enriched for hypoxia-inducible fa