ライフサイエンスコーパス: ganglia

1 n (white matter, cortex, fiber tracts, basal ganglia).

2 trigeminal ganglia than in mouse trigeminal ganglia.

3 gs of neuronal activity from the human basal ganglia.

4 at are uniquely found in adult sex segmental ganglia.

5 essing, and impaired plasticity in the basal ganglia.

6 whose cell bodies reside in cranial sensory ganglia.

7 ical roles of beta oscillations in the basal ganglia.

8 uman skin and sensory neurons in dorsal root ganglia.

9 vation and cell-body loss in the dorsal root ganglia.

10 an excess of striatal dopamine in the basal ganglia.

11 am inhibitory signaling centers in the basal ganglia.

12 utely and latently infected mouse trigeminal ganglia.

13 a-producing CD8 T cells in latently infected ganglia.

14 f dopamine in an output nucleus of the basal ganglia.

15 mography data in vivo, at least in the basal ganglia.

16 he direct and indirect pathways of the basal ganglia.

17 c parasympathetic ganglia, including enteric ganglia.

18 zed cell line derived from human dorsal root ganglia.

19 buting to acute ethanol effects on the basal ganglia.

20 lts to viral protein expression in the whole ganglia.

21 No group differences were found in the basal ganglia.

22 extensive spread of virus is observed in the ganglia.

23 ed with spotlike calcifications in the basal ganglia.

24 increased activity in the midbrain and basal ganglia.

25 imately into many cranial sensory organs and ganglia.

26 ions, including the frontal cortex and basal ganglia.

27 d white matter with heaviest burden in basal ganglia.

28 vels of phosphorylated VEGFR1 in dorsal root ganglia.

29 yngeal C neurons in the nodose/jugular (N/J) ganglia.

30 neurons, primarily located in the trigeminal ganglia.

31 er virus (VZV) pathology in skin and sensory ganglia.

32 eactivation from explanted latently infected ganglia.

33 e among the highest expressed in dorsal root ganglia.

34 ormal integration of left thalamus and basal ganglia.

35 nderlying bicycling and walking in the basal ganglia.

36 lobes (30.4%), temporal lobes (8.69%), basal ganglia (22%), cerebellum(17.39%), brainstem(9%) and tha

37 D8 T cells were also detected in the sensory ganglia 3 dpi.

38 The basal ganglia, a group of subcortical nuclei, play a crucial r

39 cribing changes in the activity of the basal ganglia across the sleep-wake cycle that contribute to o

40 ts shed light on why states of altered basal ganglia activity disrupt both motor function and cogniti

41 s pathway is conserved, as human sympathetic ganglia also contain SAMs expressing the analogous molec

42 ation-sensitive input neurons from the optic ganglia and a single layer of simple neuronal connectivi

43 and neutrophils infiltrate infected sensory ganglia and are responsible for driving the production o

44 s contribute to all sense organs and sensory ganglia and arise from a common pool of Six1/Eya2+ proge

45 ns such as the frontal lobes, thalami, basal ganglia and brainstem.

46 lex of hypomyelination with atrophy of basal ganglia and cerebellum (H-ABC).

47 me in OCD patients as nodes within the basal ganglia and cerebellum were more strongly connected to o

48 planted cultures or by homogenization of the ganglia and compare the results to viral protein express

49 rsor cells that are located within myenteric ganglia and express both Nestin and p75NTR, but not the

50 , patients with PD and MCI had a large basal ganglia and frontoparietal network with decreased fracti

51 a network with decreased FA, including basal ganglia and frontotemporoparietal regions bilaterally (P

52 striatum is the major component of the basal ganglia and is well known to play a key role in the cont

53 emporal and functional analyses of the basal ganglia and lays the foundation for an integrated approa

54 -releasing neurons with connections to basal ganglia and limbic brain regions.

55 451 in vivo retention predominantly in basal ganglia and midbrain.

56 en considered an interface between the basal ganglia and motor systems, and its ability to regulate a

57 tically and subcortically in bilateral basal ganglia and occipital cortex.

58 ue (SAT) via its actions both on sympathetic ganglia and on the SAT itself.

59 al sites of recurrent lytic infection and to ganglia and persist at the dermal-epidermal junction for

60 mmunication within rodent peripheral sensory ganglia and show that it can modulate transmission of pa

61 he central nervous system (CNS), eyes, optic ganglia and statocysts of the nudibranchs.

62 r alphaherpesviruses to establish latency in ganglia and then to reactivate and move back to peripher

63 The basal ganglia and/or thalamus were also commonly involved with

64 the selective death of sensory (dorsal root ganglia) and autonomic neurons observed in FD.

65 or region of many cranial sensory organs and ganglia), and other ectodermal domains.

66 cations: small, symmetric, sparing the basal ganglia, and a stepping stone appearance in the frontal

67 al abnormalities in total gray matter, basal ganglia, and cerebellum.

68 tum receives inhibitory input from the basal ganglia, and input from the pallium (cortex in mammals)

69 tering level in somatomotor, thalamic, basal ganglia, and limbic networks.

70 interaction between the cerebellum and basal ganglia, and put forward a hypothesis that dystonia is a

71 The basal ganglia are highly implicated in action selection and go

72 ts suggest that the PCC, thalamus, and basal ganglia are key components of a LC-noradrenergic arousal

73 The basal ganglia are known to bias movement selection according t

74 MSNs and specific circuits within the basal ganglia are preferentially vulnerable to HIV-1.

75 ortex, working closely in concert with basal ganglia, are also involved in tic production.

76 d that neuroinflammation occurs in the basal ganglia as an autoimmune response to infections.

77 Immunolabeling of ganglia associated with the vagina indicated the likely

78 Exaggerated basal ganglia beta activity (13-35 Hz) is commonly found in pa

79 racked response-set control costs, and basal ganglia (BG) activity mirrored the interaction between t

80 ease in structure and function of left basal ganglia (BG) and insula relative to control subjects and

81 ABSTRACT: Neural oscillations in the basal ganglia (BG) are well studied yet remain poorly understo

82 to the striatum is critical for normal basal ganglia (BG) function.

83 different sub-cortical structures, the basal ganglia (BG) has been investigated as a putative anatomi

84 The basal ganglia (BG) integrate inputs from diverse sensorimotor,

85 ntopeduncular nucleus (EP), one of the basal ganglia (BG) output nuclei, is an important station in i

86 Targeted lesions in select basal ganglia (BG) structures also revealed a major role for n

87 he direct and indirect pathways of the basal ganglia (BG).

88 in microglia, such as those within the basal ganglia (BG).

89 Cerebellar associative learning and basal ganglia-brainstem interaction were investigated in 17 my

90 ipheral taste organs and innervating sensory ganglia, but the underlying mechanisms remain poorly und

91 n these preparations was conveyed to central ganglia by axons in the anterior- and lateral-dorsal ner

92 reactivation in latently infected explanted ganglia by sampling media from the explanted cultures or

93 to inhibit lytic gene expression in infected ganglia by targeting ICP0 mRNA.

94 r, disorders primarily associated with basal ganglia calcifications, such as primary familial brain c

95 amine from the striatum, a part of the basal ganglia, causes some symptoms of Parkinson's disease.

96 dy the role of the recently discovered basal ganglia-cerebellar anatomical links.

97 event and that the recently discovered basal ganglia-cerebellar anatomical pathway may support the in

98 Studying this non-cortex-mediated basal ganglia-cerebellar interaction could radically change ou

99 periments about the involvement of the basal ganglia-cerebellar-thalamo-cortical system in tic genera

100 proposes a computational model of the basal ganglia-cerebellar-thalamo-cortical system to study how

101 ly, there may be an involvement of the basal ganglia, cerebellum and brainstem, with or without hemor

102 ported volumetric abnormalities in the basal ganglia, cerebellum, and prefrontal cortices.

103 g localized inactivation of a cortical-basal ganglia circuit specialized for song, we show that this

104 nt plasticity in songbirds depend on a basal ganglia circuit, which actively generates vocal variabil

105 the dorsolateral prefrontal cortex and basal ganglia circuitry are the earliest neural network connec

106 on, while top-down input from cortical-basal ganglia circuitry biases this representation to enable c

107 of adaptive motor control that rely on basal ganglia circuitry.

108 excitatory signaling center within the basal ganglia circuitry.

109 o a large extent by dysfunction of the basal ganglia circuitry.

110 llent tool to study the development of basal ganglia circuitry.

111 erate pacemaker activity that controls basal ganglia, circuitry associated with habitual and compulsi

112 Cortico-basal ganglia circuits are critical for speech and language an

113 Cortico-basal ganglia circuits are thought to mediate goal-directed le

114 map widespread functional imbalance of basal ganglia circuits in a mouse model of DYT1 dystonia overe

115 pathologically exaggerated throughout basal ganglia circuits in parkinsonism.

116 are abnormally exaggerated in cortical-basal ganglia circuits in parkinsonism.

117 g capacity depends on specific cortico-basal ganglia circuits that are affected by normal ageing.

118 vocal learning is mediated by cortico-basal ganglia circuits that include the SHELL region of latera

119 ia can upset the functional balance of basal ganglia circuits, affecting direct and indirect pathways

120 is channelled through distinct sets of basal ganglia circuits, with the GPh representing a key locus

121 opamine D1 and D2 receptors present in basal ganglia circuits.

122 hestrate these pathological rhythms in basal ganglia circuits.SIGNIFICANCE STATEMENT Chronic depletio

123 In the paired commissural ganglia (CoGs) of the stomatogastric nervous system of t

124 the Nudipleura were restricted to the buccal ganglia, commissures, and connectives.

125 rk in which the LC, PCC, thalamus, and basal ganglia comprise a functional arousal circuitry.SIGNIFIC

126 vel computational model of the healthy basal ganglia, constrained by single unit recordings from non-

127 ection by direct homogenization of explanted ganglia correlates with viral protein expression, but de

128 GABAergic dysfunction in the basal ganglia could disrupt the learning and development of co

129 ystonia was originally classified as a basal ganglia disease.

130 orward a hypothesis that dystonia is a basal ganglia disorder that can be induced by aberrant afferen

131 the empirical concept of dystonia as a basal ganglia disorder, we discovered large-scale alterations

132 psy, although SV2C with its restricted basal ganglia distribution is poorly characterized.

133 suggest that mesolimbic and non-limbic basal ganglia dopamine circuits are functionally connected and

134 In the isolated segmental ganglia, dopamine can induce a rhythmic antiphasic activ

135 f GABA or GABA reuptake inhibitor to sensory ganglia dramatically reduced acute peripherally induced

136 correlated with degeneration in dorsal root ganglia (DRG) and sciatic nerve and abundance of Schwann

137 eripheral sensory neurons in the dorsal root ganglia (DRG) are the initial transducers of sensory sti

138 eripheral sensory neurons of the dorsal root ganglia (DRG) express kainate receptors (KARs), a subfam

139 a (ENU)-induced mutation affects dorsal root ganglia (DRG) formation in ouchless mutant zebrafish lar

140 y afferent neurons isolated from dorsal root ganglia (DRG) innervating the lower gastrointestinal tra

141 ociated small diameter (<27 mum) dorsal root ganglia (DRG) neurons and on miniature (m)EPSCs recorded

142 ain-of-function mutations render dorsal root ganglia (DRG) neurons hyperexcitable.

143 FICANCE STATEMENT Small-diameter dorsal root ganglia (DRG) neurons mediating nociception and other se

144 ciceptors are a subpopulation of dorsal root ganglia (DRG) neurons that detect noxious stimuli and si

145 would result in transduction of dorsal root ganglia (DRG) or trigeminal ganglia (TG), respectively.

146 oding microRNAs (miRs) occurs in dorsal root ganglia (DRG) sensory neurons.

147 , EP4) in endometriosis lesions, dorsal root ganglia (DRG), spinal cord, thalamus and forebrain.

148 rents is well known to reside in dorsal root ganglia (DRG), the morphology and location of peripheral

149 the number of T cells in lumbar dorsal root ganglia (DRG), where CD8(+) T cells were the major subse

150 primary afferent neurons of the dorsal root ganglia (DRG).

151 zation responses to capsaicin in dorsal root ganglia (DRGs) following application of supernatants gen

152 gene expression is increased in dorsal root ganglia (DRGs) of paclitaxel-treated rats.

153 xonal growth from chicken or rat dorsal root ganglia (DRGs).

154 nfectious virus production in the trigeminal ganglia during acute infection, mouse mortality, or the

155 to host-pathogen interactions in the sensory ganglia during acute varicella and demonstrate that SVV

156 Although basal ganglia dysfunction has been proposed to underlie repeti

157 RM cells within latently infected trigeminal ganglia following virus reactivation.

158 Transcriptome analysis of trigeminal ganglia from latently HSV-1-infected, glutamine-treated

159 naling has been neglected in models of basal ganglia function and has implications for a range of pat

160 been critical to our understanding of basal ganglia function and the treatment of neurological disor

161 ve been found to preferentially target basal ganglia function to lead to impaired motivation and moto

162 tly associated with increased log left basal ganglia glutamate controlling for age, sex, race, body m

163 nteers, the median signal intensity in basal ganglia gray matter (DGErho = 4.59%) was significantly i

164 fication of distinct cell types in the basal ganglia has been critical to our understanding of basal

165 amyloid angiopathy, while those in the basal ganglia have been associated with deep perforating arter

166 Y POINTS: Neuronal oscillations in the basal ganglia have been observed to correlate with behaviours,

167 ) imaging results were normal, without basal ganglia hyperintensity, lacunae, calcification, or heavy

168 cortex, few studies have detailed the basal ganglia in autism.

169 om the brain to the spinal cord (or thoracic ganglia in insects).

170 ly through the neuronal sheath of nerves and ganglia in insects.

171 Considerable evidence implicates the basal ganglia in interval timing, yet the underlying mechanism

172 ter-wet system, where the oil was trapped in ganglia in the larger regions of the pore space.

173 ever, it is known that dysfunctions in basal ganglia, including a reduced number of striatal choliner

174 s to populate post-embryonic parasympathetic ganglia, including enteric ganglia.

175 f neuromelanin-containing cells in the basal ganglia, indicating that off-target binding to neuromela

176 accordingly homogenous, with bilateral basal ganglia involvement (98%); the characteristic "putaminal

177 isrupted expression of SV2C within the basal ganglia is a pathological feature of PD.

178 al subtypes of sensory neuron in dorsal root ganglia is distorted by Gars mutations, leading to senso

179 Cholinergic innervation of the basal ganglia is important in learning and memory.

180 Action selection in the basal ganglia is often described within the framework of a sta

181 l striatum, a major input structure of basal ganglia, is composed of two opponent pathways, direct an

182 he development of cranial sensory organs and ganglia, kidneys, hypaxial muscles and several other org

183 erge in the normal functioning cortico-basal ganglia loop during behavior.

184 None, however, displayed the basal ganglia malformations typically associated with TUBB2B m

185 e formation of fused multinucleated cells in ganglia might be associated with this condition.

186 reactivation from latency both in a sensory ganglia model system and in vivo.

187 otor circuit; while dysfunction of the basal ganglia motor circuit and disconnection between the rost

188 eased activity and connectivity in the basal ganglia motor circuit, but had no effect on progressive

189 aphia is related to dysfunction of the basal ganglia motor circuit; while dysfunction of the basal ga

190 f the midbrain dopamine and integrated basal ganglia motor systems to control movement.

191 Basal ganglia MRI signal abnormalities were observed in only 1

192 hat unexpected events recruit a fronto-basal-ganglia network for stopping.

193 ons (MSNs) are a key population in the basal ganglia network, and their degeneration causes a severe

194 information processing in the cortico-basal ganglia network.

195 ellar-thalamic-cortical and cerebellar-basal ganglia networks after locomotor adaptation.

196 ice, we explored how ageing of cortico-basal ganglia networks alters the microstructure of action thr

197 bellum-thalamo-cortical and the fronto-basal-ganglia networks regulating inhibitory control.

198 veal static properties of aged cortico-basal ganglia networks that introduce temporal limits to actio

199 cating a possible link between altered basal ganglia neurodevelopment and declined motor performance

200 were able to optically stimulate dorsal root ganglia neurons and generate action potentials with visi

201 l as in vitro effects of HOCl on dorsal root ganglia neurons and mouse bone marrow-derived dendritic

202 o induced neuronal plasticity in dorsal root ganglia neurons by increasing the number of neurites and

203 ll-diameter, capsaicin-sensitive dorsal root ganglia neurons corresponding to nociceptors (from rats

204 sponse to several pruritogens in dorsal root ganglia neurons excised from NC/Nga mice after terminati

205 urons, which account for >40% of dorsal root ganglia neurons, display resistance to rabies infection.

206 orts of ASIC3 mRNA expression in dorsal root ganglia neurons, we found that the ASIC3 antagonist APET

207 -like currents in naked mole-rat dorsal root ganglia neurons.

208 he activity of TRPV1 channels in dorsal root ganglia neurons.

209 cate a potential evolutionary shift in basal ganglia neurotransmission in humans that may favor incre

210 the globus pallidus externus (GPe), a basal ganglia nucleus not previously known to participate in b

211 rical, bilateral calcifications in the basal ganglia, nucleus gyrus and cerebral cortex.

212 tein and mRNA was detected in neurons of the ganglia of all segments of the human gastrointestinal tr

213 are present in the central brain and ventral ganglia of C. fortis whereas in the retrocerebral comple

214 f the executive and motor loops of the basal ganglia of humans, great apes, and monkeys.

215 s neurons in the spinal cord and dorsal root ganglia of immunodeficient mice with higher efficacy tha

216 significantly more neurons in the trigeminal ganglia of latently infected calves than in those of uni

217 ugmenting the amount of CXCL10 in trigeminal ganglia of latently infected CXCL10-deficient mice signi

218 rations in the sciatic nerve and dorsal root ganglia of oxaliplatin treated mice.

219 low beta band specifically within the basal ganglia of patients susceptible to freezing.

220 licated in sensorimotor control in the basal ganglia of task-performing healthy animals.

221 l loss because of apoptosis in the myenteric ganglia of the adult small intestine, total myenteric ne

222 via the dorsal root ganglia to the autonomic ganglia of the enteric nervous system (ENS) in the colon

223 ctrometry analysis were obtained directly on ganglia of the medicinal leech (Hirudo medicinalis) with

224 o collect two volumes of serial EM data from ganglia of the medicinal leech.

225 We applied this system to the segmental ganglia of the medicinal leech.

226 used by non-progressive lesions to the basal ganglia or thalamus, or both, and is characterised by ab

227 Classical schemes of basal ganglia organization posit that parkinsonian movement di

228 ogenetics, we examined the role of the basal ganglia output in interval timing.

229 nd attenuates pathological activity of basal ganglia output neurons for hours beyond stimulation.

230 e synchrony of a modeled population of basal ganglia output neurons receiving excitatory and inhibito

231 nigra pars reticulata (SNR), the major basal ganglia output nucleus, during self-initiated drinking i

232 lar and circuit complexity involving a basal ganglia output structure, the entopeduncular nucleus.

233 putative global suppressive effect on basal-ganglia output.

234 on for an integrated approach to study basal ganglia pathologies such as Parkinson's disease in silic

235 imbalance between indirect and direct basal ganglia pathways, disturbed sensory processing, and impa

236 g amount of infectious virus produced in the ganglia per reactivation event.

237 ons, and increases in white matter and basal ganglia perfusion, with effect sizes ranging from 0.4 to

238 neuroimmune-glia interactions at the sensory ganglia play a critical role in the genesis of herpetic

239 arbors of varicose neurites within myenteric ganglia/primary plexus and, concomitantly, long rectilin

240 , and regulate the development of, the basal ganglia primodia from which many GABAergic neurons origi

241 Dopamine in the basal ganglia reduces trial-to-trial neural variability when t

242 aneaat different time points during cephalic ganglia regeneration.

243 larger network of frontal control and basal ganglia regions than within-language competition.

244 Surprisingly, basal ganglia regions that receive sparse or no VTA dopaminerg

245 on is induced by LMAN, the output of a basal ganglia-related circuit that also contributes a correcti

246 dings indicate that peripheral somatosensory ganglia represent a hitherto underappreciated site of so

247 n frontal cortex and nucleus accumbens basal ganglia, respectively, were significantly regulated by M

248 rs of laryngeal sensory C neurons in the N/J ganglia retrogradely traced by 1,1'-dioctadecyl-3,3,3',3

249 variables influencing spread of virus in the ganglia should be considered when interpreting results o

250 tein-coupled receptors in murine dorsal root ganglia showed that both receptors were among the highes

251 erential damage to the hippocampus and basal ganglia (specifically nigrostriatal pathways).

252 and histological analysis of the dorsal root ganglia, spinal cord, and cerebellum.

253 non-neuronal tissues, including dorsal root ganglia, spinal cord, and keratinocytes.

254 arget activity in small-diameter dorsal root ganglia, spinal slices, and in a mouse model of pain ind

255 here is an opportunity not only to map basal ganglia structures but also to gain insights into how di

256 ased morphometry method on 3 bilateral basal ganglia structures in school-age children chronically ex

257 icant enlargement of many areas of the basal ganglia structures, preferentially affecting the putamen

258 ngle-unit data recorded from different basal ganglia subregions in rats performing a cued choice task

259 expressed on GABAergic neurons of the basal ganglia, substantia nigra, and ventral tegmental area (V

260 extensive expression of CFTR in the enteric ganglia suggests that CFTR may play a role in the physio

261 o-AMPase activity in dental pulp, trigeminal ganglia (TG) neurons, and their nerve fibers.

262 eplication in the eye, latency in trigeminal ganglia (TG), and markers of T cell exhaustion in the TG

263 latency within sensory neurons of trigeminal ganglia (TG), and TG-resident CD8(+) T cells play a crit

264 n of dorsal root ganglia (DRG) or trigeminal ganglia (TG), respectively.

265 e intestinal peptide (vip) in the trigeminal ganglia (TG).

266 within the sensory neurons of the trigeminal ganglia (TG).

267 alities, supporting the involvement of basal ganglia-thalamocortical circuits, representing emotional

268 trainment of structures throughout the basal ganglia-thalamocortical loop in the lesioned hemisphere

269 kingly, when applied to the brain-wide basal ganglia-thalamocortical network, DCM accurately reproduc

270 ons including the reticular formation, basal ganglia, thalamus, posterior cingulate cortex (PCC), pre

271 echano-activated currents in duck trigeminal ganglia than in mouse trigeminal ganglia.

272 neuroimmune-glia interactions in the sensory ganglia that account for the development of acute herpet

273 the neuroimmune interactions at the sensory ganglia that account for the genesis of herpetic neuralg

274 excitatory interneuron in the songbird basal ganglia that makes strong synaptic connections onto outp

275 re, we show in neurons of murine dorsal root ganglia that pro-nociceptive TRPM3 channels, present in

276 hin neurocircuitries that comprise the basal ganglia, the extended amygdala, and the prefrontal corte

277 reactivation from latently infected sensory ganglia, the majority never develop a recurrent herpetic

278 n mice, we show that the output of the basal ganglia through the substantia nigra pars reticulata (SN

279 s were natively expressed in rat dorsal root ganglia tissue.

280 ital, allowing spread from latently infected ganglia to epithelial tissues, where viral progeny are p

281 eories of OCD should extend beyond the basal ganglia to include the cortico-striato-thalamo-cortical

282 Instead, HSV-1 spread via the dorsal root ganglia to the autonomic ganglia of the enteric nervous

283 reduction in latent HSV-2 DNA in dorsal root ganglia to undetectable levels.

284 We obtained the basal ganglia transcriptome by RNA sequencing in the caudate a

285 tion of GABA receptor antagonists to sensory ganglia triggered or exacerbated peripherally induced no

286 including whole-brain, hippocampal and basal ganglia volumetry; white matter integrity (diffusion ten

287 MRI-visible perivascular spaces in the basal ganglia was associated with clinically diagnosed subcort

288 reactivation in latently infected trigeminal ganglia was induced by UV-B light, we demonstrated that

289 ionally, bilinguals' activation of the basal ganglia was inversely correlated with their executive fu

290 18F-AV-1451 binding to the basal ganglia was strong in all groups in vivo.

291 down in the cerebellum, but not in the basal ganglia, was sufficient to induce dystonia.

292 T1-bright basal ganglia were confined to LGI1-IgG-positive patients with

293 ured and contralateral L4 and L5 dorsal root ganglia were cultured in a compartmentalized system.

294 identified differences including that small ganglia were restricted to cervical segments, epithelial

295 The study was performed in isolated ganglia where manipulation of the activity of specific m

296 al cortex and its interaction with the basal ganglia, where a more anterior corticostriatal loop esta

297 nction and proposed roles of KARs in sensory ganglia, which include promotion of neurite outgrowth an

298 lishment of lifelong latency in host sensory ganglia with occasional reactivation causing recurrent l

299 heimer's disease, whereas those in the basal ganglia would be associated with subcortical vascular co

300 r to motor suppressing pathways in the basal ganglia, yet its neuronal heterogeneity has remained an