ライフサイエンスコーパス: basal ganglia

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

2 upstream inhibitory signaling centers in the basal ganglia.

3 sociated with spotlike calcifications in the basal ganglia.

4 ects of dopamine in an output nucleus of the basal ganglia.

5 ion tomography data in vivo, at least in the basal ganglia.

6 s to the direct and indirect pathways of the basal ganglia.

7 contributing to acute ethanol effects on the basal ganglia.

8 No group differences were found in the basal ganglia.

9 rives increased activity in the midbrain and basal ganglia.

10 ray and white matter with heaviest burden in basal ganglia.

11 in regions, including the frontal cortex and basal ganglia.

12 n-related genes co-expressed in normal human basal ganglia.

13 n to value, also influence movements via the basal ganglia.

14 (-/-) x Tfr2(mut) brain and post-mortem NBIA basal ganglia.

15 mplitude drives network activity through the basal ganglia.

16 in the amelioration of alpha-syn in vivo in basal ganglia.

17 tem function, behavior, and disorders of the basal ganglia.

18 g activity in the hippocampus, midbrain, and basal ganglia.

19 impairments of behaviors orchestrated by the basal ganglia.

20 state by virtue of its connectivity with the basal ganglia.

21 -normalized measures of other metabolites in basal ganglia.

22 bly via the subthalamic nucleus (STN) of the basal ganglia.

23 ts, allowing us to test how each engaged the basal ganglia.

24 thin widespread brain regions, including the basal ganglia.

25 lexibility in the control of volition by the basal ganglia.

26 anges in dopamine and opioid peptides in the basal ganglia.

27 an abnormal integration of left thalamus and basal ganglia.

28 mics underlying bicycling and walking in the basal ganglia.

29 cordings of neuronal activity from the human basal ganglia.

30 y processing, and impaired plasticity in the basal ganglia.

31 thological roles of beta oscillations in the basal ganglia.

32 d with an excess of striatal dopamine in the basal ganglia.

33 ontal lobes (30.4%), temporal lobes (8.69%), basal ganglia (22%), cerebellum(17.39%), brainstem(9%) a

34 The basal ganglia, a group of subcortical nuclei, play a cru

35 activity in the prefrontal cortex and in the basal ganglia, a set of subcortical nuclei implicated in

36 gs describing changes in the activity of the basal ganglia across the sleep-wake cycle that contribut

37 results shed light on why states of altered basal ganglia activity disrupt both motor function and c

38 ocations such as the frontal lobes, thalami, basal ganglia and brainstem.

39 family, we compared two models in which the basal ganglia and cerebello-thalamo-cortical loop were c

40 m complex of hypomyelination with atrophy of basal ganglia and cerebellum (H-ABC).

41 nnectome in OCD patients as nodes within the basal ganglia and cerebellum were more strongly connecte

42 Here we discuss the role of the basal ganglia and connected prefrontal regions in the et

43 epressed controls increased glutamate in the basal ganglia and dorsal anterior cingulate cortex (dACC

44 rtex and insula, including glutamate, to the basal ganglia and extended amygdala.

45 bjects, patients with PD and MCI had a large basal ganglia and frontoparietal network with decreased

46 I had a network with decreased FA, including basal ganglia and frontotemporoparietal regions bilatera

47 ed to pathophysiological changes both in the basal ganglia and in a cerebello-thalamo-cortical motor

48 The striatum is the major component of the basal ganglia and is well known to play a key role in th

49 ral, temporal and functional analyses of the basal ganglia and lays the foundation for an integrated

50 d GABA-releasing neurons with connections to basal ganglia and limbic brain regions.

51 ]-AV-1451 in vivo retention predominantly in basal ganglia and midbrain.

52 ong been considered an interface between the basal ganglia and motor systems, and its ability to regu

53 ed cortically and subcortically in bilateral basal ganglia and occipital cortex.

54 Subcortical structures, which include the basal ganglia and parts of the limbic system, have key r

55 The basal ganglia and/or thalamus were also commonly involve

56 alcifications: small, symmetric, sparing the basal ganglia, and a stepping stone appearance in the fr

57 e roles of brain circuits across the cortex, basal ganglia, and cerebellum in generating vocal behavi

58 ructural abnormalities in total gray matter, basal ganglia, and cerebellum.

59 n the olfactory bulb, lateral septal nuclei, basal ganglia, and distinct areas of the midbrain, brain

60 pretectum receives inhibitory input from the basal ganglia, and input from the pallium (cortex in mam

61 t clustering level in somatomotor, thalamic, basal ganglia, and limbic networks.

62 suring resting perfusion in the hippocampus, basal ganglia, and midbrain in people at high risk of ps

63 ional interaction between the cerebellum and basal ganglia, and put forward a hypothesis that dystoni

64 mainly in the anterior cingulate cortex, the basal ganglia, and the cerebellum has been reported in a

65 nhibitory effects in thalamic neurons of the basal ganglia- and cerebellar-receiving regions of the m

66 The subthalamic nucleus (STN) of the basal ganglia appears to have a potent role in action an

67 The basal ganglia are a critical nexus where circuits necess

68 Because the basal ganglia are evolutionarily conserved, the tectal p

69 The basal ganglia are highly implicated in action selection

70 results suggest that the PCC, thalamus, and basal ganglia are key components of a LC-noradrenergic a

71 The basal ganglia are known to be involved in the planning,

72 The basal ganglia are known to bias movement selection accor

73 hat D2 MSNs and specific circuits within the basal ganglia are preferentially vulnerable to HIV-1.

74 and cortex, working closely in concert with basal ganglia, are also involved in tic production.

75 roposed that neuroinflammation occurs in the basal ganglia as an autoimmune response to infections.

76 Exaggerated basal ganglia beta activity (13-35 Hz) is commonly found

77 vity tracked response-set control costs, and basal ganglia (BG) activity mirrored the interaction bet

78 c increase in structure and function of left basal ganglia (BG) and insula relative to control subjec

79 urons that includes multiple pathways in the basal ganglia (BG) and is endowed with feedback mechanis

80 The basal ganglia (BG) are critical for adaptive motor contr

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

82 suggesting potential dysfunction of cortico-basal ganglia (BG) circuits.

83 The basal ganglia (BG) control action selection, motor progr

84 uts into the striatum is critical for normal basal ganglia (BG) function.

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

86 The basal ganglia (BG) integrate inputs from diverse sensori

87 leus (STN) constitute the input stage of the basal ganglia (BG) network and together innervate BG dow

88 The basal ganglia (BG) network has been divided into interac

89 tory activity in the subthalamic nucleus and basal ganglia (BG) output nuclei in both Parkinson's dis

90 The entopeduncular nucleus (EP), one of the basal ganglia (BG) output nuclei, is an important statio

91 The basal ganglia (BG) promote complex sequential movements

92 Targeted lesions in select basal ganglia (BG) structures also revealed a major role

93 ep brain microglia, such as those within the basal ganglia (BG).

94 evidence supports the key involvement of the basal ganglia (BG).

95 ween the direct and indirect pathways of the basal ganglia (BG).

96 Cerebellar associative learning and basal ganglia-brainstem interaction were investigated in

97 oreover, disorders primarily associated with basal ganglia calcifications, such as primary familial b

98 of dopamine from the striatum, a part of the basal ganglia, causes some symptoms of Parkinson's disea

99 to study the role of the recently discovered basal ganglia-cerebellar anatomical links.

100 e tic event and that the recently discovered basal ganglia-cerebellar anatomical pathway may support

101 Studying this non-cortex-mediated basal ganglia-cerebellar interaction could radically cha

102 ent experiments about the involvement of the basal ganglia-cerebellar-thalamo-cortical system in tic

103 rticle proposes a computational model of the basal ganglia-cerebellar-thalamo-cortical system to stud

104 sionally, there may be an involvement of the basal ganglia, cerebellum and brainstem, with or without

105 nly reported volumetric abnormalities in the basal ganglia, cerebellum, and prefrontal cortices.

106 Schemes of basal ganglia circuit dynamics generally consider striat

107 mediator of information flow through frontal-basal ganglia circuit loops.

108 Using localized inactivation of a cortical-basal ganglia circuit specialized for song, we show that

109 acing, we show that the GPh is embedded in a basal ganglia circuit wherein it receives inhibitory inp

110 m increased efficacy of the indirect pathway basal ganglia circuit, relative to the direct pathway.

111 ependent plasticity in songbirds depend on a basal ganglia circuit, which actively generates vocal va

112 st that disruption of NALCN could impair the basal ganglia circuit, which may underlie the severe mot

113 We found in mice that separate basal ganglia circuitries mediated the hedonic and nutri

114 on to the dorsolateral prefrontal cortex and basal ganglia circuitry are the earliest neural network

115 lization, while top-down input from cortical-basal ganglia circuitry biases this representation to en

116 acologic PDE10 inhibition to acutely correct basal ganglia circuitry deficits.

117 hile much is known about the function of the basal ganglia circuitry in selection, how these nuclei c

118 hat thalamus drives asymmetric activation of basal ganglia circuitry underlying parkinsonian motor im

119 nisms of adaptive motor control that rely on basal ganglia circuitry.

120 tical excitatory signaling center within the basal ganglia circuitry.

121 n excellent tool to study the development of basal ganglia circuitry.

122 iven to a large extent by dysfunction of the basal ganglia circuitry.

123 striatal cAMP signaling in the regulation of basal ganglia circuitry.

124 e) generate pacemaker activity that controls basal ganglia, circuitry associated with habitual and co

125 Cortico-basal ganglia circuits are critical for speech and langu

126 Cortico-basal ganglia circuits are thought to mediate goal-direc

127 t beta frequencies (20-50 Hz) in the cortico-basal ganglia circuits have long been the leading theory

128 ) can map widespread functional imbalance of basal ganglia circuits in a mouse model of DYT1 dystonia

129 become pathologically exaggerated throughout basal ganglia circuits in parkinsonism.

130 that are abnormally exaggerated in cortical-basal ganglia circuits in parkinsonism.

131 earning capacity depends on specific cortico-basal ganglia circuits that are affected by normal agein

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

133 behavioral models to dissect causal cortico-basal ganglia circuits underlying discrete behavioral sy

134 dystonia can upset the functional balance of basal ganglia circuits, affecting direct and indirect pa

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

136 d by dopamine D1 and D2 receptors present in basal ganglia circuits.

137 ld orchestrate these pathological rhythms in basal ganglia circuits.SIGNIFICANCE STATEMENT Chronic de

138 chronous oscillatory activity within cortico-basal-ganglia circuits.

139 ramework in which the LC, PCC, thalamus, and basal ganglia comprise a functional arousal circuitry.SI

140 s assumes that, during action selection, the basal ganglia compute for all actions available in a giv

141 Basal ganglia connectivity is a promising biomarker for

142 t a novel computational model of the healthy basal ganglia, constrained by single unit recordings fro

143 results enhance the understanding of how the basal ganglia control gripping force, and also suggest t

144 Here we aim to define the nature of the basal ganglia control signal for force and to decode gri

145 GABAergic dysfunction in the basal ganglia could disrupt the learning and development

146 In disease, however, the basal ganglia develop amplified rhythmicity.

147 Dystonia was originally classified as a basal ganglia disease.

148 put forward a hypothesis that dystonia is a basal ganglia disorder that can be induced by aberrant a

149 with the empirical concept of dystonia as a basal ganglia disorder, we discovered large-scale altera

150 epilepsy, although SV2C with its restricted basal ganglia distribution is poorly characterized.

151 rther suggest that mesolimbic and non-limbic basal ganglia dopamine circuits are functionally connect

152 Although basal ganglia dysfunction has been proposed to underlie

153 disease and may be a diagnostic biomarker of basal ganglia dysfunction.

154 ating its potential as an indicator of early basal ganglia dysfunction.

155 Furthermore, the basal ganglia effectively influenced the cerebello-thala

156 In the basal ganglia, focused rhythmicity is an important featu

157 3R signaling has been neglected in models of basal ganglia function and has implications for a range

158 ia has been critical to our understanding of basal ganglia function and the treatment of neurological

159 A central theory of basal ganglia function is that striatal neurons expressi

160 Although perturbations of basal ganglia function produce profound changes in movem

161 uli have been found to preferentially target basal ganglia function to lead to impaired motivation an

162 easily predicted from-contemporary models of basal ganglia function.

163 g = 0.56; 95% CI, 0.02-1.09), and Glx in the basal ganglia (g = 0.39; 95% CI, 0.09-0.70) and medial t

164 The embryonic basal ganglia generates multiple projection neurons and

165 RP were also associated with CSI measures of basal ganglia glutamate and the glial marker myoinositol

166 ificantly associated with increased log left basal ganglia glutamate controlling for age, sex, race,

167 In turn, log left basal ganglia glutamate was associated with anhedonia an

168 y volunteers, the median signal intensity in basal ganglia gray matter (DGErho = 4.59%) was significa

169 dopamine inputs to a region of the songbird basal ganglia greatly impairs vocal learning but has no

170 identification of distinct cell types in the basal ganglia has been critical to our understanding of

171 The basal ganglia have a central role in motor patterning, h

172 ebral amyloid angiopathy, while those in the basal ganglia have been associated with deep perforating

173 KEY POINTS: Neuronal oscillations in the basal ganglia have been observed to correlate with behav

174 e significant elevations in glutamate in the basal ganglia (Hedges g = 0.63; 95% CI, 0.15-1.11), glut

175 ce (MR) imaging results were normal, without basal ganglia hyperintensity, lacunae, calcification, or

176 ssion may lead to increased glutamate in the basal ganglia in association with glial dysfunction and

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

178 Considerable evidence implicates the basal ganglia in interval timing, yet the underlying mec

179 However, it is known that dysfunctions in basal ganglia, including a reduced number of striatal ch

180 ence of neuromelanin-containing cells in the basal ganglia, indicating that off-target binding to neu

181 lo-thalamo-cortical loop and (2) whether the basal ganglia influence the cerebello-thalamo-cortical l

182 1.229, P < .001) abnormalities in bilateral basal ganglia/insula, which were decreased in GMV and fu

183 ystems interact, is the pivotal structure of basal ganglia involved in pathophysiological changes und

184 were accordingly homogenous, with bilateral basal ganglia involvement (98%); the characteristic "put

185 that disrupted expression of SV2C within the basal ganglia is a pathological feature of PD.

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

187 Action selection in the basal ganglia is often described within the framework of

188 Whereas hyperdopaminergic signaling in the basal ganglia is thought to cause dyskinesia, alteration

189 dorsal striatum, a major input structure of basal ganglia, is composed of two opponent pathways, dir

190 ng how the expected reward is learned in the basal ganglia, it is not known how reward uncertainty is

191 The striatum, the entry nucleus of the basal ganglia, lacks laminar or columnar organization of

192 Area X in basal ganglia, lateral magnocellular nucleus of the ante

193 Bilateral basal ganglia lesions were the most common finding in br

194 ons emerge in the normal functioning cortico-basal ganglia loop during behavior.

195 ch movement control is attributed to cortico-basal ganglia loops, yet population dynamics within thes

196 influence on synchronous activity in cortico-basal-ganglia loops remains to be fully characterized.

197 None, however, displayed the basal ganglia malformations typically associated with TU

198 Diffusion-weighted imaging in the basal ganglia may provide a noninvasive biomarker in fut

199 ise interrupts cognition via the same fronto-basal ganglia mechanism that interrupts action.

200 s were compared across 72 individuals in the basal ganglia, midbrain, thalamus, dentate nucleus, cere

201 glia motor circuit; while dysfunction of the basal ganglia motor circuit and disconnection between th

202 crographia was related to the dysfunction of basal ganglia motor circuit together with disconnections

203 icrographia by restoring the function of the basal ganglia motor circuit, but does not improve progre

204 y increased activity and connectivity in the basal ganglia motor circuit, but had no effect on progre

205 icrographia is related to dysfunction of the basal ganglia motor circuit; while dysfunction of the ba

206 h decreased activity and connectivity in the basal ganglia motor circuit; while progressive micrograp

207 erve of the midbrain dopamine and integrated basal ganglia motor systems to control movement.

208 Basal ganglia MRI signal abnormalities were observed in

209 mporal lobe atrophy scores and single voxel (basal ganglia) N-acetylaspartate (NAA)/Choline, NAA/Crea

210 ly observed across the sensorimotor cortical-basal ganglia network after cessation of voluntary movem

211 ion using a polymodal approach could combine basal ganglia network connectivity with clinical and oth

212 state functional magnetic resonance imaging basal ganglia network dysfunction and loss of dopaminerg

213 Connectivity measures of basal ganglia network dysfunction differentiated both ra

214 ctional magnetic resonance imaging to detect basal ganglia network dysfunction in rapid eye movement

215 omising biomarker for the detection of early basal ganglia network dysfunction, and may help to ident

216 tic resonance imaging dysfunction within the basal ganglia network is a feature of early Parkinson's

217 y neurons (MSNs) are a key population in the basal ganglia network, and their degeneration causes a s

218 e loss and aberrant striatal inputs into the basal ganglia network.

219 tate, possibly by bypassing the pathological basal ganglia network.

220 ere extracted from the study subjects in the basal ganglia network.

221 tating information processing in the cortico-basal ganglia network.

222 pose that unexpected events recruit a fronto-basal-ganglia network for stopping.

223 e dorsal striatum and disruptions of cortico-basal ganglia networks across a broad range of disorders

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

225 s in mice, we explored how ageing of cortico-basal ganglia networks alters the microstructure of acti

226 thesis that pathological movement-inhibiting basal ganglia networks in PD patients are bypassed durin

227 lts reveal static properties of aged cortico-basal ganglia networks that introduce temporal limits to

228 e cerebellum-thalamo-cortical and the fronto-basal-ganglia networks regulating inhibitory control.

229 , indicating a possible link between altered basal ganglia neurodevelopment and declined motor perfor

230 s indicate a potential evolutionary shift in basal ganglia neurotransmission in humans that may favor

231 s from the globus pallidus externus (GPe), a basal ganglia nucleus not previously known to participat

232 symmetrical, bilateral calcifications in the basal ganglia, nucleus gyrus and cerebral cortex.

233 ions of the executive and motor loops of the basal ganglia of humans, great apes, and monkeys.

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

235 en implicated in sensorimotor control in the basal ganglia of task-performing healthy animals.

236 lly caused by non-progressive lesions to the basal ganglia or thalamus, or both, and is characterised

237 rives tremulous network activity through the basal ganglia or the cerebello-thalamo-cortical loop and

238 as the matrix-striosome organization of the basal ganglia or the patch-interpatch organization of th

239 cally or as a result of impaired cerebellar, basal ganglia, or peripheral feedback.

240 Classical schemes of basal ganglia organization posit that parkinsonian movem

241 ng optogenetics, we examined the role of the basal ganglia output in interval timing.

242 mice and attenuates pathological activity of basal ganglia output neurons for hours beyond stimulatio

243 in the synchrony of a modeled population of basal ganglia output neurons receiving excitatory and in

244 antia nigra pars reticulata (SNR), the major basal ganglia output nucleus, during self-initiated drin

245 cellular and circuit complexity involving a basal ganglia output structure, the entopeduncular nucle

246 with a putative global suppressive effect on basal-ganglia output.

247 The contribution of basal ganglia outputs to consummatory behavior remains p

248 undation for an integrated approach to study basal ganglia pathologies such as Parkinson's disease in

249 Two basal ganglia pathways have been classically hypothesize

250 Deficits in the basal ganglia pathways modulating cortical motor activit

251 are an imbalance between indirect and direct basal ganglia pathways, disturbed sensory processing, an

252 he mutually antagonistic direct and indirect basal ganglia pathways.

253 l regions, and increases in white matter and basal ganglia perfusion, with effect sizes ranging from

254 ful for elucidating the functions of Rem2 in basal ganglia physiology.

255 at the thalamic subregions innervated by the basal ganglia preferentially interconnect with motor-rel

256 sed in, and regulate the development of, the basal ganglia primodia from which many GABAergic neurons

257 ted relative to stimulus-guided movements by basal ganglia processing.

258 We recorded basal ganglia-projecting dopamine neurons in singing zeb

259 een arthropod central complex and vertebrate basal ganglia provide an opportunity to examine whether

260 Dopamine in the basal ganglia reduces trial-to-trial neural variability

261 sure of dopaminergic innervation within five basal ganglia regions in humans, great apes, and New and

262 ited a larger network of frontal control and basal ganglia regions than within-language competition.

263 Surprisingly, basal ganglia regions that receive sparse or no VTA dopa

264 loration is induced by LMAN, the output of a basal ganglia-related circuit that also contributes a co

265 rged as key actors in the pathophysiology of basal-ganglia-related movement disorders.

266 15.3 in frontal cortex and nucleus accumbens basal ganglia, respectively, were significantly regulate

267 ults suggest that dopaminergic inputs to the basal ganglia selectively mediate reinforcement-driven v

268 lthough cortical SI may fluctuate, increased basal ganglia SI is a consistent finding and is due to r

269 childhood-onset dystonia, optic atrophy, and basal ganglia signal abnormalities on MRI.

270 s differential damage to the hippocampus and basal ganglia (specifically nigrostriatal pathways).

271 ons, there is an opportunity not only to map basal ganglia structures but also to gain insights into

272 face-based morphometry method on 3 bilateral basal ganglia structures in school-age children chronica

273 significant enlargement of many areas of the basal ganglia structures, preferentially affecting the p

274 riatum, which in turn projects to downstream basal ganglia structures.

275 rom single-unit data recorded from different basal ganglia subregions in rats performing a cued choic

276 e also expressed on GABAergic neurons of the basal ganglia, substantia nigra, and ventral tegmental a

277 Cortico-basal ganglia-thalamic (CBT) neural circuits are critica

278 lamic nucleus (STN) is an element of cortico-basal ganglia-thalamo-cortical circuitry critical for ac

279 abnormalities, supporting the involvement of basal ganglia-thalamocortical circuits, representing emo

280 ial entrainment of structures throughout the basal ganglia-thalamocortical loop in the lesioned hemis

281 Strikingly, when applied to the brain-wide basal ganglia-thalamocortical network, DCM accurately re

282 f regions including the reticular formation, basal ganglia, thalamus, posterior cingulate cortex (PCC

283 tive, excitatory interneuron in the songbird basal ganglia that makes strong synaptic connections ont

284 irectly through ascending projections to the basal ganglia that project down to brainstem locomotor n

285 ms within neurocircuitries that comprise the basal ganglia, the extended amygdala, and the prefrontal

286 physiology of and synaptic plasticity in the basal ganglia, they explain the effects of dopaminergic

287 tics in mice, we show that the output of the basal ganglia through the substantia nigra pars reticula

288 ory theories of OCD should extend beyond the basal ganglia to include the cortico-striato-thalamo-cor

289 We obtained the basal ganglia transcriptome by RNA sequencing in the cau

290 aminobutyric acid (GABA)ergic input from the basal ganglia via both the ipsilateral and the contralat

291 data, including whole-brain, hippocampal and basal ganglia volumetry; white matter integrity (diffusi

292 ty of MRI-visible perivascular spaces in the basal ganglia was associated with clinically diagnosed s

293 Additionally, bilinguals' activation of the basal ganglia was inversely correlated with their execut

294 18F-AV-1451 binding to the basal ganglia was strong in all groups in vivo.

295 knockdown in the cerebellum, but not in the basal ganglia, was sufficient to induce dystonia.

296 T1-bright basal ganglia were confined to LGI1-IgG-positive patient

297 frontal cortex and its interaction with the basal ganglia, where a more anterior corticostriatal loo

298 of Alzheimer's disease, whereas those in the basal ganglia would be associated with subcortical vascu

299 ributor to motor suppressing pathways in the basal ganglia, yet its neuronal heterogeneity has remain

300 In contrast, the ETI (arising from basal ganglia, zona incerta (ZI), anterior pretectum, an