ライフサイエンスコーパス: corticostriatal

1 Previous evidence has implicated corticostriatal abnormalities in the pathophysiology of

2 As training progressed, variability in corticostriatal activity became progressively more corre

3 se results provide the first dynamic view of corticostriatal activity during bond formation, revealin

4 Therefore, a chronic decrease in corticostriatal activity during withdrawal is regulated

5 In this study, we highlight the key role of corticostriatal activity in determining the timing of in

6 resynaptic potentiation (PPP) that increased corticostriatal activity in direct pathway medium spiny

7 in G2019S mutants, supporting that abnormal corticostriatal activity is involved.

8 correlated with deficient reorganisation of corticostriatal activity.

9 n, which promoted a reversible depression in corticostriatal activity.

10 We first review constitutive corticostriatal adaptations that are elicited by and sha

11 However, inhibiting corticostriatal afferent activity during sensitization s

12 Corticostriatal afferents can engage parvalbumin-express

13 fect that was normalized by inhibiting these corticostriatal afferents immediately before the drug pr

14 Optogenetic stimulation of S1-corticostriatal afferents in ex vivo recordings produced

15 cally, in vivo optogenetic stimulation of S1-corticostriatal afferents produced task-specific behavio

16 eld recordings and electrical stimulation of corticostriatal afferents revealed that histamine, actin

17 eurons (SPNs), an effect not observed for M1-corticostriatal afferents.

18 ly, we reported that Sapap3 deletion reduces corticostriatal alpha-amino-3-hydroxy-5-methyl-4-isoxazo

19 s, show widespread structural differences in corticostriatal and limbic networks.

20 We find that corticostriatal and spiny neurons both show precise sing

21 nt of habits but instead through interacting corticostriatal and striato-striatal processes that resu

22 used to measure synaptic transmission in the corticostriatal and thalamostriatal circuits of Sapap3 K

23 tural plasticity of excitatory synapses from corticostriatal and thalamostriatal pathways and their p

24 SAPAP isoforms at corticostriatal and thalamostriatal synapses were detect

25 e are two main excitatory synaptic circuits, corticostriatal and thalamostriatal.

26 mates, and delineate additional loops in the corticostriatal architecture, consisting of interconnect

27 Corticostriatal atrophy is a cardinal manifestation of H

28 to regulate neuronal interactions along the corticostriatal axis and beyond.

29 investigated neuronal oscillations along the corticostriatal axis in rats during rest and treadmill r

30 The corticostriatal axis is the main input stage of the basa

31 o effects of enhanced glutamate release from corticostriatal axons and postsynaptic PKA and discovere

32 STATEMENT Motor learning in mice depends on corticostriatal BDNF supply, and regulation of BDNF expr

33 ns of the striatum, implicating cortical and corticostriatal brain circuits.

34 is dependent upon dopamine D2/3 signaling in corticostriatal brain regions.

35 effect not only in cell culture, but also in corticostriatal brain slice cultures.

36 gly, when proteotoxicity was assessed in rat corticostriatal brain slices, either flanking region alo

37 kinetic rats and that this rewiring involves corticostriatal but not thalamostriatal contacts onto MS

38 neurons (SPNs) and a concomitant increase in corticostriatal circuit activity.

39 We demonstrate that Hoxb8 mutants contain corticostriatal circuit defects.

40 related behaviors, focusing attention on the corticostriatal circuit for mediating the behavioral abn

41 st that Foxp2-Mef2C signaling is critical to corticostriatal circuit formation.

42 ve our understanding of how nicotine changes corticostriatal circuit function and communication durin

43 We recreated the corticostriatal circuit in microfluidic chambers, pairin

44 tinuation phase of the SCT suggests that the corticostriatal circuit is involved in the control of in

45 r data show that astrocyte engagement in the corticostriatal circuit is markedly altered in HD.

46 otein contributes to the degeneration of the corticostriatal circuit is not well understood.

47 re the rules for astrocyte engagement in the corticostriatal circuit of adult wild-type (WT) and Hunt

48 dial prefrontal cortex (mPFC), a node in the corticostriatal circuit that is thought to play a role i

49 tivity map of five major neuron types in the corticostriatal circuit, as well as an activity-based ma

50 n increased inflammation and altered DAergic corticostriatal circuitry and behavior in patients with

51 Z3 in the development and functioning of the corticostriatal circuitry and provides evidence that dys

52 initiation, suggesting dynamic modulation of corticostriatal circuitry contributes to the choreograph

53 Thus, our results support a novel role for corticostriatal circuitry in pain regulation.

54 cipitate these changes through modulation of corticostriatal circuitry involved in reinforcement lear

55 ic pathway that may drive changes in DAergic corticostriatal circuitry is inflammation.

56 Our results indicate that variation in corticostriatal circuitry may play a role in the relatio

57 ng whether functional connectivity of dorsal corticostriatal circuitry, which is disrupted in psychos

58 connectivity to examine the impact of DUP on corticostriatal circuitry.

59 sms were related to activity in sensorimotor corticostriatal circuitry.

60 tions with distant cortical areas outside of corticostriatal circuitry.

61 ing new questions on the architecture of the corticostriatal circuitry.SIGNIFICANCE STATEMENT Project

62 rebrain and suggest that striosome-targeting corticostriatal circuits can underlie neural processing

63 s and histamine's role in the development of corticostriatal circuits have remained understudied.

64 cal studies that have focused on the role of corticostriatal circuits in context-induced reinstatemen

65 reasing evidence implicates abnormalities in corticostriatal circuits in the pathophysiology of obses

66 FoxP2 is enriched in corticostriatal circuits of both human and songbird brai

67 tive to neutral autobiographical memories in corticostriatal circuits that also responded to monetary

68 re, different forms of a signal exist within corticostriatal circuits that evolve across a sequence o

69 hought to require synaptic plasticity within corticostriatal circuits that route information through

70 ngs indicate that Cdh8 delineates developing corticostriatal circuits where it is a strong candidate

71 nes, which are interconnected with separable corticostriatal circuits, and are crucial for the organi

72 nvestigated how histamine affects developing corticostriatal circuits, both acutely and longer-term,

73 d controls longer-term changes in developing corticostriatal circuits, thus providing insight into th

74 ce statistics relates to plasticity in motor corticostriatal circuits, while selecting the most proba

75 ance in the caudate leading to dysfunctional corticostriatal circuits.

76 rogressive dysfunction and neuronal death in corticostriatal circuits.

77 l representations of sequence progression in corticostriatal circuits.

78 pal dependence, a timescale known to require corticostriatal circuits.

79 sive-compulsive disorder, and dysfunction of corticostriatal circuits.

80 ticity in visual, motivational and executive corticostriatal circuits.

81 ible for synaptic loss in HD, we developed a corticostriatal coculture model that features age-depend

82 We report here that corticostriatal cocultures prepared from YAC128 HD mice

83 ally defined type of cortical interneuron in corticostriatal communication.

84 n neither case, however, was the strength of corticostriatal connections globally scaled.

85 Continuing investigations of corticostriatal connections in rodents emphasize an intr

86 Dopamine (DA) modulates corticostriatal connections.

87 As a result, striatum and corticostriatal connectivity are highly sensitive to acu

88 ses were performed on a composite measure of corticostriatal connectivity derived from the significan

89 Neuronal dysfunction and altered corticostriatal connectivity have been postulated to be

90 Stronger corticostriatal connectivity in response to rewards pred

91 These findings suggest that decreased corticostriatal connectivity may serve as a target for a

92 We propose that late development of corticostriatal connectivity sets the stage for optimal

93 d is underpinned by striatal activations and corticostriatal connectivity similar to other human affi

94 Furthermore, disturbance to corticostriatal connectivity was more pervasive in treat

95 may be constrained by ongoing maturation of corticostriatal connectivity.

96 tment response was significantly mediated by corticostriatal connectivity.

97 al-directed learning revealed dysfunction in corticostriatal control associated with a profound defic

98 in 72 subjects in fMRI, we investigated the corticostriatal correlates of goal-directed learning and

99 tiation of glutamatergic transmission at the corticostriatal D2->D1 synapse.

100 imultaneously and nonsimultaneously recorded corticostriatal datasets.

101 Finally, these corticostriatal deregulations resulted in a behavioral p

102 k demonstrates Nrp2 to be a key regulator of corticostriatal development, maintenance, and function,

103 not model-free, learning is associated with corticostriatal dopamine tone.

104 hese data suggest that during motor learning corticostriatal dynamics encode the refinement of specif

105 and synaptic abnormalities that may underlie corticostriatal dysfunction relevant to OCD, we used the

106 Theta-burst stimulation of corticostriatal fibres produces long-term potentiation (

107 hat challenges and refines existing views of corticostriatal function and expose neuronal projection-

108 A data-driven computational model of corticostriatal function closely replicated the temporal

109 target for future therapies aimed to restore corticostriatal function in HD.

110 aptic mechanisms of inhibitory modulation of corticostriatal function that probably contribute to the

111 ng-related in vivo modulation of presynaptic corticostriatal function.

112 rize risk- and resilience-related changes in corticostriatal functional circuits in individuals expos

113 ectrophysiological activity, and (v) altered corticostriatal functional connectivity and plasticity.

114 ncreased striatal activation and potentiated corticostriatal functional connectivity between the nucl

115 We evaluated corticostriatal functional connectivity differences by p

116 iated reward-related striatal activation and corticostriatal functional connectivity in depressed ind

117 ncluding assessment of social behaviors, and corticostriatal functional connectivity was evaluated in

118 Our results indicated that corticostriatal functional dysconnectivity in psychosis

119 nce of major OCD symptom dimensions on brain corticostriatal functional systems in a large sample of

120 in the xCT(-/-) mice; in tests sensitive to corticostriatal functioning we recorded increased repeti

121 Corticostriatal gene expression profiles are predominate

122 Our convergent data demonstrate how corticostriatal GluN2B circuits govern the ability to le

123 Finally, inhibition of corticostriatal glutamate release by TAAR1 showed mechan

124 ceptors exert marked inhibitory control over corticostriatal glutamate release in the DLS, yet the si

125 f RO5166017 prevented the increase of evoked corticostriatal glutamate release provoked by dopamine d

126 In contrast to corticostriatal glutamatergic inputs onto FSIs, which ar

127 tment of marijuana dependence and underscore corticostriatal glutamatergic neurotransmission as a pos

128 d (ii) deleting CB1 receptors selectively in corticostriatal glutamatergic or striatal GABAergic neur

129 glutamatergic neurons, and (ii) manipulating corticostriatal glutamatergic projections remotely with

130 to modulate medium spiny neuron responses to corticostriatal glutamatergic signaling acutely, and we

131 tors (M4Rs) promoted long-term depression of corticostriatal glutamatergic synapses, by suppressing r

132 Indeed, disrupted plasticity at corticostriatal glutamatergic synapses, the gateway of t

133 insic excitability and pruning of excitatory corticostriatal glutamatergic synapses.

134 BID rats showed hypersensitivity of corticostriatal glutamatergic terminals (lower frequency

135 INTERPRETATION: Hypersensitivity of corticostriatal glutamatergic terminals can constitute a

136 iously hypothesized increased sensitivity of corticostriatal glutamatergic terminals in the rodent wi

137 mate upon local light-induced stimulation of corticostriatal glutamatergic terminals.

138 regulation emerge, we recorded stepwise from corticostriatal (HVC) neurons and their target spiny and

139 riggers increased SPN excitatory synapse and corticostriatal hyperconnectivity.

140 PDE10 inhibition restored corticostriatal input and boosted cortically driven indi

141 on the interplay between incoming excitatory corticostriatal inputs and the internal striatal state.

142 al mouse striatum controls synaptogenesis of corticostriatal inputs and vocalization in neonates.

143 Here, we find that corticostriatal inputs from whisker-related primary soma

144 sic striatal dysfunction or abnormalities in corticostriatal inputs.

145 Convergent evidence suggests that corticostriatal interactions act as a gate to select the

146 is known about the development of functional corticostriatal interactions, and in particular, virtual

147 These observations extend current models of corticostriatal interactions, suggesting more complex mo

148 nformative reward properties are encoded via corticostriatal interactions.

149 rd properties were differentially encoded in corticostriatal interactions.

150 We show that loss of corticostriatal, interhemispheric, and intrahemispheric

151 vated motor memory altered offline task-free corticostriatal interregional functional connectivity, r

152 This slow remodeling of corticostriatal iSPN circuitry is likely to play a role

153 located, almost everywhere the proportion of corticostriatal labeled neurons in layers III and/or VI

154 regions, the laminar distribution pattern of corticostriatal labeled neurons largely varied independe

155 h functional and structural abnormalities in corticostriatal-limbic brain regions, which may explain

156 Our results describe a corticostriatal long-range inhibitory circuit (CS-SOM in

157 Dopaminergic modulation of both corticostriatal long-term depression (LTD) and long-term

158 hese impairments are associated with altered corticostriatal long-term potentiation (LTP) and specifi

159 The caudate nucleus is a part of the visual corticostriatal loop (VCSL), receiving input from differ

160 vide evidence for the contribution of visual corticostriatal loop and the caudate nucleus on generati

161 ith the basal ganglia, where a more anterior corticostriatal loop establishes task-set selection, whi

162 al level through catecholamine influences on corticostriatal loops.

163 emonstrated a key role for cAMP signaling in corticostriatal LTD.

164 riatal disturbances in HD and underlie early corticostriatal LTP and cognitive defects.

165 Our results demonstrate that TBS evokes corticostriatal LTP, and that optogenetic activation of

166 ological similarities and differences in the corticostriatal mechanisms of context-induced reinstatem

167 We here present a corticostriatal model identifying three mechanisms that

168 A data-driven computational model of the corticostriatal network closely replicated the temporal

169 gest a clear functional dichotomy within the corticostriatal network, pointing to disparate temporal

170 uld be the result of dopamine dysfunction in corticostriatal networks (salience, central executive ne

171 hown that cognitive control engages multiple corticostriatal networks and brainstem nuclei, but theor

172 tanding of the relationship between distinct corticostriatal networks and intertemporal preferences i

173 ivity is associated with altered function of corticostriatal networks, the specific neural substrates

174 electively connected but broadly distributed corticostriatal networks.

175 function are associated with alterations in corticostriatal neurocircuitry, which may reflect abnorm

176 eurons (n = 153) and intratelencephalic-type corticostriatal neurons (n = 126) in the M1 of two monke

177 f both sexes to identify thalamostriatal and corticostriatal neurons during extracellular recordings,

178 Here, we demonstrate that S100a10 corticostriatal neurons exhibit distinct serotonin respo

179 Corticostriatal neurons in motor and somatosensory corte

180 present study shows that the distribution of corticostriatal neurons in the various layers of the pri

181 udy, we analyzed the laminar distribution of corticostriatal neurons projecting to different parts of

182 of these neurons reveals that stimulation of corticostriatal neurons promotes conditioned reward-seek

183 Whereas corticostriatal neurons provide a more accurate represen

184 vely for synaptic plasticity associated with corticostriatal neurons representing different frequenci

185 ed projection targets reveal that individual corticostriatal neurons show response tuning to reward-p

186 and the laminar distribution of the labeled corticostriatal neurons was analyzed quantitatively.

187 ound-evoked responses of thalamostriatal and corticostriatal neurons, our work demonstrates that thes

188 ype neurons (-50%) but essentially absent in corticostriatal neurons.

189 corticoamygdala neurons compared with nearby corticostriatal neurons.

190 get layer 2 corticoamygdala over neighboring corticostriatal neurons.

191 ful at corticoamygdala neurons compared with corticostriatal neurons.

192 a previously unrecognized role in regulating corticostriatal neurotransmission and influences social

193 st time, that GABAergic synapse formation in corticostriatal pairs depends on two parallel, but poten

194 l for the development and maintenance of the corticostriatal pathway and may shed novel insights on n

195 n neurodevelopmental disorders linked to the corticostriatal pathway and Semaphorin signaling.SIGNIFI

196 aphorin signaling.SIGNIFICANCE STATEMENT The corticostriatal pathway controls sensorimotor, learning,

197 e, we investigated potential sites along the corticostriatal pathway for the integration of sound sig

198 dent modulation of activity propagation in a corticostriatal pathway important to song variability, a

199 ntegrated with reward signals throughout the corticostriatal pathway, potentially contributing to ada

200 Corticostriatal pathways are an ideal neural substrate f

201 human affiliative bonds; highlight specific corticostriatal pathways as defining distinct coparental

202 onnectivity patterns differentiated distinct corticostriatal pathways associated with two stable copa

203 Findings suggest that corticostriatal pathways contribute to the natural time

204 he shifting dynamics of functionally defined corticostriatal pathways during skill learning in mice u

205 s aberrant learning results from maladaptive corticostriatal plasticity and learned motor inhibition.

206 gulatory mechanisms underlying bidirectional corticostriatal plasticity are not fully understood.

207 Our results indicate that Hebbian corticostriatal plasticity can be induced by classical r

208 Corticostriatal plasticity was required for the reductio

209 ine and opiates, and alter the regulation of corticostriatal plasticity.

210 eby heightened D1R-SPN activity can regulate corticostriatal plasticity.

211 DCS and that DCS-induced learning results in corticostriatal plasticity.

212 els and the strength of excitatory inputs on corticostriatal plasticity.

213 ng and decision computations can emerge from corticostriatal plasticity.

214 We observe frequency-dependent corticostriatal potentiation in vivo over the course of

215 ging studies provide insights into executive corticostriatal processes related to extraordinary inhib

216 ne (cell-autonomous model) or by mhtt in the corticostriatal projection cell-cell interaction model,

217 The function of this corticostriatal projection in pain states, however, is n

218 s), whereas the latter type included crossed corticostriatal projection neurons (cCStrPNs) and crosse

219 We demonstrate the role of corticostriatal projection neurons in auditory decisions

220 pression during motor learning is highest in corticostriatal projection neurons in cortical layer II/

221 rning depends on synaptic plasticity between corticostriatal projections and striatal medium spiny ne

222 B1R heteromer (i) is essentially absent from corticostriatal projections and striatonigral neurons, a

223 How discrete, anatomically defined corticostriatal projections function in vivo to encode s

224 NF as a potential regulator of plasticity in corticostriatal projections in male and female mice.

225 urologically plausible network of converging corticostriatal projections that may support the integra

226 cator GCaMP6 to assess presynaptic Ca(2+) in corticostriatal projections to the DLS.

227 increased inflammation in depression affects corticostriatal reward circuitry to lead to deficits in

228 Depression is associated with alterations in corticostriatal reward circuitry.

229 rp2), influence dendritic spine maintenance, corticostriatal short-term plasticity, and learning in a

230 on striatal spiny projection neurons (SPNs), corticostriatal short-term plasticity, intrinsic physiol

231 that synaptic transmission was depressed in corticostriatal slices after perfusion with cocaine (10

232 lar, and structural changes were assessed in corticostriatal slices.

233 We found that the cortex, via corticostriatal somatostatin neurons (CS-SOM), has a dir

234 imental paradigm that achieves bidirectional corticostriatal STDP in vivo through modulation by behav

235 a neuronal phenomenon; astrocytes respond to corticostriatal stimulation and this astrocyte response

236 These data suggest that corticostriatal stimulation can compensate for deficits

237 Mef2c suppresses corticostriatal synapse formation and striatal spinogene

238 Bidirectional long-term plasticity at the corticostriatal synapse has been proposed as a central c

239 spines and presynaptic modifications at the corticostriatal synapse in the Nrp2 (-/-) mouse, but doe

240 n mice to isolate the source and target of a corticostriatal synapse that regulates the performance o

241 re we explore how dopaminergic plasticity at corticostriatal synapses alters competition between stri

242 stamine on longer-term changes at developing corticostriatal synapses and show that histamine facilit

243 etylcholine receptor reduces transmission at corticostriatal synapses and that this effect is dramati

244 t in increased transmission at glutamatergic corticostriatal synapses at early presymptomatic stages

245 Strengthening of the corticostriatal synapses depends on the second messenger

246 ry discrimination preferentially potentiates corticostriatal synapses from neurons representing eithe

247 iGlu (u) We report findings from individual corticostriatal synapses in acute slices prepared from m

248 Our findings suggest a model in which the corticostriatal synapses made by neurons tuned to differ

249 trophysiological and biochemical analyses at corticostriatal synapses of EAAT3(glo)/CMKII mice reveal

250 by adenosine A1 receptor (A1R) activation at corticostriatal synapses of the direct pathway [cortico-

251 We show that long-term depression (LTD) at corticostriatal synapses of the direct pathway is not st

252 e number, reduces short-term facilitation at corticostriatal synapses, and impairs goal-directed lear

253 spines, or the density or ultrastructure of corticostriatal synapses, indicating that the observed f

254 In contrast to corticostriatal synapses, thalamostriatal synaptic activ

255 lutamate concentration ([Glu]) at individual corticostriatal synapses, we can now quantify the time c

256 and can also modify long-term plasticity of corticostriatal synapses.

257 d to strengthening of a subset of excitatory corticostriatal synapses.

258 iation and decreased long-term depression in corticostriatal synapses.

259 spike-timing dependent plasticity (STDP) at corticostriatal synapses.

260 we uncovered decreased neurotransmission at corticostriatal synapses.

261 rtical projections, neuronal morphology, and corticostriatal synapses.

262 in the number but not strength of excitatory corticostriatal synapses.

263 controlling the induction of potentiation at corticostriatal synapses.

264 PAP4, is present at thalamostriatal, but not corticostriatal, synapses.

265 t iSPN intrinsic excitability and excitatory corticostriatal synaptic connectivity were lower in PD m

266 by the ratio of axo-spinous to axo-dendritic corticostriatal synaptic contacts was reduced.

267 al or striatal neurons partially ameliorates corticostriatal synaptic deficits, further restoration o

268 e (HD) mutant Huntingtin (mHtt) causes early corticostriatal synaptic dysfunction and eventual neurod

269 Thus, corticostriatal synaptic dysfunction early in HD is attr

270 paralleled by molecular changes in CPNs and corticostriatal synaptic dysfunctions.

271 ease is associated with early alterations in corticostriatal synaptic function that precede cell deat

272 Corticostriatal synaptic integration is partitioned amon

273 cellular basis for regulating bidirectional corticostriatal synaptic plasticity and may help to iden

274 at histamine permits NMDA receptor-dependent corticostriatal synaptic plasticity during an early crit

275 But how this interaction modulates corticostriatal synaptic plasticity underlying learned a

276 results reveal some of the prerequisites for corticostriatal synaptic plasticity, and explain recent

277 ese inputs are not fully understood, and the corticostriatal synaptic processes that support normal a

278 es the internalization of AMPARs and reduces corticostriatal synaptic strength, dephosphorylates DARP

279 egulating the development and maintenance of corticostriatal synaptic transmission are unclear.

280 ting at H(3) receptors, negatively modulates corticostriatal synaptic transmission from the first pos

281 M1) from excitatory cortical neurons impairs corticostriatal synaptic transmission in the dorsolatera

282 tes, increased excitatory synapses, enhanced corticostriatal synaptic transmission, and increased MSN

283 Corticostriatal systems are known to mediate choice lear

284 These findings highlight how corticostriatal systems contribute to reward processing,

285 xp2 phenotype reflects a different tuning of corticostriatal systems involved in declarative and proc

286 ects on cognition and emotion through limbic corticostriatal systems.

287 in ACC/OFC to determine the extent to which corticostriatal terminal fields overlapped with these co

288 enriched in adult layer V pyramidal neurons, corticostriatal terminals, and in developing and adult s

289 tein 2) immunoreactivity was reduced next to corticostriatal terminals.

290 Together, local phase-amplitude coupling and corticostriatal theta phase coupling mediated the tempor

291 gesting that falls reflect disruption of the corticostriatal transfer of movement-related cues and th

292 al and synaptic changes in CPNs and impaired corticostriatal transmission and plasticity.

293 derlying PDE10A inhibitor-induced changes in corticostriatal transmission are only partially understo

294 hus, stimulation of PDE10A acts to attenuate corticostriatal transmission in a manner largely depende

295 ynaptic, but not presynaptic, D2Rs inhibited corticostriatal transmission in an endocannabinoid-depen

296 Dopaminergic modulation of corticostriatal transmission is critically involved in r

297 ic investigation of the processes regulating corticostriatal transmission is key to understanding DLS

298 logical interventions that reverse excessive corticostriatal transmission may provide a novel approac

299 nNOS to limit cGMP production and excitatory corticostriatal transmission.

300 ds modified the ratio of direct and indirect corticostriatal weights within opposing action channels.