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3 se results provide the first dynamic view of corticostriatal activity during bond formation, revealin
5 al and electrochemical recordings to examine corticostriatal activity in adolescent mice exposed to c
6 In this study, we highlight the key role of corticostriatal activity in determining the timing of in
7 resynaptic potentiation (PPP) that increased corticostriatal activity in direct pathway medium spiny
14 fect that was normalized by inhibiting these corticostriatal afferents immediately before the drug pr
15 ly, we reported that Sapap3 deletion reduces corticostriatal alpha-amino-3-hydroxy-5-methyl-4-isoxazo
16 d by adjusting effective connectivity within corticostriatal and cerebellar-striatal brain systems, t
17 by a change in effective connectivity within corticostriatal and cerebellar-striatal brain systems.
18 e tracer, we characterized the topography of corticostriatal and corticofugal projections arising in
19 m pyramidal neurons in layers 5A/B including corticostriatal and corticospinal neurons, implicating t
22 nt of habits but instead through interacting corticostriatal and striato-striatal processes that resu
23 used to measure synaptic transmission in the corticostriatal and thalamostriatal circuits of Sapap3 K
24 tural plasticity of excitatory synapses from corticostriatal and thalamostriatal pathways and their p
29 investigated neuronal oscillations along the corticostriatal axis in rats during rest and treadmill r
31 o effects of enhanced glutamate release from corticostriatal axons and postsynaptic PKA and discovere
32 ion neurons was associated with increases in corticostriatal BDNF, with assessments done at 10 weeks
37 gly, when proteotoxicity was assessed in rat corticostriatal brain slices, either flanking region alo
38 kinetic rats and that this rewiring involves corticostriatal but not thalamostriatal contacts onto MS
41 related behaviors, focusing attention on the corticostriatal circuit for mediating the behavioral abn
44 tinuation phase of the SCT suggests that the corticostriatal circuit is involved in the control of in
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 specific neural correlates of HI within the corticostriatal circuitry and determined how they intera
52 initiation, suggesting dynamic modulation of corticostriatal circuitry contributes to the choreograph
55 cipitate these changes through modulation of corticostriatal circuitry involved in reinforcement lear
56 ex predicted pain persistence, implying that corticostriatal circuitry is causally involved in the tr
59 he hippocampus and its interactions with the corticostriatal circuitry via the application of model-b
60 ocused primarily on the contributions of the corticostriatal circuitry, involved in trial-and-error r
64 rebrain and suggest that striosome-targeting corticostriatal circuits can underlie neural processing
65 n within and/or between limbic and executive corticostriatal circuits contributes to such symptoms.
67 cal studies that have focused on the role of corticostriatal circuits in context-induced reinstatemen
69 reasing evidence implicates abnormalities in corticostriatal circuits in the pathophysiology of obses
71 tive to neutral autobiographical memories in corticostriatal circuits that also responded to monetary
72 idence detection of oscillatory processes in corticostriatal circuits that can be mapped onto the sta
73 re, different forms of a signal exist within corticostriatal circuits that evolve across a sequence o
74 hought to require synaptic plasticity within corticostriatal circuits that route information through
75 ngs indicate that Cdh8 delineates developing corticostriatal circuits where it is a strong candidate
76 nes, which are interconnected with separable corticostriatal circuits, and are crucial for the organi
77 ist that may interact to persistently sculpt corticostriatal circuits, potentially influencing action
83 also provide bidirectional modulation of the corticostriatal circuits; (3) dopaminergic and GABAergic
84 ible for synaptic loss in HD, we developed a corticostriatal coculture model that features age-depend
88 t of these interactions aligned closely with corticostriatal conduction delays, demonstrating highly
89 pair BDNF-TrkB survival signaling within the corticostriatal connection that is most affected in HD.
92 ses were performed on a composite measure of corticostriatal connectivity derived from the significan
97 d is underpinned by striatal activations and corticostriatal connectivity similar to other human affi
103 al-directed learning revealed dysfunction in corticostriatal control associated with a profound defic
104 in 72 subjects in fMRI, we investigated the corticostriatal correlates of goal-directed learning and
105 its in cortical axonal projections including corticostriatal, corticospinal, and corticothalamic trac
108 hese data suggest that during motor learning corticostriatal dynamics encode the refinement of specif
109 How GABA abnormalities might contribute to corticostriatal dysfunction in OCD deserves further stud
112 hat challenges and refines existing views of corticostriatal function and expose neuronal projection-
115 aptic mechanisms of inhibitory modulation of corticostriatal function that probably contribute to the
119 ectrophysiological activity, and (v) altered corticostriatal functional connectivity and plasticity.
120 ncreased striatal activation and potentiated corticostriatal functional connectivity between the nucl
121 iated reward-related striatal activation and corticostriatal functional connectivity in depressed ind
122 ncluding assessment of social behaviors, and corticostriatal functional connectivity was evaluated in
125 nce of major OCD symptom dimensions on brain corticostriatal functional systems in a large sample of
129 ceptors exert marked inhibitory control over corticostriatal glutamate release in the DLS, yet the si
130 f RO5166017 prevented the increase of evoked corticostriatal glutamate release provoked by dopamine d
132 tment of marijuana dependence and underscore corticostriatal glutamatergic neurotransmission as a pos
133 d (ii) deleting CB1 receptors selectively in corticostriatal glutamatergic or striatal GABAergic neur
134 glutamatergic neurons, and (ii) manipulating corticostriatal glutamatergic projections remotely with
135 tors (M4Rs) promoted long-term depression of corticostriatal glutamatergic synapses, by suppressing r
138 ological studies showing overactivity of the corticostriatal glutamatergic system in models of parkin
141 iously hypothesized increased sensitivity of corticostriatal glutamatergic terminals in the rodent wi
143 regulation emerge, we recorded stepwise from corticostriatal (HVC) neurons and their target spiny and
146 on the interplay between incoming excitatory corticostriatal inputs and the internal striatal state.
147 al mouse striatum controls synaptogenesis of corticostriatal inputs and vocalization in neonates.
148 ptic integration between thalamostriatal and corticostriatal inputs, which might alter the action sel
150 is known about the development of functional corticostriatal interactions, and in particular, virtual
154 vated motor memory altered offline task-free corticostriatal interregional functional connectivity, r
157 h functional and structural abnormalities in corticostriatal-limbic brain regions, which may explain
161 hese impairments are associated with altered corticostriatal long-term potentiation (LTP) and specifi
162 The caudate nucleus is a part of the visual corticostriatal loop (VCSL), receiving input from differ
163 vide evidence for the contribution of visual corticostriatal loop and the caudate nucleus on generati
164 ith the basal ganglia, where a more anterior corticostriatal loop establishes task-set selection, whi
169 ological similarities and differences in the corticostriatal mechanisms of context-induced reinstatem
170 ased glutamate release following PCE, normal corticostriatal modulation by dopamine was reestablished
171 A data-driven computational model of the corticostriatal network closely replicated the temporal
172 gest a clear functional dichotomy within the corticostriatal network, pointing to disparate temporal
173 uld be the result of dopamine dysfunction in corticostriatal networks (salience, central executive ne
174 tanding of the relationship between distinct corticostriatal networks and intertemporal preferences i
175 ivity is associated with altered function of corticostriatal networks, the specific neural substrates
177 function are associated with alterations in corticostriatal neurocircuitry, which may reflect abnorm
178 eurons (n = 153) and intratelencephalic-type corticostriatal neurons (n = 126) in the M1 of two monke
180 elrhodopsin-2 (ChR2)-mediated stimulation of corticostriatal neurons during the task biased decisions
183 Both corticospinal and callosally projecting corticostriatal neurons in layer 5B formed within-class
184 and projection-class specific, restricted to corticostriatal neurons in upper layer 5B and not neighb
185 of these neurons reveals that stimulation of corticostriatal neurons promotes conditioned reward-seek
186 vely for synaptic plasticity associated with corticostriatal neurons representing different frequenci
187 ed projection targets reveal that individual corticostriatal neurons show response tuning to reward-p
188 rons (callosal projection neurons similar to corticostriatal neurons) similarly received a paucity of
195 ned serotonergic modulation of rat and mouse corticostriatal neurotransmission and find that serotoni
197 dent modulation of activity propagation in a corticostriatal pathway important to song variability, a
198 AR) signaling is important for modulation of corticostriatal pathways and prefrontal activity during
200 human affiliative bonds; highlight specific corticostriatal pathways as defining distinct coparental
201 onnectivity patterns differentiated distinct corticostriatal pathways associated with two stable copa
203 he shifting dynamics of functionally defined corticostriatal pathways during skill learning in mice u
204 ndings suggest that integrity of dissociable corticostriatal pathways underlies individual difference
205 s aberrant learning results from maladaptive corticostriatal plasticity and learned motor inhibition.
207 gulatory mechanisms underlying bidirectional corticostriatal plasticity are not fully understood.
209 l task in rodents to investigate the role of corticostriatal plasticity in abstract skill learning.
212 wever, dopamine denervation induces aberrant corticostriatal plasticity that degrades established syn
214 DA receptors impairs the development of this corticostriatal plasticity, and disrupts the ability to
215 lpha-syn, and deficits in dopamine-dependent corticostriatal plasticity, which, in the absence of ove
219 Dopamine denervation gives rise to abnormal corticostriatal plasticity; however, its role in the sym
221 ging studies provide insights into executive corticostriatal processes related to extraordinary inhib
222 ne (cell-autonomous model) or by mhtt in the corticostriatal projection cell-cell interaction model,
224 s), whereas the latter type included crossed corticostriatal projection neurons (cCStrPNs) and crosse
227 B1R heteromer (i) is essentially absent from corticostriatal projections and striatonigral neurons, a
229 urologically plausible network of converging corticostriatal projections that may support the integra
233 translational profiling to show that layer 5 corticostriatal pyramidal cells expressing p11 (S100a10)
234 was associated with selective disruption of corticostriatal resting functional MR imaging correlatio
235 increased inflammation in depression affects corticostriatal reward circuitry to lead to deficits in
237 cue-dependent behaviors are modified through corticostriatal signaling whereby short-term increases i
238 that synaptic transmission was depressed in corticostriatal slices after perfusion with cocaine (10
243 imental paradigm that achieves bidirectional corticostriatal STDP in vivo through modulation by behav
244 teration of NMDA receptor composition at the corticostriatal synapse contributes not only to the clin
246 Bidirectional long-term plasticity at the corticostriatal synapse has been proposed as a central c
247 n mice to isolate the source and target of a corticostriatal synapse that regulates the performance o
248 etylcholine receptor reduces transmission at corticostriatal synapses and that this effect is dramati
249 ine responses and point to depotentiation at corticostriatal synapses as a possible therapeutic targe
250 t in increased transmission at glutamatergic corticostriatal synapses at early presymptomatic stages
251 ry discrimination preferentially potentiates corticostriatal synapses from neurons representing eithe
253 Our findings suggest a model in which the corticostriatal synapses made by neurons tuned to differ
255 INTERPRETATION: The dynamic alterations at corticostriatal synapses that occur in response to PCE p
265 The dynamics of thalamostriatal, but not corticostriatal, synapses were modulated by histamine le
267 t iSPN intrinsic excitability and excitatory corticostriatal synaptic connectivity were lower in PD m
269 al or striatal neurons partially ameliorates corticostriatal synaptic deficits, further restoration o
270 e (HD) mutant Huntingtin (mHtt) causes early corticostriatal synaptic dysfunction and eventual neurod
272 ease is associated with early alterations in corticostriatal synaptic function that precede cell deat
273 cellular basis for regulating bidirectional corticostriatal synaptic plasticity and may help to iden
275 es the internalization of AMPARs and reduces corticostriatal synaptic strength, dephosphorylates DARP
278 bjects, involved widespread dysregulation of corticostriatal systems characterized most prominently b
280 xp2 phenotype reflects a different tuning of corticostriatal systems involved in declarative and proc
281 endent individuals had abnormal structure of corticostriatal systems, and variability in the extent o
282 associated with pronounced dysregulation of corticostriatal systems, characterized most prominently
283 oordinated activity in the corticospinal and corticostriatal systems, which are involved in different
286 in ACC/OFC to determine the extent to which corticostriatal terminal fields overlapped with these co
288 lutamate release that was most pronounced in corticostriatal terminals with a low probability of rele
292 Together, local phase-amplitude coupling and corticostriatal theta phase coupling mediated the tempor
294 unidirectional signaling from higher-order (corticostriatal) to lower-order (corticospinal) output n
296 derlying PDE10A inhibitor-induced changes in corticostriatal transmission are only partially understo
297 hus, stimulation of PDE10A acts to attenuate corticostriatal transmission in a manner largely depende
298 ic investigation of the processes regulating corticostriatal transmission is key to understanding DLS
299 logical interventions that reverse excessive corticostriatal transmission may provide a novel approac
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