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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 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
8  in G2019S mutants, supporting that abnormal corticostriatal activity is involved.
9 n, which promoted a reversible depression in corticostriatal activity.
10  correlated with deficient reorganisation of corticostriatal activity.
11                 We first review constitutive corticostriatal adaptations that are elicited by and sha
12                          However, inhibiting corticostriatal afferent activity during sensitization s
13                                              Corticostriatal afferents can engage parvalbumin-express
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
20 s, show widespread structural differences in corticostriatal and limbic networks.
21                                 We find that corticostriatal and spiny neurons both show precise sing
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
25                            SAPAP isoforms at corticostriatal and thalamostriatal synapses were detect
26 e are two main excitatory synaptic circuits, corticostriatal and thalamostriatal.
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 ion neurons was associated with increases in corticostriatal BDNF, with assessments done at 10 weeks
33               Glutamatergic abnormalities in corticostriatal brain circuits are thought to underlie o
34 ns of the striatum, implicating cortical and corticostriatal brain circuits.
35 is dependent upon dopamine D2/3 signaling in corticostriatal brain regions.
36 effect not only in cell culture, but also in corticostriatal brain slice cultures.
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
39 neurons (SPNs) and a concomitant increase in corticostriatal circuit activity.
40    We demonstrate that Hoxb8 mutants contain corticostriatal circuit defects.
41 related behaviors, focusing attention on the corticostriatal circuit for mediating the behavioral abn
42 st that Foxp2-Mef2C signaling is critical to corticostriatal circuit formation.
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  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
53                             Dysregulation of corticostriatal circuitry has long been thought to be cr
54   Thus, our results support a novel role for corticostriatal circuitry in pain regulation.
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
57 ic pathway that may drive changes in DAergic corticostriatal circuitry is inflammation.
58       Our results indicate that variation in corticostriatal circuitry may play a role in the relatio
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
61 tions with distant cortical areas outside of corticostriatal circuitry.
62 connectivity to examine the impact of DUP on corticostriatal circuitry.
63 sms were related to activity in sensorimotor corticostriatal circuitry.
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.
66                       Although plasticity in corticostriatal circuits has been implicated in learning
67 cal studies that have focused on the role of corticostriatal circuits in context-induced reinstatemen
68 arning, and the interaction between multiple corticostriatal circuits in selection and learning.
69 reasing evidence implicates abnormalities in corticostriatal circuits in the pathophysiology of obses
70                         FoxP2 is enriched in corticostriatal circuits of both human and songbird brai
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
78 rogressive dysfunction and neuronal death in corticostriatal circuits.
79 l representations of sequence progression in corticostriatal circuits.
80 pal dependence, a timescale known to require corticostriatal circuits.
81 tion and motor-skill learning, in particular corticostriatal circuits.
82 ance in the caudate leading to dysfunctional corticostriatal circuits.
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
85                          We report here that corticostriatal cocultures prepared from YAC128 HD mice
86 ement binding protein (CREB), in rat primary corticostriatal cocultures.
87 ally defined type of cortical interneuron in corticostriatal communication.
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.
90 n neither case, however, was the strength of corticostriatal connections globally scaled.
91                    As a result, striatum and corticostriatal connectivity are highly sensitive to acu
92 ses were performed on a composite measure of corticostriatal connectivity derived from the significan
93             Neuronal dysfunction and altered corticostriatal connectivity have been postulated to be
94                                     Stronger corticostriatal connectivity in response to rewards pred
95        These findings suggest that decreased corticostriatal connectivity may serve as a target for a
96          We propose that late development of corticostriatal connectivity sets the stage for optimal
97 d is underpinned by striatal activations and corticostriatal connectivity similar to other human affi
98                  Furthermore, disturbance to corticostriatal connectivity was more pervasive in treat
99  may be constrained by ongoing maturation of corticostriatal connectivity.
100 tment response was significantly mediated by corticostriatal connectivity.
101                       Tolcapone also changed corticostriatal connectivity: specifically, by inducing
102              There is a dramatic increase in corticostriatal contacts onto spines and dendrites that
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
106                                      We used corticostriatal cultures from mice in which MSN subtypes
107 imultaneously and nonsimultaneously recorded corticostriatal datasets.
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
110 cell recordings combined with stimulation of corticostriatal fibers in rats and mice.
111                   Theta-burst stimulation of corticostriatal fibres produces long-term potentiation (
112 hat challenges and refines existing views of corticostriatal function and expose neuronal projection-
113         A data-driven computational model of corticostriatal function closely replicated the temporal
114 target for future therapies aimed to restore corticostriatal function in HD.
115 aptic mechanisms of inhibitory modulation of corticostriatal function that probably contribute to the
116 ng-related in vivo modulation of presynaptic corticostriatal function.
117 tributes to steeper discounting by impairing corticostriatal function.
118 vels attenuates impulsive choice by changing corticostriatal function.
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
123                                              Corticostriatal functional correlations were decreased i
124                   Our results indicated that corticostriatal functional dysconnectivity in psychosis
125 nce of major OCD symptom dimensions on brain corticostriatal functional systems in a large sample of
126                                              Corticostriatal gene expression profiles are predominate
127          Our convergent data demonstrate how corticostriatal GluN2B circuits govern the ability to le
128                       Finally, inhibition of corticostriatal glutamate release by TAAR1 showed mechan
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
131                               In contrast to corticostriatal glutamatergic inputs onto FSIs, which ar
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
136              Indeed, disrupted plasticity at corticostriatal glutamatergic synapses, the gateway of t
137 insic excitability and pruning of excitatory corticostriatal glutamatergic synapses.
138 ological studies showing overactivity of the corticostriatal glutamatergic system in models of parkin
139          BID rats showed hypersensitivity of corticostriatal glutamatergic terminals (lower frequency
140          INTERPRETATION: Hypersensitivity of corticostriatal glutamatergic terminals can constitute a
141 iously hypothesized increased sensitivity of corticostriatal glutamatergic terminals in the rodent wi
142 mate upon local light-induced stimulation of corticostriatal glutamatergic terminals.
143 regulation emerge, we recorded stepwise from corticostriatal (HVC) neurons and their target spiny and
144 riggers increased SPN excitatory synapse and corticostriatal hyperconnectivity.
145                    PDE10 inhibition restored corticostriatal input and boosted cortically driven indi
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
149            Convergent evidence suggests that corticostriatal interactions act as a gate to select the
150 is known about the development of functional corticostriatal interactions, and in particular, virtual
151 nformative reward properties are encoded via corticostriatal interactions.
152 rd properties were differentially encoded in corticostriatal interactions.
153                         We show that loss of corticostriatal, interhemispheric, and intrahemispheric
154 vated motor memory altered offline task-free corticostriatal interregional functional connectivity, r
155                      This slow remodeling of corticostriatal iSPN circuitry is likely to play a role
156  craving measures correlated positively with corticostriatal-limbic activations.
157 h functional and structural abnormalities in corticostriatal-limbic brain regions, which may explain
158                       In cocaine dependence, corticostriatal-limbic hyperactivity appears to be linke
159                       Our results describe a corticostriatal long-range inhibitory circuit (CS-SOM in
160              Dopaminergic modulation of both corticostriatal long-term depression (LTD) and long-term
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
165 al level through catecholamine influences on corticostriatal loops.
166 emonstrated a key role for cAMP signaling in corticostriatal LTD.
167 riatal disturbances in HD and underlie early corticostriatal LTP and cognitive defects.
168      Our results demonstrate that TBS evokes corticostriatal LTP, and that optogenetic activation of
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
176             Relatively decreased activity in corticostriatal neurocircuitry during multiple phases of
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
179       In the motor cortex, corticospinal and corticostriatal neurons are closely intermingled, raisin
180 elrhodopsin-2 (ChR2)-mediated stimulation of corticostriatal neurons during the task biased decisions
181            Connections involving presynaptic corticostriatal neurons had greater synaptic depression,
182                                              Corticostriatal neurons in layer 5A and corticocortical
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
189 n-derived neurotrophic factor (BDNF), within corticostriatal neurons.
190 ory microcircuit formed by corticospinal and corticostriatal neurons.
191 ype neurons (-50%) but essentially absent in corticostriatal neurons.
192 corticoamygdala neurons compared with nearby corticostriatal neurons.
193 get layer 2 corticoamygdala over neighboring corticostriatal neurons.
194 ful at corticoamygdala neurons compared with corticostriatal neurons.
195 ned serotonergic modulation of rat and mouse corticostriatal neurotransmission and find that serotoni
196                                              Corticostriatal or striatal deletion of Grin2b (encoding
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
199                                              Corticostriatal pathways are an ideal neural substrate f
200  human affiliative bonds; highlight specific corticostriatal pathways as defining distinct coparental
201 onnectivity patterns differentiated distinct corticostriatal pathways associated with two stable copa
202                        Findings suggest that corticostriatal pathways contribute to the natural time
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.
206         It is proposed that viewing aberrant corticostriatal plasticity and learning as a provisional
207 gulatory mechanisms underlying bidirectional corticostriatal plasticity are not fully understood.
208            Our results indicate that Hebbian corticostriatal plasticity can be induced by classical r
209 l task in rodents to investigate the role of corticostriatal plasticity in abstract skill learning.
210                   These results suggest that corticostriatal plasticity is necessary for abstract ski
211            Consequently, mitigating aberrant corticostriatal plasticity represents an important thera
212 wever, dopamine denervation induces aberrant corticostriatal plasticity that degrades established syn
213                                              Corticostriatal plasticity was required for the reductio
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
216 els and the strength of excitatory inputs on corticostriatal plasticity.
217 ine and opiates, and alter the regulation of corticostriatal plasticity.
218 eby heightened D1R-SPN activity can regulate corticostriatal plasticity.
219  Dopamine denervation gives rise to abnormal corticostriatal plasticity; however, its role in the sym
220               We observe frequency-dependent corticostriatal potentiation in vivo over the course of
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,
223                         The function of this corticostriatal projection in pain states, however, is n
224 s), whereas the latter type included crossed corticostriatal projection neurons (cCStrPNs) and crosse
225                            Our data identify corticostriatal projection neurons as critical for the r
226                   We demonstrate the role of corticostriatal projection neurons in auditory decisions
227 B1R heteromer (i) is essentially absent from corticostriatal projections and striatonigral neurons, a
228           How discrete, anatomically defined corticostriatal projections function in vivo to encode s
229 urologically plausible network of converging corticostriatal projections that may support the integra
230 cator GCaMP6 to assess presynaptic Ca(2+) in corticostriatal projections to the DLS.
231  monkeys disclosed a specific arrangement of corticostriatal projections.
232  share the dual pattern of focal and diffuse corticostriatal projections.
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
236 Depression is associated with alterations in corticostriatal reward circuitry.
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
239               Interestingly, co-treatment of corticostriatal slices with NR2A antagonist (NVP-AAM077)
240              Here, we show that treatment of corticostriatal slices with NR2A antagonist NVP-AAM077 o
241 lar, and structural changes were assessed in corticostriatal slices.
242                We found that the cortex, via corticostriatal somatostatin neurons (CS-SOM), has a dir
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
245                             Mef2c suppresses corticostriatal synapse formation and striatal spinogene
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
252  reverse the temporal order of plasticity at corticostriatal synapses in rats and mice.
253    Our findings suggest a model in which the corticostriatal synapses made by neurons tuned to differ
254                   The dynamic alterations at corticostriatal synapses that occur in response to PCE p
255   INTERPRETATION: The dynamic alterations at corticostriatal synapses that occur in response to PCE p
256                               In contrast to corticostriatal synapses, thalamostriatal synaptic activ
257 rtical projections, neuronal morphology, and corticostriatal synapses.
258 in the number but not strength of excitatory corticostriatal synapses.
259 controlling the induction of potentiation at corticostriatal synapses.
260  and can also modify long-term plasticity of corticostriatal synapses.
261 ly in direct-pathway MSNs without effects on corticostriatal synapses.
262 d to strengthening of a subset of excitatory corticostriatal synapses.
263 iation and decreased long-term depression in corticostriatal synapses.
264  spike-timing dependent plasticity (STDP) at corticostriatal synapses.
265     The dynamics of thalamostriatal, but not corticostriatal, synapses were modulated by histamine le
266 PAP4, is present at thalamostriatal, but not corticostriatal, synapses.
267 t iSPN intrinsic excitability and excitatory corticostriatal synaptic connectivity were lower in PD m
268 by the ratio of axo-spinous to axo-dendritic corticostriatal synaptic contacts was reduced.
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
271                                        Thus, corticostriatal synaptic dysfunction early in HD is attr
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
274           But how this interaction modulates corticostriatal synaptic plasticity underlying learned a
275 es the internalization of AMPARs and reduces corticostriatal synaptic strength, dephosphorylates DARP
276                   Thus, this study reveals a corticostriatal system associated with contextual facili
277                                              Corticostriatal systems are known to mediate choice lear
278 bjects, involved widespread dysregulation of corticostriatal systems characterized most prominently b
279                 These findings highlight how corticostriatal systems contribute to reward processing,
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
284 CD) is associated with disturbances of brain corticostriatal systems.
285 ects on cognition and emotion through limbic corticostriatal systems.
286  in ACC/OFC to determine the extent to which corticostriatal terminal fields overlapped with these co
287                                              Corticostriatal terminals have presynaptic GABA(B) recep
288 lutamate release that was most pronounced in corticostriatal terminals with a low probability of rele
289 inhibition at GABAB receptors on presynaptic corticostriatal terminals.
290  that these two forms of LTD act on the same corticostriatal terminals.
291 ns, with higher connection probability among corticostriatal than among corticospinal neurons.
292 Together, local phase-amplitude coupling and corticostriatal theta phase coupling mediated the tempor
293  asymmetric, essentially unidirectional from corticostriatal to corticospinal.
294  unidirectional signaling from higher-order (corticostriatal) to lower-order (corticospinal) output n
295                             The "rectifying" corticostriatal-to-corticospinal connectivity implies a
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
300 nNOS to limit cGMP production and excitatory corticostriatal transmission.

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