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1 rs correlating with information derived from striatal (11)C-DTBZ data using the DSI Studio toolbox.
2 ts were significantly associated with higher striatal (11)C-DTBZ distribution volume ratios (least af
3 se analyses to identify group differences in striatal [(18) F]-fluorodopa uptake (K(i) ).
4          However, at baseline and over time, striatal [(18) F]-fluorodopa uptake in mutation carriers
5 l or clozapine counteracted the reduction of striatal A(2A)R-D(2)R heteromers.
6  prognosis and subtyping based on functional striatal abnormalities (FSA).
7 entration, which coincides with elevation of striatal acetylcholine (ACh) levels.
8                                              Striatal activation could be augmented by circulating se
9                                    Decreased striatal activity may have been due to decreased cortica
10 dystonic patients or to the normal levels of striatal activity reported in healthy animals.
11  understand the mechanisms supporting proper striatal activity.
12              The cerebral cortex is the main striatal afferent, and progressive cortico-striatal disc
13 ession differentially in layers II/III and V striatal afferents from motor cortex and that cortical B
14  cortical and subcortical regions with known striatal afferents.
15 tivity and the latter with dorsal cingulate, striatal and anterior insular activity.
16 ts in ASD and to a hyperconnectivity between striatal and cortical brain areas.
17 sure synaptic DA availability in CHR both in striatal and extra-striatal brain regions.
18 r responses to stimulation of SNr-projecting striatal and GPe neurons, including biphasic and excitat
19  for genes expressed in T-cells, but also in striatal and hippocampal neurons.
20 -containing varicosities diffusely innervate striatal and mesolimbic networks, including the nucleus
21       Together, our data reveal that ventral striatal and midbrain reward networks form a reinforcing
22 FC (DPFC), insula and their mesial temporal, striatal and posterior connection sites, as well as in t
23 ntified structural and functional changes in striatal and prefrontal brain regions, among others.
24     Multimodal MRI in vivo indicates cortico-striatal and thalamo-striatal functional network deficit
25 n three-dimensional cultures to form cortico-striatal assembloids.
26 n-coupled receptor 88 (GPR88) in a number of striatal-associated disorders.
27 ly altered with respect to the activation of striatal astrocyte G protein-coupled receptor (GPCR) sig
28                       Furthermore, selective striatal astrocyte stimulation of the G(i)-GPCR pathway
29                                          The striatal astrocyte-converted neurons showed action poten
30  characterize neurogenesis by Notch-depleted striatal astrocytes in vivo.
31 elevance to the striatum, we discovered that striatal astrocytes mount context-specific molecular res
32 cal HFS increases calcium (Ca(2+)) levels in striatal astrocytes through activation of metabotropic g
33                       After stroke, however, striatal astrocytes undergo neurogenesis in mice, trigge
34  induce impairment of motor coordination and striatal atrophy.
35 acts connecting midbrain somatodendritic and striatal axonal compartments of dopaminergic neurons.
36 atially distant midbrain somatodendritic and striatal axonal compartments.
37           While most research has focused on striatal-based feedback learning, open questions remain
38 xhibited Pb-related alterations in behavior, striatal BDNF levels, frontal cortical Th total percenta
39 icit was defined as less than 65% of putamen striatal binding ratio expected for the individual's age
40                          To identify whether striatal brain regions are activated in Npas2 mutant fem
41  across the nervous system, including in the striatal brain regions.
42 ailability in CHR both in striatal and extra-striatal brain regions.
43 s with respect to frontocortical, limbic and striatal brain volume, functional activation elicited by
44                            Using an HD mouse striatal cell model and HD mouse organotypic brain slice
45  transcriptomic analyses of caudate/putamen (striatal) cell type-specific gene expression changes in
46  neuro2a neuroblastoma cells and mouse brain striatal cells, and performed gene expression profiling.
47 effect on normal HTT protein levels in mouse striatal cells, human cells and HD mouse models.
48 d exerts critical sex-specific influences on striatal cellular estrogenic mechanisms.
49                We focus on simulation at the striatal cellular/microcircuit level, in which the molec
50                  These results indicate that striatal ChIs are essential for the control of complex m
51       Synchronized pauses in the activity of striatal cholinergic interneurons (ChINs) are correlated
52 ctivity of VP neurons, GPe cells (actor) and striatal cholinergic interneurons (critic) while monkeys
53 d laterodorsal tegmental nuclei synapse with striatal cholinergic interneurons and give rise to excit
54 pamine D2 receptor it is highly expressed in striatal cholinergic interneurons and therefore is poise
55 omplex movement control in rodents, and that striatal cholinergic interneurons are an essential node
56              Habit formation is modulated by striatal cholinergic interneurons.
57  M(4)-autoreceptor-Galpha (i/o) signaling in striatal cholinergic interneurons.
58 ssociated with losses of basal forebrain and striatal cholinergic neurons, suggesting that falls refl
59   Baseline PANDAS sera decreased activity of striatal CINs, but not of parvalbumin-expressing GABAerg
60  baseline sera did not alter the activity of striatal CINs.
61 voxels were not matched to any mouse cortico-striatal circuit (mouse->human: 85% unassigned; mouse->m
62 ed response to anticipation across a cortico-striatal circuit (striatum, ACC, insula).
63 n positive affect and identify a hippocampal-striatal circuit associated with this bidirectional rela
64 pport a novel mechanism for the selection of striatal circuit components, where fluctuating levels of
65 uggest that the identified trans-species ACC-striatal circuit relationship with nicotine dependence s
66 e relationships between regions of a cortico-striatal circuit supporting reward processing and both c
67  modulate the activity of a specific cortico-striatal circuit to ameliorate motor symptoms and recove
68 ore global hyporeactivity across the cortico-striatal circuit.
69 s demonstrates adaptations in insula-ventral striatal circuitry and metabolic regulatory hormones tha
70 ty fingerprint matching, we compared cortico-striatal circuits across humans, non-human primates, and
71                                              Striatal circuits must be modulated for behavioral flexi
72 frontal and ventromedial prefrontal cortical-striatal circuits-pathways critically implicated in goal
73 ntributor to cholinergic transmission in the striatal complex.
74 prefrontal cortical, anterior cingulate, and striatal connections and the different methodologies use
75 y may have been due to decreased cortical to striatal connectivity consistent with glutamatergic and
76              Ketamine thus normalized fronto-striatal connectivity in TRD participants but disrupted
77 ia, as well as a significant upregulation of striatal D(2)R without changes in A(2A)R expression in P
78                       By combining RNAseq of striatal D2R neurons and histological analyses, we ident
79 male rats with dual cortical cholinergic and striatal DA losses (DL rats) exhibit cued turning defici
80 ession, degeneration of LC fibers, decreased striatal DA metabolism, and age-dependent behaviors remi
81                                              Striatal DA signals can be evoked by direct activation o
82 ally, despite decreased DAT levels in males, striatal DA uptake was enhanced, but was not due to enha
83                                          The striatal damage and progression of HD are associated wit
84 striatum attenuates brain atrophy, preserves striatal DARPP32 levels and reduces mutant HTT (mHTT) ag
85                              Following intra-striatal delivery, pathological mHTT-positive protein ag
86 perturbations of histamine levels can impact striatal development.
87   Similarly, SP-immunostained terminals from striatal direct pathway neurons were more abundant in gl
88 coincident decreased distal spine density in striatal direct pathway striatal projection neurons.
89 n striatal afferent, and progressive cortico-striatal disconnection characterizes HD.
90                                              Striatal dopamine (DA) is critical for action and learni
91 tible with a haloperidol-induced increase in striatal dopamine (e.g., because of a presynaptic mechan
92                                              Striatal dopamine activity was assessed as K(i)(cer) val
93  present a novel form of interaction between striatal dopamine and acetylcholine dynamics.
94                   Data suggest that aberrant striatal dopamine and cortico-thalamic dysconnectivity a
95 ng, calcium signals at somata and axons, and striatal dopamine concentrations.
96                                              Striatal dopamine D2 receptors (D2Rs) are important for
97 ngs demonstrate significant heterogeneity of striatal dopamine function in schizophrenia.
98 cannabis use affects either acute or chronic striatal dopamine is inconclusive.
99 odels declines in concert with extracellular striatal dopamine levels rather than insufficient dopami
100                We hypothesized that aberrant striatal dopamine links topographically with aberrant co
101         While some evidence suggests altered striatal dopamine may underlie the association, direct e
102  magnetic resonance imaging to determine how striatal dopamine release shapes local and global respon
103 triatal stimulation is sufficient to inhibit striatal dopamine release, and that a novel mGlu(1) posi
104 ns and medial prefrontal cortex, and ex vivo striatal dopamine reuptake.
105 ized by motor and nonmotor symptoms, reduced striatal dopamine signaling, and loss of dopamine neuron
106               Sub-chronic ketamine increased striatal dopamine synthesis capacity (Cohen's d = 2.5) a
107                                              Striatal dopamine synthesis capacity at presentation pre
108   Patients with schizophrenia show increased striatal dopamine synthesis capacity in imaging studies.
109             Results demonstrate that reduced striatal dopamine synthesis capacity links topographical
110                                              Striatal dopamine synthesis capacity predicted the worse
111 ort was greater for participants with higher striatal dopamine synthesis capacity, whereas methylphen
112 nderwent an [(18)F]DOPA PET scan to quantify striatal dopamine synthesis capacity.
113 er based on 18F-DOPA-PET was used to measure striatal dopamine synthesis capacity; correlation coeffi
114 s reveal distinct neuromodulatory actions of striatal dopamine that extend well beyond its sites of p
115  is suggested by theoretical models based on striatal dopamine's topographic modulation of cortico-th
116 order is associated with blunted presynaptic striatal dopamine.
117 duces the cost of mental labor by increasing striatal dopamine.
118 tergic neuron hyperactivity drives increased striatal dopaminergic activity, which underlies the deve
119 orrelational tractography) and the degree of striatal dopaminergic denervation based on (11)C-DTBZ PE
120 o investigate interindividual variability of striatal dopaminergic function in patients with schizoph
121       FSA revealed a spectrum of severity in striatal dysfunction across neuropsychiatric disorders,
122 In study 2, this specific prefrontal-ventral striatal dysfunction was associated with fewer days of a
123   FSA scores provide a personalized index of striatal dysfunction, ranging from normal to highly path
124 d anxiety-like behavior], dopamine function [striatal expression of tyrosine hydroxylase (Th)], gluco
125                  These findings suggest that striatal fast spiking interneurons play an important rol
126   These data causally implicate the minority striatal fast-spiking interneuron population as a key co
127  beta oscillations, we show that networks of striatal fast-spiking interneurons (FSIs) are capable of
128                       Parvalbumin-expressing striatal fast-spiking interneurons comprise ~1% of the t
129                                              Striatal field recordings and electrical stimulation of
130 differences in predispositional insula-based striatal-frontal circuits, highlighting the circuit's po
131 ergic Rit2 expression differentially impacts striatal function and DA-dependent behaviors in males an
132 many important contributions from neurons in striatal function, far less is known about the role of a
133                    Ketamine increased fronto-striatal functional connectivity in TRD participants tow
134  vivo indicates cortico-striatal and thalamo-striatal functional network deficits and reduced glutama
135  mTOR signaling as an important regulator of striatal functions through an intricate mechanism involv
136 cytes are emerging as critical regulators of striatal functions.
137 choline/glutamate cotransmission to regulate striatal functions.
138  with intriguing consequences for opioid and striatal functions.
139                                      Ambient striatal GABA tone on striatal projection neurons can be
140                     Past work has shown that striatal GABA tonically inhibits dopamine release, but w
141 that DA release is under tonic inhibition by striatal GABA.
142 GD10, MIA; (3) no alterations in cortical or striatal GAD1 mRNA of polyI:C offspring, but an expected
143                   These results suggest that striatal Gadd45b functions as a dopamine-induced gene th
144                             However, whether striatal GATs and astrocytes determine DA output are unk
145 To further assess downstream consequences on striatal gene expression, we used next-generation RNA se
146 the cellular and subcellular localization of striatal GluD1 immunoreactivity (GluD1-IR) in mice and m
147                             In both species, striatal GluD1-IR displayed a patchy pattern of distribu
148    These results suggest that an increase in striatal glutamate levels may underlie acute cannabis-in
149 sign was used to investigate whether altered striatal glutamate, as measured using proton magnetic re
150  deeper understanding of GluD1 regulation of striatal glutamatergic synapses, but also suggest possib
151 istry for histamine-containing axons reveals striatal histaminergic innervation by the second postnat
152                                      Loci of striatal hyperactivity recapitulated the spatial distrib
153                 We conclude that dorsomedial striatal iMSNs control approach-avoidance conflicts in e
154 ibed a dose-dependent effect of a unilateral striatal injection of vasoconstrictive endothelin-1 (ET-
155                 Despite the importance of DA striatal innervation, processes involved in establishmen
156  multiple parallel closed loops that provide striatal input.
157  transfer of movement-related cues and their striatal integration with movement sequencing.
158  notable subcortical innovation: an abundant striatal interneuron type in primates that had no molecu
159    No reduction in SP+ striatal perikarya or striatal interneurons was seen in Q175 mice at 18 months
160 icant correlation was found between baseline striatal K(i)(cer) values and time to relapse after anti
161                      Consequently, the giant striatal Kv3.3-expressing PV neuron may link compromised
162 vigation (thought to rely on hippocampal and striatal learning mechanisms respectively).
163                                              Striatal lesion core and globus pallidus of Abeta + ET1
164 d distant regions with synaptic links to the striatal lesion such as white matter (subcortical white
165 the updating of brain activity in prefrontal-striatal-limbic circuits.
166         Morphologically, the complexities of striatal median spiny neurons (MSNs), parvalbumin-positi
167 ion of the dopamine D2 receptor (D2R) in the striatal medium spiny neurons (MSNs) (iMSN-D2RKO).
168 t recordings and dendritic spine analyses on striatal medium spiny neurons (MSNs) in drug-naive rAAV-
169 ough dysregulation of synaptic signalling in striatal medium spiny neurons, adult nigral dopaminergic
170 Galpha (i/o) signaling in SNc DA neurons and striatal medium spiny neurons, respectively.
171  We observed no changes in the morphology of striatal medium spiny neurons, the density of dendritic
172 city between corticostriatal projections and striatal medium spiny neurons.
173 e [(35)S]GTPgammaS binding assay using mouse striatal membranes but was inactive in membranes from GP
174 ine transporter protein, dopamine uptake, or striatal methamphetamine and amphetamine metabolite leve
175                                       Higher striatal mGluR5 availability in alcohol-dependent users
176                       Also, normalization of striatal mGluR5 to control levels was associated with re
177 his paper, we propose a biophysical model of striatal microcircuits that comprehensively describes th
178 RAMINT approach retained only 31 explanatory striatal miRNA-mRNA pairs that are precisely associated
179 es: 1) extended amygdala module, 2) midbrain striatal module, and 3) cortico-hippocampo-thalamic modu
180 tterns for the nucleus accumbens and cortico-striatal motor circuits (posterior/lateral putamen) were
181 d spine density and thin-spine morphology on striatal MSNs; both phenomena mimicking changes seen in
182                                    We mapped striatal network dysfunction in HD mice to ultimately mo
183      We tested this hypothesis in the fronto-striatal network of nonhuman primates during reversal le
184  underpinned by atrophy in a thalamo-cortico-striatal network.
185 relationship between prefrontal cortical and striatal neural interactions, and cognitive flexibility,
186 demonstrate that Gadd45b knockdown decreases striatal neuron action potential burst duration in vitro
187 n unforeseen heterogeneity in D2R-expressing striatal neuronal populations, underlying specific D2R's
188 rimarily expressed in SNc DA neurons (RGS6), striatal neurons (RGSs 4 and 9), or microglia (RGS10), m
189  that histamine acutely modulates developing striatal neurons and synapses and controls longer-term c
190              Knockout of GluD1 expression in striatal neurons elicits cognitive deficits and disrupts
191                       It remains unclear how striatal neurons encode motor parameters and use them to
192                 Supporting this theory, many striatal neurons exhibit such graded changes without bur
193 ccurs in the cerebellar granular neurons and striatal neurons in Tubb4a(D249N/D249N) mice.
194      In vitro, dopamine treatment in primary striatal neurons increases Gadd45b mRNA expression throu
195 e postmortem evidence of Nurr1 expression in striatal neurons of l-DOPA-treated PD patients.
196                        In medium-size, spiny striatal neurons of the direct pathway, dopamine D(1)- a
197 riatum (DLS) was undetectable in HD mice and striatal neurons show blunted electrophysiological respo
198 rained to self-administer heroin and primary striatal neurons treated with chronic morphine in vitro.
199                                   No loss of striatal neurons was seen out to 18 months, but ENK+ and
200 Indeed, rAAV-mediated expression of Nurr1 in striatal neurons was sufficient to overcome LID-resistan
201  to independent effects on oligodendrocytes, striatal neurons, and cerebellar granule cells in the co
202 rected against the nuclei of Purkinje cells, striatal neurons, and hippocampal neurons.
203 nd inhibition of direct and indirect pathway striatal neurons, respectively.
204 the intrinsic excitability of direct pathway striatal neurons.
205 tin (HTT) fragments that preferentially kill striatal neurons.
206                                  The lack of striatal Nolz1 expression results in nigral to pallidal
207  rats displayed mild LID and no induction of striatal Nurr1 despite receiving a high dose of l-DOPA.
208                      These data suggest that striatal Nurr1 is an important mediator of the formation
209 ortical neurons send axonal projections into striatal organoids and form synaptic connections.
210                                              Striatal oscillatory activity is associated with movemen
211 ation, it's unclear how compartment-specific striatal output is dynamically achieved, particularly co
212              However, it remains unclear how striatal output neurons encode and facilitate movement.
213 ne shift the balance of compartment-specific striatal output.
214                                          The striatal pathologies resemble those in human HD, but are
215 s of disease burden (r = -0.42 to -0.69) and striatal pathology (r = 0.71-0.60) in individuals with p
216 ments that target this functional prefrontal-striatal pathology could improve early treatment outcome
217 iatal shape deflation and disease burden and striatal pathology in individuals with prodromal Hunting
218 ciations with measures of disease burden and striatal pathology.
219 romote locomotion; however, their effects on striatal pathway function in vivo remain unclear.
220 to impair PDE10A function due to the loss of striatal PDE10A protein levels, but here we show that th
221                          No reduction in SP+ striatal perikarya or striatal interneurons was seen in
222 seen out to 18 months, but ENK+ and DARPP32+ striatal perikarya were fewer by 6 months, due to dimini
223                        Here, we demonstrated striatal phenotypes in heterozygous Disc1 mutant mice, w
224 he mechanisms behind how mTOR is involved in striatal physiology and its relative role in distinct ne
225 erneurons comprise ~1% of the total neuronal striatal population, are enriched dorsolaterally and are
226              Much is known about frontal and striatal processes that support cognitive control, but f
227                                      Thalamo-striatal progressive volumetric deficit associated with
228                 We show that the ablation of striatal projecting neurons reduces learning speed, wher
229 atal synapses of the direct pathway [cortico-striatal projection neuron (dSPN)] in the dorsolateral s
230 ment, presumably through their modulation of striatal projection neuron (SPN) activity.
231  in nigral to pallidal lineage conversion of striatal projection neuron subtypes.
232 ed mice, (1) D2 dopamine receptor expressing striatal projection neurons (D2-SPNs) discharge at highe
233  activity of D2 dopamine receptor-expressing striatal projection neurons (D2-SPNs), parvalbumin-expre
234 deling and experimental work suggesting that striatal projection neurons (SPNs) are capable of genera
235  adaptations of gamma-aminobutyric acidergic striatal projection neurons (SPNs) evoked by drugs of ab
236                Ambient striatal GABA tone on striatal projection neurons can be determined by plasma
237 interneurons (FSIs) in the striatum to train striatal projection neurons to gate relevant and suppres
238 putative fast-spiking interneurons (FSIs) to striatal projection neurons was enhanced in striosomes c
239 vestigate the effects of dopamine release on striatal projection neurons.
240 tal spine density in striatal direct pathway striatal projection neurons.
241                                      Cortico-striatal projections are critical components of forebrai
242 ts emphasize an intricate architecture where striatal projections originate from different combinatio
243 ionally determined that in l-DOPA-naive rats striatal rAAV-Nurr1 overexpression (1) increased cortica
244 ficant differences in DA transmission in any striatal region between converters and nonconverters, al
245 or cingulate cortex did as well, but neither striatal region did in either animal.
246 es had good test-rest reproducibility across striatal regions (K(i)(cer) ICC: 0.68-0.94, SUVRc ICC: 0
247 ructural connectivity between prefrontal and striatal regions as critical nodes for action selection.
248 pha exhibits nuclear expression in all three striatal regions before adulthood and disappears in a re
249 S2 regulates reward and activity in specific striatal regions in a sex and time of day (TOD)-specific
250 urthermore, focal activation of two distinct striatal regions induces either licking or turning, cons
251  flow of information between dACC and fronto-striatal regions is secured through different pathways,
252 uron is much larger than PV neurons in other striatal regions, displays characteristic electrophysiol
253 nding dominates models of estrogen action in striatal regions.
254 ting a dichotomous role of BDNF signaling in striatal regions.
255 t prefrontal, right parahippocampal and left striatal regions; also, a gradient of decreasing respons
256 le in distinct neuronal populations in these striatal-related diseases still remain to be clarified.
257 erfunction, which could be targeted to treat striatal-related monogenic disorders associated with the
258 d individuals showing blunted (hyporeactive) striatal response to monetary rewards.
259 cted functional disruption of the prefrontal-striatal responses to stress images and to alcohol cues
260 r amygdala responsivity to neutral faces, or striatal responsivity to monetary losses.
261  of robust sex differences in prefrontal and striatal resting state networks that may contribute to d
262 t, mood symptoms are associated with blunted striatal reward prediction error signals in a large comm
263 al questions regarding the interpretation of striatal 'reward' signals in the context of effort deman
264                                              Striatal RGS4 has been shown to exacerbate motor symptom
265                  siRNA-mediated knockdown of striatal Rgs4 in DIO-susceptible rats decreased food int
266 and that overweight humans exhibit increased striatal Rgs4 protein.
267 onsolidate reinforcement learning theory and striatal RPEs as key factors subtending the formation of
268 ate of torque development values and greater striatal shape deflation and disease burden and striatal
269                      Pathological changes in striatal shape were evaluated using magnetic resonance i
270 indirect SPN pathways by recruiting distinct striatal signaling pathways, epigenetic and genetic resp
271  freely moving animals has revealed opposing striatal signals, with greater response to increasing ef
272 ervate the striatum in both constitutive and striatal-specific Nolz1 mutant embryos.
273               LRRK2 is a kinase expressed in striatal spiny projection neurons (SPNs), cells which lo
274         Whole-cell patch-clamp recordings of striatal spiny projection neurons and histamine superfus
275        Findings were similar using a cortico-striatal staging system and continuous PET measurements.
276 ation of mGlu(1) signaling following thalamo-striatal stimulation is sufficient to inhibit striatal d
277 he critical role of a reduction in prefronto-striatal structural connectivity in accounting for actio
278 ion is associated with a localized effect on striatal structure, having a prior ADI is a strong predi
279 ration between caudate nucleus and putamen-a striatal sub-division unique to primates-with both dopam
280 specific D1R and D2R dysfunction in distinct striatal sub-regions.
281                                     Distinct striatal subfields are involved in voluntary movement ge
282  SST downregulation in specific cortical and striatal subregions, with additional deficits in somatos
283 e morphological and molecular differences of striatal subregions.
284 a twofold increase in hnRNP H protein in the striatal synaptosome of H1(+/-) mice with no change in w
285 , successfully characterizes the hippocampal-striatal system as a general system for decision making
286  whether ketamine affects the brain's fronto-striatal system, which is known to drive motivational be
287 -SPN plasticity within functionally relevant striatal territories to reshape volitional action.
288 h the following: dysfunction within cortical-striatal-thalamic-cortical (CSTC) brain circuits implica
289  could prevent the initial excitation of the striatal tic focus-a hypothesis we have previously intro
290         Gene-level transcriptome analysis of striatal tissue from 114 kb congenics vs Hnrnph1 mutants
291  analysis of wild-type and Nolz1(-/-) mutant striatal tissue led to the identification of several sec
292 and chemogenetics we show the involvement of striatal tyrosine hydroxylase-expressing interneurons in
293 ently to the "salience" network, the ventral striatal/ventromedial prefrontal "reward" network, and t
294 ile HIV serostatus was associated with lower striatal volume (B = -0.59; 95% CI = [-1.08 - -0.10]), c
295  ADI was independently associated with lower striatal volume (B=-0.73; 95% CI =[-1.36 - -0.09]).
296 However, a large number of human and macaque striatal voxels were not matched to any mouse cortico-st
297                                          Top striatal weighted edges are enriched in modulators of de
298 o change in baseline extracellular dopamine, striatal whole-tissue dopamine, dopamine transporter pro
299                       Accordingly, different striatal zones collect specific combinations of signals
300 s may project in different ways to different striatal zones, which can be targets of specific combina

 
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