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1                Results: In the ROI analyses, extrastriatal (123)I-FP-CIT binding ratios in the hypoth
2                         In the ROI analyses, extrastriatal (123)I-FP-CIT binding ratios in the hypoth
3    Therefore, we examined the time course of extrastriatal (123)I-FP-CIT binding.
4 l DAT binding, there would be differences in extrastriatal (123)I-FP-CIT SPECT binding to SERT betwee
5                         However, the role of extrastriatal A(2A)Rs in modulating psychomotor activity
6 ration of a predominant facilitatory role of extrastriatal A(2A)Rs.
7 ian fear conditioning, while inactivation of extrastriatal A2ARs in the forebrain inhibits fear condi
8 tative population may reflect possible early extrastriatal and extracerebral pathology of PD.
9                This deficit extends to other extrastriatal areas and predicts subclinical psychopatho
10 alpha desynchronization, while ventrolateral extrastriatal areas ipsilateral to the attended hemifiel
11 tantia nigra pars compacta but also in other extrastriatal areas of the brain.
12  in (11)C-raclopride BP in both striatal and extrastriatal areas, including amygdala, temporal and fr
13 n of synaptic transmission and plasticity in extrastriatal areas, including the hippocampus.
14 opamine signaling in the striatum but not in extrastriatal areas.
15 hat dopamine denervation of the striatum and extrastriatal basal ganglia profoundly alters the transm
16 ltivariate striatal connectivity pattern and extrastriatal baseline D2 receptor binding potential and
17 sporter (SERT), predominantly represented in extrastriatal binding.
18                             The inability of extrastriatal brain areas to regulate the formation of d
19 udate nucleus and putamen) and the SERT-rich extrastriatal brain regions (thalamus, hypothalamus, and
20 nts of [(18)F]fallypride in the striatal and extrastriatal brain regions and the correlations of thes
21 sure amphetamine-induced dopamine release in extrastriatal brain regions in the non-human primates wa
22 iography using [3H]7-OH-DPAT in striatal and extrastriatal brain regions of the common marmoset (Call
23 measure the capacity for dopamine release in extrastriatal brain regions.
24 D) was measured pre- and post amphetamine in extrastriatal brain regions.
25 dopamine transmission in the striatum and in extrastriatal brain regions.
26 s dopamine transmission in both striatal and extrastriatal brain regions.
27 re, selective inactivation of the A(2A)Rs in extrastriatal cells by administering the A(2A)R antagoni
28 /3) receptor ligand, to measure striatal and extrastriatal D(2/3) nondisplaceable binding potential (
29  source of variability for quantification of extrastriatal D2 receptors with [123I]epidepride.
30 allypride PET studies to assess striatal and extrastriatal D2-like receptor uptake in a placebo-contr
31 positive associations of striatal as well as extrastriatal DA D(2/3) receptors to BOLD response in th
32 In advanced Parkinson's disease, significant extrastriatal decreases in [(18)F]dopa K(i)(o) were obse
33                         However, the role of extrastriatal dopamine receptors (DRs) in BG information
34 ssing by highlighting the functional role of extrastriatal dopamine receptors.
35              We measured amphetamine-induced extrastriatal dopamine release before and after treatmen
36 e possibility of measuring both striatal and extrastriatal dopamine release during activation paradig
37 paminergic deficit, we examined striatal and extrastriatal dopamine release in severely cannabis-depe
38  to the ability to explore both striatal and extrastriatal dopamine release simultaneously.
39                 To measure both striatal and extrastriatal dopamine release, the height of dopamine r
40 pport the use of (18)F-fallypride to measure extrastriatal dopamine release.
41 onization of neuronal discharge, the role of extrastriatal dopamine, and expanded intrinsic and input
42  system must be changed to take into account extrastriatal dopaminergic projections and intrastriatal
43 o investigate the mesencephalic striatal and extrastriatal dopaminergic projections together with ext
44                   To investigate the role of extrastriatal DRs, we studied their distribution and fun
45 spines, indicating that these spines receive extrastriatal excitatory afferents.
46  but are also present at lower levels in the extrastriatal forebrain (i.e., hippocampus, cortex), int
47                                        These extrastriatal forebrain A2AR behavioral effects were ass
48 y left hemi-Parkinson's disease, significant extrastriatal increases in [(18)F]dopa K(i)(o) were obse
49 medial VS or ventrolateral VS, suggesting an extrastriatal mechanism.
50                                     However, extrastriatal mechanisms have increasingly been the focu
51 erved not only in striatal areas but also in extrastriatal "motor" regions, bilaterally.
52  disease progression in distributed, largely extrastriatal networks.
53 esults indicate that A(2A)Rs in striatal and extrastriatal neurons exert an opposing modulation of ps
54 evidence for the critical role of A(2A)Rs in extrastriatal neurons in modulating psychomotor behavior
55 sults identify a critical role of A(2A)Rs in extrastriatal neurons in providing a prominent excitator
56 odulation of excitatory neurotransmission of extrastriatal origin.
57 ase or medication and are posited to rely on extrastriatal, possibly prefrontal, structures.
58 have studied the progression of striatal and extrastriatal post-synaptic dopaminergic changes in a gr
59 ET, we have objectively localized changes in extrastriatal, pre-synaptic dopaminergic function in Par
60 e differential effects of psychostimulant in extrastriatal regions and other uptake inhibitors in the
61 ng in dopamine release in SCZ involving most extrastriatal regions and the midbrain; and a significan
62 knockout mice and examined both striatal and extrastriatal regions at molecular and cellular levels.
63 , BP(ND-8 h), and BP(ND-MRTM2) in any of the extrastriatal regions explored.
64       There were no changes in D2/D3 BPND in extrastriatal regions in either group.
65 pread deficit extending to many cortical and extrastriatal regions including the midbrain.
66 ask induced increased ligand displacement in extrastriatal regions of the reward circuit, including t
67  decrease in (18)F-fallypride binding in the extrastriatal regions points to the importance of dopami
68 wever, because receptor density was lower in extrastriatal regions than in the striatum, the counting
69   The reproducibility of outcome measures in extrastriatal regions was good.
70 ecific [3H]7-OH-DPAT binding in striatal and extrastriatal regions were not different to those in nor
71  in FFG, whereas D1 BP in striatal and other extrastriatal regions were unrelated to neural activity
72                                       In the extrastriatal regions, a single acquisition at 5 or 8 h
73 levels correlated well with l-DOPA levels in extrastriatal regions, such as hippocampus, amygdala, be
74  dopamine release in associative striatum vs extrastriatal regions.
75 -DPAT binding was found in both striatal and extrastriatal regions.
76 the binding potential of (18)F-fallypride in extrastriatal regions: thalamus (-20%), amygdala (-39%)
77  assessed D2/3R availability in striatal and extrastriatal reward regions in 14 OB and 14 age- and ge
78 kinetic model in detecting both striatal and extrastriatal reward-induced dopamine release, using hum
79 iatal dopaminergic projections together with extrastriatal serotonin transporter binding in Parkinson
80 frame for assessing (123)I-FP-CIT binding to extrastriatal SERT is between 2 and 3 h after injection
81 OR transgene in the striatum, rather than in extrastriatal sites, is needed for the restoration of op
82  receptors, either within the striatum or in extrastriatal sites, regulate D2 receptor-mediated Fos e
83 seline binding potential across cortical and extrastriatal subcortical regions (t25 = 3.01, P = .01,
84 g to most cortical regions and even to other extrastriatal subcortical regions not previously conside
85  soma-dendritic shape, and intrastriatal and extrastriatal synaptic interactions of these neurons are
86 lyses indicate that alpha phase in early and extrastriatal visual areas modulated HFA power in downst
87 wer modulated local alpha phase in early and extrastriatal visual areas, with suppressed interareal i