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1 lopmental trajectories of tissue iron in the basal ganglia.
2 made by the corresponding systems within the basal ganglia.
3 ward-related and motivational signals in the basal ganglia.
4 (STN) neurons form a key network within the basal ganglia.
5 turation of tissue iron concentration in the basal ganglia.
6 affects learning and action selection in the basal ganglia.
7 nent in the striatum, the central hub of the basal ganglia.
8 a key, yet an understudied component of the basal ganglia.
9 key, centrally positioned network within the basal ganglia.
10 striatum is the main input structure of the basal ganglia.
11 lates with deposition of amyloid-beta in the basal ganglia.
12 ough dopamine-mediated interactions with the basal ganglia.
13 aints for future computational models of the basal ganglia.
14 aints for future computational models of the basal ganglia.
15 choice between GO and NO-GO pathways in the basal ganglia.
16 ex, frontal gyrus, amygdala, hippocampus and basal ganglia.
17 induced at specific coordinates in the right basal ganglia.
18 ed throughout the cerebellum, brainstem, and basal ganglia.
19 prediction errors that drive learning in the basal ganglia.
20 reduced vision /cataract or calcification of basal ganglia.
21 n subtype that preferentially innervates the basal ganglia.
22 the cerebral cortex, the cerebellum, and the basal ganglia.
23 d attention-related visual processing in the basal ganglia.
24 ease conditions associated with the mPFC and basal ganglia.
25 making systems residing in the brain, in our basal ganglia.
26 including white matter-enhancing lesions and basal ganglia abnormalities that could be related to sev
29 l output will pave the way toward dissecting basal ganglia activity in both physiological and patholo
30 d to be permitted or triggered by changes in basal ganglia activity through gating- or rebound-like m
34 demonstrated abundant nitrergic cells in the basal ganglia, amygdaloid complex, preoptic area, basal
35 carrier status, mutation site within PSEN1, basal ganglia amyloid-beta as measured by Pittsburgh com
36 84% versus 63.3%; P = 0.006) and showed more basal ganglia amyloid-beta deposition (Pittsburgh compou
37 was significantly positively correlated with basal ganglia amyloid-beta deposition, Clinical Dementia
38 ers with motor findings more frequently were basal ganglia amyloid-beta positive (84% versus 63.3%; P
40 memory (learning and memory that rely on the basal ganglia and associated circuitry) can explain nume
41 ional direct pathways running from cortex to basal ganglia and between basal ganglia and cerebellum i
42 ivated astroglia in the cortex, hippocampus, basal ganglia and brainstem; therefore, by measuring imi
44 hy including Hypomyelination with Atrophy of Basal Ganglia and Cerebellum (H-ABC), a rare hypomyelina
45 ing from cortex to basal ganglia and between basal ganglia and cerebellum in the pathophysiology of m
47 inputs from upstream centers, including the basal ganglia and cortex, to regulate and modulate behav
48 relationship between neuronal firing in the basal ganglia and cortical gamma activity during movemen
49 port for models that link beta activity with basal ganglia and dopamine for the allocation of neural
50 he anatomy, physiology, and circuitry of the basal ganglia and highlight the mechanisms that underlie
51 Subtype 2 showed increased volume in the basal ganglia and internal capsule, and otherwise normal
52 normal and stable anatomy, except for larger basal ganglia and internal capsule, not explained by ant
53 he striatum is the main input nucleus of the basal ganglia and is a key site of sensorimotor integrat
54 gene expression patterns and found that the basal ganglia and medium spiny neurons were most enriche
56 imultaneous intracranial recordings from the basal ganglia and motor cortex, we found that response-c
58 of the ventral telencephalon from which the basal ganglia and olfactory tubercles originate, where i
59 mal and patients demonstrate the role of the basal ganglia and other interconnected structures, such
60 ciated with blunted reward activation in the basal ganglia and other regions such as the medial prefr
61 from the frontal and occipital white matter, basal ganglia and pons was used to obtain a global cereb
62 the nervous system, such as the spinal cord, basal ganglia and pontine nuclei in the brainstem, can b
63 ic nucleus (STN) is a pivotal element of the basal ganglia and serves as target for deep brain stimul
64 ificity and multi-network integration in the basal ganglia and thalamus of individual human subjects.
66 hology, myelin and iron concentration of the basal ganglia and thalamus were estimated from 182 MRI d
67 racterize the functional interaction between basal ganglia and thalamus, we demonstrated that patient
69 havior both via ascending projections to the basal ganglia and through descending projections to brai
70 d target engagement (lowering of iron in the basal ganglia), and seemed to somewhat slow disease prog
74 ing and correlating the variable cerebellar, basal ganglia, and neocortical neuropathology with the v
76 nderstand the functional organization of the basal ganglia, and with the discovery of the neurotoxin
79 ursts of beta frequency band activity in the basal ganglia are associated with slowing of voluntary m
84 hat D2 MSNs and specific circuits within the basal ganglia are preferentially vulnerable to HIV-1.
86 h brain slices we show that within each bird basal ganglia Area X-projecting (HVC(X)) neurons share s
88 gly connected with the prefrontal cortex and basal ganglia, areas which have been implicated in inter
89 and marked deposition of amyloid-beta in the basal ganglia, autosomal dominant Alzheimer's disease co
91 in brain regions linked to ASD, such as the basal ganglia (BG) and the dorsomedial prefrontal cortex
93 nds to treatments that decrease pathological basal ganglia (BG) beta oscillations (10-17 Hz in primat
94 antia nigra pars reticulata (SNr), where the basal ganglia (BG) direct and indirect pathways converge
97 ter sensory-motor cortical loop and an inner basal ganglia (BG) loop, controlling their respective ha
103 ars reticulata (SNr), the main output of the basal ganglia, blocks signaled active avoidance, while i
104 ere located in the following areas: level of basal ganglia (caudate nucleus, putamen, corpus callosum
107 ays a distinct role in the prefrontal cortex-basal ganglia circuit for reinforcement learning and is
109 plausible biophysical models of the cortico-basal ganglia circuit that could explain the functional
115 Our findings provide insights into cortical-basal ganglia circuits and global brain organization und
116 ulates glutamatergic transmission in cortico-basal ganglia circuits and represents a major target of
118 ical and fundamental studies have identified basal ganglia circuits as critical for this process.
119 y oscillations (15 to 35 Hz) in cortical and basal ganglia circuits become abnormally synchronized in
120 scenarios emerge that shed new light on how basal ganglia circuits modulate self-paced movement init
121 ing and to establish that downstream cortico-basal ganglia circuits serve a learning role that is onl
122 l spatial attention, then the involvement of basal ganglia circuits should incorporate the subject's
123 or symptoms are attributed to dysfunction of basal ganglia circuits under conditions of low dopamine.
126 apturing prefrontal, anterior cingulate, and basal ganglia connections linked to the limbic system.
127 on has both behaviour-independent effects on basal ganglia connectivity, as well as behaviour-depende
128 demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-b
129 lanation for these diverse roles is that the basal ganglia control the level of commitment to particu
130 (47.4%) developed T1 hyperintensities of the basal ganglia, corresponding to accumulated lipid phagoc
132 unique but complementary spatial patterns of basal ganglia degeneration that are strikingly reminisce
133 cifications, necrotic and calcified areas in basal ganglia, dentato-olivary dysplasia and severe hypo
134 telencephalic signaling center important for basal ganglia development known in other vertebrates (i.
136 ons (SPNs) are thought to contribute to many basal ganglia disorders, including early-onset neurodeve
138 tory of tissue iron concentration across the basal ganglia during adolescence and provide evidence th
139 ly, the increase in beta oscillations in the basal ganglia during sleep paralleled decreased NREM sle
141 established physiological criteria to define basal ganglia dysfunction, correlations between individu
142 ous research has linked SHANK3 deficiency to basal ganglia dysfunction, motor stereotypies, and socia
143 related directed medial prefrontal cortex to basal ganglia effective connectivity is abnormally incre
147 tes, and executive function, mediated by the basal ganglia, extended amygdala, and frontal cortex, re
148 mplex modes of information processing in the basal ganglia for different motor and nonmotor functions
150 red in the basal ganglia in PD and models of basal ganglia function and dysfunction were proposed.
152 ing.SIGNIFICANCE STATEMENT Current models of basal ganglia function are often based on a distinction
153 pathways provides striking predictions about basal ganglia function that have been used to develop de
154 sting parallel functional pathway concept of basal ganglia function to include the study of limbic-mo
155 nals in the striatum play a critical role in basal ganglia function, such as reinforcement and motor
158 g mice of either sex, we found that the main basal ganglia GABAergic output in the midbrain, the subs
160 anatomy of the medial prefrontal cortex and basal ganglia has been extensively studied and the forme
161 The ventral pallidum, located in the ventral basal ganglia, has long been recognized as an obligatory
164 Whereas subcortical structures such as the basal ganglia have been widely explored in relation to m
165 n CD36 protein with age in several cortices, basal ganglia, hippocampus, and midbrain, a decrease wit
168 ticipation or an even more prominent role of basal ganglia in focal seizures, the mode of interaction
169 ation of potential volumetric changes of the basal ganglia in patients with PD who underwent staged S
170 e physiological changes that occurred in the basal ganglia in PD and models of basal ganglia function
173 intracerebral electrode contact explored the basal ganglia, in either their putaminal or caudate part
176 Ndufs4 deletion in GABAergic neurons causes basal ganglia inflammation without motor or respiratory
177 t in the integration of limbic, sensory, and basal ganglia information to guide effective response st
179 ings suggest that the broken balance between basal ganglia inhibition and thalamus synchronization ca
181 of the motor system by including cerebellar-basal ganglia interactions, and compared the modulatory
183 r, the normative developmental trajectory of basal ganglia iron concentration during adolescence and
184 r, our results suggest a prolonged period of basal ganglia iron enrichment that extends into the mid-
188 lar nucleus (PF), an excitatory input to the basal ganglia, is targeted with deep-brain stimulation t
189 m(2)/sec; right, 1.15 x10(3)mum(2)/sec), and basal ganglia (left, 1.26 x10(3)mum(2)/sec; right, 1.23
190 years +/- 0.32; right, 1.45 years +/- 0.33), basal ganglia (left, 1.79 years +/- 0.31; right, 1.70 ye
191 in connectivity between the habenula and the basal ganglia, limbic, and sensory systems was already p
192 on effective connectivity within the cortico-basal ganglia loops at rest, as well as further modulati
193 esults demonstrate that activity through the basal ganglia may play an important and distinct role am
196 he striatum is the main input nucleus of the basal ganglia, mediating motor and cognitive functions.
197 extremity hemiparesis, we propose a cortico-basal ganglia model capable of performing reaching tasks
198 n's disease, leading to abnormal function of basal ganglia motor circuits and the accompanying charac
202 pected nogo signal recruited the same fronto-basal-ganglia network which is usually assigned to stopp
204 ther, these findings demonstrate that fronto-basal ganglia networks buttress action-selection under r
205 previous findings on the essential role for basal ganglia networks in absence seizures, in particula
206 ry of beta bursting, both locally and across basal ganglia networks, impacts on motor performance in
207 ry of beta bursting, both locally and across basal ganglia networks, may impact on motor performance.
210 logical methods to detail the progression of basal ganglia neuron type-specific pathology and the def
211 s issue by defining the firing properties of basal ganglia neurons around the emergence of cortical b
213 ally control the flow of information through basal ganglia nuclei that eventually project back to the
216 ursts of beta frequency band activity in the basal ganglia of patients with Parkinson's disease (PD)
219 tical injury had an AUC of 0.67 (0.60-0.73), basal ganglia or thalamic injury had an AUC of 0.81 (0.7
221 osphodiesterase 10A (PDE10A) activity in the basal ganglia orchestrates the control of coordinated mo
222 sampled single-unit activity from connected basal ganglia output and thalamic nuclei (globus pallidu
223 a convergence, illuminating how synchrony of basal ganglia output during motor learning or in patholo
224 y in the ventral thalamus, a major target of basal ganglia output, is often assumed to be permitted o
226 ing the impact of the subthalamic nucleus on basal ganglia output; then, at ~160 ms, suppression was
227 ow direct and indirect pathways can modulate basal ganglia outputs to facilitate movement initiation,
231 plementing this complex balancing act is the basal ganglia pathway, but its roles have not yet been e
235 ought to be nodes in circuits extending, via basal ganglia pathways, from mood-related neocortical re
238 ject to the subthalamic nucleus (STN) of the basal ganglia, play a key role in inhibiting impulsive r
239 ons of primate anterior cingulate cortex and basal ganglia predict the moment of gaining information
240 TEMENT The striatum is the main input of the basal ganglia processing information from different brai
241 kdown of Sgce in the cerebellum, but not the basal ganglia, produced motor symptoms, likely due to ab
242 dynamic functional connectivity between the basal ganglia (r = - 0.53, P = 0.003) and thalamic netwo
243 m represents the main input structure of the basal ganglia, receiving massive excitatory input from t
244 RPE signals in the ventral pallidum (VP), a basal ganglia region functionally linked to reward-seeki
246 centration using R2* relaxometry within four basal ganglia regions, including the caudate, putamen, n
249 left temporoparietal region, but not in the basal ganglia, relative to typically-developing matched
250 ting locomotion by releasing dopamine in the basal ganglia, spinal networks, and the mesencephalic lo
251 phase-locked action potential firing in each basal ganglia structure was shifted during burst initiat
252 Neuronal ensemble recordings in multiple basal ganglia structures of parkinsonian rats revealed t
254 ntal cortex with reward prediction errors in basal ganglia support exploration of latent task represe
255 IM1 in neurotransmitter release at prominent basal ganglia synapses, and provide evidence that RIM1-d
257 entify a novel intrinsic property of cortico-basal ganglia synchrony that suggests the phase of ongoi
259 the beta band, restrict the capacity of the basal ganglia system to encode physiologically relevant
261 medial temporal lobe, cerebellum, brainstem, basal ganglia, thalami, and orbitofrontal and sensorimot
262 CHD were demonstrated bilaterally within the basal ganglia, thalami, corpus callosum, occipital, temp
263 yelination and iron concentration within the basal ganglia-thalamic circuit over 2 years post-SCI.
264 tive and reorganizational changes across the basal ganglia-thalamic circuitry occur early after SCI a
265 Abnormally increased beta bursts in cortical-basal ganglia-thalamic circuits are associated with rigi
268 and temporal aspects of large-scale cortical-basal ganglia-thalamic interactions using dynamic functi
269 hat dynamic interactions within the cortical-basal ganglia-thalamic loop might play a role in the mod
270 ple known targets of plasticity (the cortico-basal ganglia-thalamic network), suggesting that feedbac
273 (mPFC) is a critical component of a cortico-basal ganglia-thalamo-cortical loop regulating limbic an
274 ease (PD), gamma oscillatory activity in the basal ganglia-thalamo-cortical network is altered and th
278 erspective of the interactive pathways among basal ganglia, thalamus and cortex, to explore the impri
279 etrical lesions found on neuroimaging in the basal ganglia, thalamus, and brainstem and by a loss of
281 synchronization in the insular, cerebellum, basal ganglia, thalamus, operculum, frontoparietal corti
282 nificant hippocampal inhibition of amygdala, basal-ganglia, thalamus, orbital frontal cortex, inferio
283 these changes in interactive profiles of the basal ganglia-thalamus network in the current history gr
284 of both the thalamocortical network and the basal ganglia-thalamus network with resting state functi
286 e, we show that a major input station of the basal ganglia, the caudate nucleus, plays a causal role
294 Mild worsening was identified in post-ATI basal ganglia total choline MRS, suggesting an alteratio
296 D n = 19,099, control sample n = 34,194), 2) basal ganglia volumes, and 3) fractional anisotropy in t
297 A key role in this process is played by the basal ganglia, where neural activity and plasticity are
298 (2+) currents in HVC neurons that target the basal ganglia, whereas tutor exposure increased the rest
299 s through their ascending projections to the basal ganglia, which in turn project to the mesencephali
300 ry brings together models of learning in the basal ganglia with the incentive salience theory in a si