The cerebellum communicates with the basal ganglia

Hoshi, Eiji; Tremblay, Léon; Féger, J.; Carras, Peter L.; Strick, Peter L.

doi:10.1038/nn1544

Cited by 761 publications

(652 citation statements)

References 14 publications

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“…Second, we suggest that compensation could occur more directly through projections from the cerebellum to the basal ganglia. For instance, recent evidence in monkeys indicates that the dentate nucleus communicates via a disynaptic connection with the input stage of basal ganglia processing in the striatum (Hoshi et al, 2005). This finding in monkeys supported previous work in the rat (Ichinohe et al, 2000).…”

Section: Compensation and Hyperactivation In The Cerebellumsupporting

confidence: 82%

“…We also examined the correlations with the right cerebellum because there are contralateral projections to motor areas and there is also a disynaptic connection with the contralateral (left) putamen (Hoshi et al, 2005). The left cerebellum was tested for correlations as a control condition because we did not anticipate correlations between the left cerebellum and left motor areas.…”

Section: Relation Between Hypo-and Hyper-activationmentioning

confidence: 99%

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Role of hyperactive cerebellum and motor cortex in Parkinson's disease

et al. 2007

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Previous neuroimaging studies have found hyperactivation in the cerebellum and motor cortex and hypoactivation in the basal ganglia in patients with Parkinson's disease (PD) but the relationship between the two has not been established. This study examined whether cerebellar and motor cortex hyperactivation is a compensatory mechanism for hypoactivation in the basal ganglia or is a pathophysiological response that is related to the signs of the disease. Using a BOLD contrast fMRI paradigm PD patients and healthy controls performed automatic and cognitively controlled thumb pressing movements. Regions of interest analysis quantified the BOLD activation in motor areas, and correlations between the hyperactive and hypoactive regions were performed, along with correlations between the severity of upper limb rigidity and BOLD activation. There were three main findings. First, the putamen, supplementary motor area (SMA) and pre-SMA were hypoactive in PD patients. The left and right cerebellum and the contralateral motor cortex were hyperactive in PD patients. Second, PD patients had a significant negative correlation between the BOLD activation in the ipsilateral cerebellum and the contralateral putamen. The correlation between the putamen and motor cortex was not significant. Third, the BOLD activation in the motor cortex was positively correlated with the severity of upper limb rigidity, but the BOLD activation in the cerebellum was not correlated with rigidity. Further, the activation in the motor cortex was not correlated with upper extremity bradykinesia. These findings provide new evidence supporting the hypothesis that hyperactivation in the ipsilateral cerebellum is a compensatory mechanism for the defective basal ganglia. Our findings also provide the first evidence from neuroimaging that hyperactivation in the contralateral primary motor cortex is not a compensatory response but is directly related to upper limb rigidity.Mailing Address: David E. Vaillancourt, Ph.D. Departments of Movement Sciences University of Illinois at Chicago 808 South Wood Street, 690 CME (MC 994) Chicago, Illinois 60612 Tel: (312) 355-2058 Fax: (312) 355-2305 court1@uic.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroimage. Author manuscript; available in PMC 2008 March 1. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptSporadic Parkinson's disease (PD) results from degeneration of the nigrostriatal dopaminergic system leading to resting tremor, rigidity, bradykinesia and akinesia. According to the classic model ...

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Section: Compensation and Hyperactivation In The Cerebellumsupporting

confidence: 82%

Section: Relation Between Hypo-and Hyper-activationmentioning

confidence: 99%

Role of hyperactive cerebellum and motor cortex in Parkinson's disease

et al. 2007

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“…Though DAT are found in both brain regions the concentration in cerebellum is low (Glaser et al, 2006;Sanchez-Gonzalez et al, 2005). However, DA regulation of metabolism in these brain regions could be indirect via striato-thalamic or striato-cerebellar pathways (Hoshi et al, 2005). Inasmuch as DAT regulate not only the concentration of extracellular DA but also the duration in the extrasynaptic space, these findings could be interpreted to indicate that chronically high DA concentrations as occur in DAT −/− lead to increases in BGluM in thalamus and cerebellum.…”

Section: Dat −/− Mice Have Significantly Greater Baseline Bglum Thanmentioning

confidence: 96%

The effects of cocaine on regional brain glucose metabolism is attenuated in dopamine transporter knockout mice

Thanos

Michaelides

Benveniste

et al. 2008

Synapse

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Cocaine's ability to block the dopamine transporter (DAT) is crucial for its reinforcing effects. However the brain functional consequences of DAT blockade by cocaine are less clear since they are confounded by its concomitant blockade of norepinephrine and serotonin transporters. To separate the dopaminergic from the non-dopaminergic effects of cocaine on brain function we compared the regional brain metabolic responses to cocaine between dopamine transporter deficient (DAT −/− ) mice with that of their DAT +/+ littermates. We measured regional brain metabolism (marker of brain function) with 2-[18F]-fluoro-2-deoxy-D-glucose (FDG) and microPET (μPET) before and after acute cocaine administration (i.p. 10 mg/kg). Scans were conducted 2 weeks apart. At baseline DAT −/− mice had significantly greater metabolism in thalamus and cerebellum than DAT +/+ . Acute cocaine decreased whole brain metabolism and this effect was greater in DAT +/+ (15%) than in DAT −/− mice (5%). DAT +/+ mice showed regional decreases in the olfactory bulb, motor cortex, striatum, hippocampus, thalamus and cerebellum whereas DAT −/− mice showed decreases only in thalamus. The differential pattern of regional responses to cocaine in DAT −/− and DAT +/+ suggests that most of the brain metabolic changes from acute cocaine are due to DAT blockade. Cocaine-induced decreases in metabolism in thalamus (region with dense noradrenergic innervation) in DAT −/− suggest that these were mediated by cocaine's blockade of norepinephrine transporters. The greater baseline metabolism in DAT −/− than DAT +/+ mice in cerebellum (brain region mostly devoid of DAT) suggests that dopamine indirectly regulates activity of these brain regions.

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“…Although the amygdala does not share any direct, monosynaptic connections with the cerebellum in nonhuman primates, the recent use of rabies virus as a transneuronal anatomical tracer has indicated multi-synaptic connections between the cerebellum and the prefrontal cortex (especially the dorsolateral prefrontal cortex, Kelly and Strick, 2003), and also between the cerebellum and putamen (Hoshi et al, 2005). It is possible that neonatal amygdala damage could influence metabolism in the cerebellum through these intermediary structures, since the amygdala possesses light, bidirectional connections with the dorsolateral prefrontal cortex and unidirectional connections with the putamen (Amaral et al, 1992, Ghashghaei et al, 2007, and both were significantly hypometabolic for amygdalalesioned animals.…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

Effects of neonatal amygdala or hippocampus lesions on resting brain metabolism in the macaque monkey: A microPET imaging study

et al. 2008

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Longitudinal analysis of animals with neonatal brain lesions enables the evaluation of behavioral changes during multiple stages of development. Interpretation of such changes, however, carries the caveat that permanent neural injury also yields morphological and neurochemical reorganization elsewhere in the brain that may lead either to functional compensation or to exacerbation of behavioral alterations. We have measured the long-term effects of selective neonatal brain damage on resting cerebral glucose metabolism in nonhuman primates. Sixteen rhesus monkeys (Macaca mulatta) received neurotoxic lesions of either the amygdala (n = 8) or hippocampus (n = 8) when they were 2-weeks-old. Four years later, these animals, along with age-and experience-matched sham-operated control animals (n = 8), were studied with high-resolution positron emission tomography (microPET) and 2-deoxy-2[ 18 F]fluoro-D-glucose ([ 18 F]FDG) to detect areas of altered metabolism. The groups were compared using an anatomically-based region of interest analysis. Relative to controls, amygdala-lesioned animals displayed hypometabolism in three frontal lobe regions, as well as in the neostriatum and hippocampus. Hypermetabolism was also evident in the cerebellum of amygdala-lesioned animals. Hippocampal-lesioned animals only showed hypometabolism in the retrosplenial cortex. These results indicate that neonatal amygdala and hippocampus lesions induce very different patterns of long-lasting metabolic changes in distant brain regions. These observations raise the possibility that behavioral alterations in animals with neonatal lesions may be due to the intended damage, to consequent brain reorganization or to a combination of both factors.The study of neurodevelopmental disorders within a clinical setting is inherently complex since each patient's specific behavioral and cognitive deficits stem from a unique interaction between genetic, neurobiological and environmental factors. Longitudinal analysis of animal models provides a complementary approach, since genetic, neurobiological and environmental factors * Corresponding Author: David G. Amaral, Ph.D., The M.I.N.D. Institute, University of California, Davis, 2825 50 th Street, Sacramento, CA 95817,, Email: dgamaral@ucdavis.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroimage. Author manuscript; available in PMC 2009 January 15. Published in final edited form as:Neuroimage. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript can be selectively manipulated and tightly controlle...

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The cerebellum communicates with the basal ganglia

Cited by 761 publications

References 14 publications

Role of hyperactive cerebellum and motor cortex in Parkinson's disease

Role of hyperactive cerebellum and motor cortex in Parkinson's disease

The effects of cocaine on regional brain glucose metabolism is attenuated in dopamine transporter knockout mice

Effects of neonatal amygdala or hippocampus lesions on resting brain metabolism in the macaque monkey: A microPET imaging study

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