Altered cerebellar and prefrontal cortex function in rhesus monkeys that previously self-administered cocaine.

Altered cerebellar and prefrontal cortex function in rhesus monkeys that previously self-administered cocaine.
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DOI:
10.1007/s00213-014-3560-z
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发表时间:
2014-10
期刊:
影响因子:
3.4
通讯作者:
Bradberry, Charles W.
Bradberry, Charles W.
中科院分区:
医学3区
文献类型:
--
作者:
Porter, Jessica N.;Minhas, Davneet;Lopresti, Brian J.;Price, Julie C.;Bradberry, Charles W.

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Differences in brain function in cocaine users can occur even when frank deficits are not apparent, indicating neuroadaptive consequences of use. Using monkeys to investigate altered metabolic activity following chronic cocaine self-administration allows an assessment of altered function due to cocaine use, without the confound of pre-existing differences or polysubstance use often present in clinical studies. To evaluate alterations in metabolic function during a working memory task in prefrontal cortex and the cerebellum following one year of chronic cocaine self-administration followed by a 20 month drug-free period. [18F] Fluorodeoxyglucose PET imaging was used to evaluate changes in relative regional metabolic activity associated with a delayed match to sample working memory task. Chronic cocaine animals were compared to a control group, and region of interest analyses focused on the dorsolateral prefrontal cortex (DLPFC) and cerebellum. Despite no differences in task performance, in the cocaine group, the cerebellum showed greater metabolic activity during the working memory task (relative to the control task) compared to the control group. There was also a trend towards a significant difference between the groups in DLPFC activity (p=0.054), with the cocaine group exhibiting lower DLPFC metabolic activity during the delay task (relative to the control task) than the control group. The results support clinical indications of increased cerebellar activity associated with chronic cocaine exposure. Consistent with evidence of functional interactions between cerebellum and prefrontal cortex, these changes may serve to compensate for potential impairments in functionality of DLPFC.
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