Windels François, Kiyatkin Eugene A
Cellular Neurobiology Branch, National Institute on Drug Abuse - Intramural Research Program, National Institutes of Health, DHHS, Baltimore, Maryland 21224, USA.
Neuroreport. 2006 Jul 17;17(10):1071-5. doi: 10.1097/01.wnr.0000221845.43126.7d.
It is hypothesized that substantia nigra pars reticulata neurons become overactive during a deficit of dopamine transmission. In this study, we examined how acute dopamine receptor blockade (SCH23390 and eticlopride) affects impulse activity of substantia nigra pars reticulata neurons and their response to iontophoretic gamma-amino-n-butyric acid in awake, unrestrained rats. No changes in discharge rate were found during complete dopamine receptor blockade, but these neurons showed a diminished response to gamma-amino-n-butyric acid, suggesting gamma-amino-n-butyric acid receptor hyposensitivity. This may result from tonic increase in gamma-amino-n-butyric acid input from the striatum and globus pallidus, which are activated during dopamine receptor blockade. As substantia nigra pars reticulata neurons are autoactive and resistant to tonic increases in gamma-amino-n-butyric acid input, changes in their responsiveness to phasic gamma-amino-n-butyric acid inputs, not tonic increase discharge rate, may underlie movement disturbance following dopamine deficit.
据推测，在多巴胺传递不足时黑质网状部神经元会变得过度活跃。在本研究中，我们研究了急性多巴胺受体阻断（SCH23390和依托必利）如何影响清醒、不受束缚大鼠黑质网状部神经元的冲动活动及其对离子导入γ-氨基丁酸的反应。在完全多巴胺受体阻断期间未发现放电率变化，但这些神经元对γ-氨基丁酸的反应减弱，提示γ-氨基丁酸受体低敏。这可能是由于纹状体和苍白球的γ-氨基丁酸输入在多巴胺受体阻断期间被激活而出现的紧张性增加所致。由于黑质网状部神经元具有自发放电且对γ-氨基丁酸输入的紧张性增加具有抗性，它们对相位性γ-氨基丁酸输入反应性的变化而非紧张性放电率增加，可能是多巴胺缺乏后运动障碍的基础。
