Comparison of the effects of chronic haloperidol treatment on A9 and A10 dopamine neurons in the rat.
Comparison of the effects of chronic haloperidol treatment on A9 and A10 dopamine neurons in the rat.
复制标题
长期氟哌啶醇治疗对大鼠 A9 和 A10 多巴胺神经元的影响比较。
DOI：
10.1016/0024-3205(83)90929-3
复制
发表时间：
1983
期刊：
影响因子：
6.1
通讯作者：
Wang,RY
中科院分区：
文献类型：
--
作者：
White,FJ;Wang,RY
采用细胞外单细胞记录技术比较慢性氟哌啶醇(CHAL)对A9和A10多巴胺(DA)神经元的影响。CHAL使自发活动的A9和A10 DA细胞的数量随时间而减少，并在许多仍然活跃的DA细胞中诱导出不规则的放电模式。这两种影响在A10比A9发生得更早，程度也更大。静脉注射DA激动剂阿朴吗啡，既能逆转DA神经元活性的减少，又能逆转DA神经元的不规则放电模式，提示这两种效应都是去极化失活过程所致。损毁伏隔核(NAC)可阻止A10DA神经元去极化失活的发展，表明这一过程主要是通过NAC-A10反馈通路介导的。结果提示，CHAL引起的DA细胞去极化失活的缓慢发展可能是抗精神病药物长期治疗临床效应延迟起效的原因之一。
The effects of chronic haloperidol (CHAL) treatment on A9 and A10 dopamine (DA) neurons were compared using extracellular single cell recording techniques. CHAL caused a time-dependent reduction in the number of spontaneously active A9 and A10 DA cells and induced an irregular firing pattern in many of the DA cells that remained active. Both of these effects occurred earlier and to a greater extent in A10 than in A9. Intravenous injection of the DA agonist apomorphine reversed both the reduction of active DA neurons and the irregular discharge pattern, suggesting that both effects were due to the process of depolarization inactivation. Lesions of the nucleus accumbens (NAc) produced by ibotenic acid prevented the development of depolarization inactivation of A10 DA neurons, indicating that this process is mediated primarily by NAc — A10 feedback pathways. The results suggest that the slow development of depolarization inactivation of DA cells produced by CHAL may contribute to the delayed onset of the clinical effects of long-term treatment with antipsychotic drugs.