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大鼠脑尾状核与伏隔核中可释放多巴胺调节的体内比较。

In vivo comparison of the regulation of releasable dopamine in the caudate nucleus and the nucleus accumbens of the rat brain.

作者信息

Kuhr W G, Bigelow J C, Wightman R M

出版信息

J Neurosci. 1986 Apr;6(4):974-82. doi: 10.1523/JNEUROSCI.06-04-00974.1986.

DOI:10.1523/JNEUROSCI.06-04-00974.1986
PMID:3486259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6568443/
Abstract

In vivo voltammetry has been used to measure the release of dopamine evoked by electrical stimulation of the medial forebrain bundle (MFB). Simultaneous measurements have been made with voltammetric-sensing electrodes ipsilateral to the stimulating electrode in the nucleus accumbens and the caudate nucleus of the anesthetized rat. During the stimulation, the species observed in both regions is voltammetrically identical to dopamine. Further evidence for the identity of dopamine is provided by anatomical, physiological, pharmacological, and postmortem data. Postmortem analysis of these brain regions after a single stimulation demonstrates that dopamine levels are unchanged, while dihydroxyphenylacetic acid (DOPAC) levels are increased in both regions. Systemic application of synthesis inhibitors results in a decrease in evoked release for each brain region. Amfonelic acid results in a restoration of stimulated release after synthesis inhibition. Evoked release is affected differently by pargyline in the two brain regions. The evoked release of dopamine is significantly elevated in the nucleus accumbens as a result of pargyline administration, but similar effects are not seen in the caudate nucleus. Tissue levels of dopamine are increased in both brain regions by pargyline, but the increase is significantly greater in the accumbens. Electrolytic lesions of the striatonigral pathway or systemic administration of picrotoxin eliminates the pargyline-induced difference in evoked release of dopamine. Amphetamine causes a reduction in stimulated release in the caudate nucleus with little effect on that observed in the nucleus accumbens.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

体内伏安法已被用于测量由电刺激内侧前脑束(MFB)诱发的多巴胺释放。已在麻醉大鼠的伏隔核和尾状核中,使用与刺激电极同侧的伏安传感电极进行了同步测量。在刺激过程中,在这两个区域观察到的物质在伏安法上与多巴胺相同。解剖学、生理学、药理学和死后数据为多巴胺的一致性提供了进一步证据。单次刺激后对这些脑区的死后分析表明,多巴胺水平未发生变化,而两个区域中的二羟基苯乙酸(DOPAC)水平均有所升高。全身应用合成抑制剂会导致每个脑区诱发释放减少。氨苯蝶啶可在合成抑制后恢复刺激释放。在两个脑区中,优降宁对诱发释放的影响不同。施用优降宁后,伏隔核中多巴胺的诱发释放显著升高,但在尾状核中未观察到类似效果。优降宁使两个脑区的多巴胺组织水平均升高,但伏隔核中的升高幅度明显更大。纹状体黑质通路的电解损伤或全身施用苦味毒可消除优降宁诱导的多巴胺诱发释放差异。苯丙胺可使尾状核中的刺激释放减少,而对伏隔核中观察到的刺激释放影响很小。(摘要截短于250字)