Gerhardt G A, Friedemann M, Brodie M S, Vickroy T W, Gratton A P, Hoffer B J, Rose G M
Department of Psychiatry, University of Colorado Health Sciences Center, Denver 80262.
Brain Res. 1989 Oct 9;499(1):157-63. doi: 10.1016/0006-8993(89)91146-3.
The action of cholecystokinin (CCK) on presynaptic function of dopaminergic nerve terminals has been the subject of much debate in the literature. In efforts to resolve some of the reported ambiguities, high speed in vivo electrochemical recordings were carried out in the caudate nucleus and nucleus accumbens of the urethane anesthetized rat, to determine effects of locally applied sulfated (CCK-8S) and unsulfated (CCK-8US) CCK octapeptide. Locally-applied CCK-8S and CCK-8US caused no increase in the baseline electrochemical signals recorded from either brain region. However, locally applied CCK-8S potentiated the potassium-evoked overflow of dopamine (DA) into the extracellular space in both the caudate and nucleus accumbens. In contrast, pressure ejection of CCK-8US produced no significant effects on the potassium-evoked overflow of DA in either structure. These data support a facilitatory effect of CCK-8S on potassium-evoked overflow from DA-containing nerve terminals in the urethane anesthetized rat that is likely mediated through a peripheral type CCK receptor.
胆囊收缩素（CCK）对多巴胺能神经末梢突触前功能的作用在文献中一直是众多争论的主题。为了解决一些已报道的模糊问题，在乌拉坦麻醉大鼠的尾状核和伏隔核中进行了高速体内电化学记录，以确定局部应用的硫酸化（CCK-8S）和未硫酸化（CCK-8US）CCK八肽的作用。局部应用CCK-8S和CCK-8US均未使从任一脑区记录到的基线电化学信号增加。然而，局部应用CCK-8S增强了尾状核和伏隔核中钾诱发的多巴胺（DA）向细胞外空间的溢出。相反，CCK-8US的压力喷射对任一结构中钾诱发的DA溢出均无显著影响。这些数据支持CCK-8S对乌拉坦麻醉大鼠中含DA神经末梢钾诱发溢出具有促进作用，这可能是通过外周型CCK受体介导的。
