Freeman A S, Chiodo L A, Lentz S I, Wade K, Bannon M J
Laboratory of Neurophysiology, Sinai Research Institute, Detroit, MI 48235.
Brain Res. 1991 Aug 2;555(2):281-7. doi: 10.1016/0006-8993(91)90353-w.
Cholecystokinin octapeptide (CCK-8) is colocalized within a majority of dopamine (DA)-containing neurons of the rat midbrain. Exogenous CCK-8 can modulate the electrophysiological activity of DA neurons, at least in part, by direct actions on the somatodendritic region of these cells. If CCK-8 is somatodendritically released from DA neurons, it may influence DA cell function as has been shown for DA itself. In the present study, radioimmunoassay was used to determine if CCK-8 is released in vitro from slices of rat midbrain under basal and depolarizing (30 mM potassium) conditions. Low levels of CCK-8 were detected in the basal incubation medium. Thirty mM potassium caused about a 3-fold increase in the release of CCK-8. This stimulated release was abolished in calcium-free medium. The D2 receptor agonist quinpirole, but not the D1 agonist SKF 38393, attenuated the potassium-stimulated release of CCK-8 but did not affect basal release. These results show that CCK-8, like DA, can be released from midbrain slices, presumably from DA/CCK-8-containing neurons. This finding is in accordance with the possibility that CCK-8 plays a role in the regulation of DA neuronal function at the level of the cell body, where it might influence the excitability of the DA cell membrane.
胆囊收缩素八肽（CCK - 8）与大鼠中脑大多数含多巴胺（DA）的神经元共定位。外源性CCK - 8至少部分地通过直接作用于这些细胞的树突体区域来调节DA神经元的电生理活动。如果CCK - 8从DA神经元的树突体释放，它可能会像DA本身那样影响DA细胞功能。在本研究中，采用放射免疫分析法来确定在基础条件和去极化（30 mM钾）条件下，CCK - 8是否能从大鼠中脑切片中体外释放。在基础孵育培养基中检测到低水平的CCK - 8。30 mM钾使CCK - 8的释放增加了约3倍。这种刺激释放的现象在无钙培养基中消失。D2受体激动剂喹吡罗能减弱钾刺激的CCK - 8释放，但D1激动剂SKF 38393则不能，且两者均不影响基础释放。这些结果表明，CCK - 8与DA一样，可以从中脑切片中释放，推测是从含DA/CCK - 8的神经元释放。这一发现符合CCK - 8在细胞体水平调节DA神经元功能中发挥作用的可能性，在该水平它可能影响DA细胞膜的兴奋性。
