Hutchison J B, Strupish J, Nahorski S R
Brain Res. 1986 Apr 9;370(2):310-4. doi: 10.1016/0006-8993(86)90485-3.
The release of immunoreactive cholecystokinin (CCK) and dopamine was monitored simultaneously from superfused rat striatal slices. Exposure of the tissue to medium containing elevated K+ or veratrine, induced a marked release of both substances. The addition of dopamine (10(-7) and 10(-6) M), the dopamine agonist pergolide (10(-7) M), the D2-antagonist sulpiride (1 microM) or the D1-antagonist (SCH 23390) had no significant effect on basal overflow or on evoked release of CCK. On the other hand, preincubation of striatal slices with D-amphetamine (10(-5) M) enhanced basal and veratrine-stimulated dopamine release but markedly suppressed evoked CCK release. Sulpiride blocked this action of amphetamine whereas SCH 23390 was ineffective. The data suggests that whereas it is difficult to observe any effects of exogenous dopamine agonists or antagonists on evoked CCK release, endogenously released dopamine appears to interact with D2-receptors to suppress evoked CCK release from rat striatal slices.
对灌流的大鼠纹状体切片中免疫反应性胆囊收缩素（CCK）和多巴胺的释放进行了同步监测。将组织暴露于含高钾或藜芦碱的培养基中，会诱导这两种物质的显著释放。添加多巴胺（10⁻⁷和10⁻⁶ M）、多巴胺激动剂培高利特（10⁻⁷ M）、D2拮抗剂舒必利（1 μM）或D1拮抗剂（SCH 23390）对CCK的基础释放或诱发释放均无显著影响。另一方面，用右旋苯丙胺（10⁻⁵ M）预孵育纹状体切片可增强基础和藜芦碱刺激的多巴胺释放，但显著抑制诱发的CCK释放。舒必利可阻断苯丙胺的这一作用，而SCH 23390则无效。数据表明，虽然很难观察到外源性多巴胺激动剂或拮抗剂对诱发的CCK释放有任何影响，但内源性释放的多巴胺似乎与D2受体相互作用，以抑制大鼠纹状体切片中诱发的CCK释放。
