Liu J K, Kato T
Laboratory of Molecular Recognition, Graduate School of Integrated Science, Yokohama City University, Japan.
Brain Res. 1996 Sep 30;735(1):30-5. doi: 10.1016/s0006-8993(96)00577-x.
The release of cholecystokinin (CCK) and dopamine (DA) was measured simultaneously in the medial frontal cortex of the rat using an in vivo microdialysis technique coupled to either enzyme immunoassay or high performance liquid chromatography with electrochemical detection method. Basal levels of CCK-like immunoreactivity (CCK-LI) and DA in the dialysates were 0.29 +/- 0.05 pg/50 microliters and 4.98 +/- 0.56 fmol/20 microliters respectively. After perfusion of 100 micrograms/ml veratrine into rat medial frontal cortex through the microdialysis probe, the release of those neurotransmitters was significantly enhanced. Perfusion of 10 mM NMDA induced significant increases of CCK-LI and DA levels. Co-perfusion of 1 mM SCH23390, a D1 receptor antagonist, suppressed NMDA-evoked CCK-LI release and slightly raised NMDA-evoked DA release. Treatment with scopolamine, a muscarinic receptor antagonist, suppressed veratrine-induced CCK-LI and DA release, but did not change NMDA-evoked CCK-LI and DA release. These results suggest that NMDA may regulate CCK-LI release through the activation of D1 receptor existing on the afferent CCK neurons or interneurons in rat medial frontal cortex, and changes of endogenous CCK release may be involved in NMDA receptor-mediated long-term potentiation.
采用体内微透析技术结合酶免疫测定法或高效液相色谱电化学检测法，同时测定大鼠内侧前额叶皮质中胆囊收缩素（CCK）和多巴胺（DA）的释放。透析液中CCK样免疫反应性（CCK-LI）和DA的基础水平分别为0.29±0.05 pg/50微升和4.98±0.56 fmol/20微升。通过微透析探针将100微克/毫升藜芦碱灌注到大鼠内侧前额叶皮质后，这些神经递质的释放显著增强。灌注10 mM N-甲基-D-天冬氨酸（NMDA）可使CCK-LI和DA水平显著升高。共同灌注1 mM SCH23390（一种D1受体拮抗剂）可抑制NMDA诱发的CCK-LI释放，并略微提高NMDA诱发的DA释放。用毒蕈碱受体拮抗剂东莨菪碱处理可抑制藜芦碱诱导的CCK-LI和DA释放，但不改变NMDA诱发的CCK-LI和DA释放。这些结果表明，NMDA可能通过激活大鼠内侧前额叶皮质传入CCK神经元或中间神经元上存在的D1受体来调节CCK-LI释放，内源性CCK释放的变化可能参与NMDA受体介导的长时程增强。
