Add time:09/01/2019         Source:sciencedirect.com

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 μl and 4.98 ± 0.56 fmol/20 μl, respectively. After perfusion of 100 μ/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.

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