Migaud M, Roques B P, Durieux C
Département de Pharmacochimie Moléculaire et Structurale, U266 INSERM-URA D 1500 CNRS, Faculté de Pharmacie, Paris, France.
Neuropharmacology. 1994 Jun;33(6):737-43. doi: 10.1016/0028-3908(94)90113-9.
In rat hippocampal slices, BC 264 (0.1-1 microM), a highly potent and selective CCK-B agonist, was found to increase basal release of endogenous glutamate and aspartate but not that of GABA. The natural peptide cholecystokinin octapeptide (CCK8) at 1 microM, induced the same effect. The selective CCK-B receptor antagonist, L-365,260, completely reversed these responses, confirming that they are related to CCK-B receptor activation. In the absence of extracellular Ca2+, the increase in excitatory amino acid release was completely abolished. In contrast to the basal release, the potassium evoked release of aspartate and glutamate was not modified by BC 264.
在大鼠海马切片中,发现高效且选择性的CCK - B激动剂BC 264(0.1 - 1微摩尔)可增加内源性谷氨酸和天冬氨酸的基础释放量,但不增加GABA的基础释放量。1微摩尔的天然肽八肽胆囊收缩素(CCK8)可诱导相同的效应。选择性CCK - B受体拮抗剂L - 365,260可完全逆转这些反应,证实它们与CCK - B受体激活有关。在无细胞外Ca2 +的情况下,兴奋性氨基酸释放的增加被完全消除。与基础释放不同,BC 264未改变钾离子诱发的天冬氨酸和谷氨酸释放。