摘要
本工作用受体激动剂^(125)I-Bolton Hunter-CCK-8(^(125)I-BH-CCK)、CCK-A受体拮抗剂Devazepide、CCK-B受体拮抗剂L-365,260与脑组织切片共同孵育,以确定大鼠伏核、杏仁核、中脑导水管周围灰质等脑区内CCK受体的类型。结果显示:1μM未标记的CCK-8与^(125)I-BH-CCK及脑组织切片共同孵育,可完全竞争标记配体与受体的结合,说明这种结合是特异性的。30μM Devazepide可抑制脚间核处受体与标记配体的结合,但不能抑制伏核、杏仁核、中脑导水管周围灰质、大脑皮质及脊髓内受体与标记配体的结合;当剂量增大到90μM时,也只产生部分抑制。而用L-365,260只需90μM即可完全竞争伏核、杏仁核、中脑导水管周围灰质、大脑皮质及脊髓内受体与标记配体的结合。以上结果提示:脚间核部位的CCK受体为CCK-A受体;伏核、杏仁核、中脑导水管周围皮质、大脑皮质及脊髓内的CCK受体为CCK-B受体。
In vitro characterization of CCK receptors by autoradiographic receptor analysis in rat brain sections was performed using ^(125)I-Bolton Hunter CCK-8 (^(125)I-BH-CCK) as radiolabeled receptor ligand, and highly selective CCK-A receptor antagonist Devazepide and CCK-B receptor antagonist L-365, 260 as competitive inhibitors. The result showed that in nucleus aecumbens, amygdala, PAG. interpeduncular nucleus (IPN) and spinal cord, the labelling was abolished after incubation of the section with 1 μM cold CCK-8, indicating that the radiolabeled CCK binding was specific. In the IPN of the rat, ^(125)I-BH-CCK binding was selectively inhibited by 30 nM Devazepide. indicating that these receptors resemble CCK-A receptors. In nucleus accumbens, amygdala, PAG and spinal cord, ^(125)I-BH-CCK binding was significantly inhibited by Devazepide at 90 μM but not at 30 nM, and was totally abolished by 90 nM L-363, 260, indicating that these receptors are CCK-B receptors.
出处
《神经解剖学杂志》
CSCD
北大核心
1992年第2期177-180,共4页
Chinese Journal of Neuroanatomy
基金
国家自然科学基金及NIDA基金
关键词
伏核
杏仁核
中脑导水管
周围灰质
nucleus accumbens
amygdala
PAG
devazepide (formerly L364
718
MK-329)
L-365
260
CCK receptor
autoradiography
