缩胆囊素诱导的新生儿大鼠脐带腹根去极化。

S K Long
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引用次数: 1

摘要

1. 硫酸化胆囊收缩素八肽(CCK8S, 0.03 ~ 1.00微米)、五肽(CCK5)和四肽(CCK4)在体外诱导新生大鼠腹根浓度依赖性去极化。2. CCK5与CCK8S等能,但CCK4较弱(等能摩尔比为17.5)。3.河豚毒素(0.1 μ m)、Mg2+离子(0.75 μ m)和NMDA受体拮抗剂2-氨基-5-磷酸戊酸酯(AP5, 10 μ m)均可抑制cck8s诱导的去极化。这些结果表明,cck8s诱导的去极化主要是通过神经元间部位释放兴奋性氨基酸介导的。4. 选择性CCKA和CCKB受体拮抗剂L-364,718和L-365,260均抑制cck8s诱导的去极化。1 μ m L-364,718和L-365,260存在时CCK8S的剂量比分别为4.5和11.2,表明该反应主要是通过刺激CCKB受体介导的。5. 这些结果表明,新生大鼠半脐带制备是一种适合进行功能性CCK受体检测的组织。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cholecystokinin-induced ventral root depolarization of neonate rat hemicord in vitro.

1. Sulphated cholecystokinin octapeptide (CCK8S, 0.03-1.00 microM), pentapeptide (CCK5) and tetrapeptide (CCK4) elicited concentration dependent depolarizations of neonate rat ventral roots in vitro. 2. CCK5 was equipotent with CCK8S although CCK4 was weaker (equipotent molar ratio 17.5). 3. CCK8S-induced depolarizations were depressed by tetrodotoxin (0.1 microM), Mg2+ ions (0.75 mM) and the NMDA receptor antagonist 2-amino-5-phosphonopentanoate (AP5, 10 microM). These results suggest that CCK8S-induced depolarizations were predominantly mediated through the release of an excitatory amino acid from interneuronal sites. 4. The selective CCKA and CCKB receptor antagonists, L-364,718 and L-365,260 both depressed CCK8S-induced depolarizations. CCK8S dose ratios in the presence of 1 microM L-364,718 or L-365,260 were 4.5 and 11.2 respectively, suggesting the response was mediated predominantly through stimulation of CCKB receptors. 5. These results suggest that the neonate rat hemicord preparation is a suitable tissue for functional CCK receptor assays.

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