Alescio-Lautier B, Rao H, Paban V, Devigne C, Soumireu-Mourat B
Laboratoire de Neurobiologie des Comportements, URA CNRS 372-Universitede Provence, Marseille, France.
Eur J Pharmacol. 1995 Dec 29;294(2-3):763-70. doi: 10.1016/0014-2999(95)00632-x.
We have previously shown that [Arg8]vasopressin bilaterally administered into the ventral hippocampus of mice at a dose of 0.025 ng/animal 10 min prior to the retention session, improved long-term retrieval processes and relearning of a Go-No-Go visual discrimination task. The purpose of the present study was to determine whether the vasopressin V1 receptor antagonist, -beta-mercapto-beta,beta-cyclopentamethylenepropionyl1, O-Me-Tyr2,Arg8]vasopressin, d(CH2)5Tyr(Me)vasopressin), is able to block the behavioral effect of arginine-vasopressin in the ventral hippocampus. We first tested the effect of three doses of d(CH2)5Tyr(Me)vasopressin (0.025, 1, and 6.3 ng/animal) in the same experimental conditions as used for arginine-vasopressin. The results showed a dose-dependent deleterious effect of the vasopressin V1 receptor antagonist on retrieval and relearning, suggesting the involvement of endogenous arginine-vasopressin in the ventral hippocampus for these memory processes. Second, we tested the ability of d(CH2)5Tyr(Me)vasopressin to block the enhancing effect of experimentally administered arginine-vasopressin. The antagonist was injected at a dose of 0.025 ng, which had no intrinsic effect on behavior, or at a dose of 1 ng, which had a weak deleterious effect on behavior, followed by administration of 0.025 ng of arginine-vasopressin. The results showed that even at the weakest dose (0.025 ng), d(CH2)5Tyr(Me)vasopressin blocked the enhancing effect of arginine-vasopressin on retrieval and relearning. Thus, as for other behaviors and structures, the antagonist microinjected into the ventral hippocampus prevents the enhancing effect of arginine-vasopressin on long-term retrieval and relearning. However, the exclusive involvement of the vasopressin V1 receptors remain to demonstrate vis-a-vis oxytocin receptors.
我们之前已经表明，在记忆巩固阶段前10分钟，以0.025 ng/只动物的剂量将[精氨酸8]加压素双侧注射到小鼠腹侧海马中，可改善长期记忆提取过程以及对视觉辨别任务（Go-No-Go任务）的再学习。本研究的目的是确定加压素V1受体拮抗剂——β-巯基-β,β-环戊亚甲基丙酰基1、O-甲基酪胺2、精氨酸8]加压素（d(CH2)5Tyr(Me)加压素）——是否能够阻断精氨酸加压素在腹侧海马中的行为效应。我们首先在与精氨酸加压素相同的实验条件下测试了三个剂量的d(CH2)5Tyr(Me)加压素（0.025、1和6.3 ng/只动物）的效应。结果显示，加压素V1受体拮抗剂对记忆提取和再学习具有剂量依赖性的有害作用，这表明内源性精氨酸加压素参与了腹侧海马中的这些记忆过程。其次，我们测试了d(CH2)5Tyr(Me)加压素阻断实验性给予的精氨酸加压素增强效应的能力。拮抗剂分别以对行为无内在影响的0.025 ng剂量或对行为有微弱有害作用的1 ng剂量注射，随后给予0.025 ng的精氨酸加压素。结果表明，即使在最弱剂量（0.025 ng）下，d(CH2)5Tyr(Me)加压素也能阻断精氨酸加压素对记忆提取和再学习的增强效应。因此，与其他行为和结构一样，微注射到腹侧海马中的拮抗剂可阻止精氨酸加压素对长期记忆提取和再学习的增强效应。然而，加压素V1受体的唯一参与相对于催产素受体仍有待证明。
