Abstract

Experiments were designed to investigate the release of endogenous vasopressin (AVP) as related to passive avoidance behavior and the significance of circulating AVP levels for memory processes using a radioimmunoassay (RIA) and bioassay (AD activity). The levels in plasma obtained from eye plexus blood were very high. A good correlation was found between AD activity and immunoreactive AVP (y = 21.10 + 3.00x, r = 0.895, n = 59). Vasopressin levels in eye plexus blood of male rats were significantly higher than in female rats. The rate of AVP release in Wistar and Brattleboro homozygous normal rats at the 24 h retention test was related to the intensity of the electric footshock during the learning trial and the avoidance latency at the 24 h retention test. The release of AVP immediately after the learning trial was much higher than after the 24 h retention test. Blood levels were not different whether rats received electric footshock or not and were not related to the intensity of the aversive stimulus or to passive avoidance latencies at the 24 h retention test. Brattleboro homozygous diabetes insipidus rats, which had no detectable vasopressin levels in eye plexus blood failed to show passive avoidance behavior even after exposure to high shock intensity. Rats heterozygous for diabetes insipidus exhibited maximal avoidance when a high shock intensity was used. Plasma AVP levels of these rats were however not different from those measured in non-shocked rats either after the learning trial or the 24 h retention test. Passive avoidance behavior was markedly attenuated in male Wistar rats treated with AVP antiserum icv either before the learning trial or the 24 h retention test. This treatment prevented AVP release at the retention trial but not after the learning trial. These results suggest that the long term memory effect originates from AVP of central origin.

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