cholecystokinin and Amnesia

It has been reported that a nonapeptide (Val-Pro-Val-Glu-Ala-Val-Asp-Pro-Met) called V-9-M is produced from procholecystokinin in the brain. Since this peptide is particularly abundant in the hippocampus, septum, and amygdala. V-9-M may be involved in memory processes. The present study was attempted to observe the effect of V-9-M on memory processes of rat performing a one-trial passive avoidance task and a platform jumping active avoidance task. The results indicate that injection of V-9-M into the lateral ventricle of the rat prevents experimental amnesia induced by electroconvulsive shock in passive avoidance testing, and that this effect is not significantly affected by cholecystokinin-8 antagonists. V-9-M also causes a long-lasting enhancement of memory in the active avoidance task. These results suggest that V-9-M may participate in the facilitation of memory.

Topics: Amnesia; Animals; Avoidance Learning; Cholecystokinin; Electroshock; Injections, Intraventricular; Injections, Subcutaneous; Male; Memory; Peptide Fragments; Proglumide; Protein Precursors; Rats; Rats, Inbred Strains; Time Factors

The effects of cholecystokinin octapeptide (CCK-8), cholecystokinin tetrapeptide amide (CCK-4), beta-endorphin, proglumide, and naloxone on passive avoidance behavior were studied in rats. Intracerebroventricular (i.c.v.) injection of beta-endorphin (1-10 micrograms) had no significant influence on the latency of the avoidance response in intact rats. Also, beta-endorphin (0.05-5 micrograms, i.c.v.) did not affect the response in rats treated with electroconvulsive shock (ECS). The preventive effect of CCK-8 (0.1-1.0 micrograms, i.c.v.) on ECS-induced amnesia was partly antagonized by beta-endorphin (0.05-10 micrograms, i.c.v.). Intraperitoneal (i.p.) injection of naloxone (1-10 mg/kg) could not prevent ECS-induced amnesia, but continuous subcutaneous infusion of this drug (2 mg/day, 7 days) completely abolished the amnesia. Naloxone (1 and 10 mg/kg, i.p.) also partly antagonized amnesia induced by proglumide (1 and 10 micrograms, i.c.v.) and prevented it when induced by CCK-4 (5 and 10 micrograms, i.c.v.). The results indicate the facilitating action of naloxone and the inhibitory effect of beta-endorphin on memory, suggesting that the endogenous opiate systems are involved in some way in the memory processes.

Topics: Amnesia; Animals; Avoidance Learning; beta-Endorphin; Cholecystokinin; Electroshock; Injections, Intraperitoneal; Injections, Intraventricular; Male; Naloxone; Proglumide; Rats; Rats, Inbred Strains