Study summary · research use only
Vasoactive intestinal peptide (VIP): an amnestic neuropeptide
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This mouse study examined vasoactive intestinal peptide (VIP) effects on memory using a left-right footshock avoidance task in a T-maze. VIP into the third ventricle produced amnesia, and a 10-fold lower dose produced amnesia when given into the rostral hippocampus; VIP given 24 hr after training did not impair retention tested a week later. The VIP receptor antagonist [4-Cl-D-Phe6,Leu17]VIP enhanced retention when given into the rostral hippocampus, but not when given 24 hr after training. VIP's amnestic effect was blocked by peripheral arecoline, naloxone, and ST 587, but not cholecystokinin octapeptide, and by central arecoline but not neuropeptide Y. The authors concluded VIP is a potent amnestic peptide involved in memory modulation.
Abstract
Vasoactive intestinal peptide (VIP) is a neuropeptide present in high concentrations in the hippocampus. The studies reported here demonstrate that VIP administered into the third ventricle of the brain caused amnesia in mice trained on a left-right footshock avoidance task in a T-maze. VIP resulted in amnesia when administered directly into the rostral portion of the hippocampus at a 10-fold lower dose than was needed to produce amnesia when VIP was administered intracerebroventricularly. When VIP was administered 24 hr after training, it failed to impair retention measured a week later. VIP receptor antagonist ([4-Cl-D-Phe6,Leu17]VIP) enhanced retention when administered into the rostral portion of the hippocampus, suggesting that VIP plays a physiological role in memory modulation. VIP receptor antagonist administered 24 hr after training did not facilitate retention. To gain some insight as to how VIP may be affecting memory processing, we determined if some memory-improving compounds showed a selective ability to block amnesia induced by VIP. The amnestic effect of VIP was blocked by peripheral administration of the memory-enhancing agents, arecoline, naloxone and ST 587 (a noradrenergic receptor agonist) but not by cholecystokinin octapeptide. Central administration of arecoline, but not neuropeptide Y, blocked the amnestic effect of VIP. It is concluded that VIP is a potent amnestic peptide.
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