Abstract

Animal research indicated that vasopressin (VP) exerts its principle behavioral influence, the improvement of memory formation, through an action on septo-hippocampal and connected limbic structures. Here human research is reviewed with the notion of a comparable effect of VP in healthy humans. Although the human studies yielded less consistent results than those in rats, they indicate that VP is able to improve declarative memory formation which is the type of memory essentially relying on hippocampal function. The effect appears to center on the encoding process for memory. In examinations of event-related brain potentials (ERPs) VP was consistently found to increase the 'mismatch negativity' (MMN) and the P3 components which are ERP potentials closely linked to the hippocampal processing of novel, unexpected and salient events. Enhanced processing of these stimulus aspects is considered to precipitate memory encoding. The regulation of voluntary selective attention and arousal do not appear to be primary targets of VP effects in humans. A mediation of effects by peripheral changes can be excluded since the central nervous effects were observed in studies using intranasal VP administration providing a direct access to brain functions.

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