Abstract

Abstract When an individual encounters stressors such as physical pain, internal malaise, or drought conditions, a constellation of physiological and behavioral responses are evoked that aid the individual in coping with the stressors and learning strategies to minimize exposure to these stressors. Vasopressin (VP) plays an important role in modulating these responses and this role is complex. Acute painful stimuli such as electric footshock stimulate hormonal and neural release of VP and this in turn can contribute to analgesia and facilitate maintenance of behaviors that allow the individual to avoid future painful encounters in the same environmental context. The effect of VP on avoidance maintenance is consistent no matter when during the stressful situation it is released. Two hypotheses have emerged to account for the action of VP on shock avoidance maintenance. One states that central VP is necessary for optimal mnemonic processing of aversive environmental stimuli and the other states that VP produces nonspecific effects on arousal systems that modulate memory processes. There is evidence to support both positions. Internal malaise induced by consumption of toxic substances also stimulates hormonal release of VP and this in turn facilitates a reduction in exposure to the toxic substance and modulates maintenance of behaviors that avoid future contact with the toxic substance. The hormonal and neural release of low levels of VP promotes relinquishing avoidance behavior when it is present after the first exposure to the stressor but the release of high levels of VP facilitates maintenance. It is suggested that low doses of VP reduce the sensory impact of toxins while high doses of VP have aversive stimulus properties that are additive with the properties of toxins. Finally, scarcity of water stimulates hormonal release of VP, which directly promotes water retention. The neural changes in VP release during the conditions of water restriction can affect avoidance behavior maintenance when an individual encounters other stressors. It facilitates maintaining avoidance behavior for physical pain stressors and relinquishing avoidance behavior for internal malaise stressors. The picture emerging is that VP has variable effects on learning and memory processes. Some of these effects are due to its direct action on the neural systems mediating these processes while other effects are due to its action on modulatory neural systems, such as those mediating the aversive properties of VP and those mediating arousal.

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