A facilitatory role of vasopressin in hypoxia/hypoglycemia-induced impairment of dopamine release from rat striatal slices.

The excitatory amino acid, glutamate plays a crucial role in the pathogenesis of brain damage caused by anoxia and/or hypoglycemia. Although vasopressin (VP) also acts as an excitatory transmitter in the CNS, little is known about its effect on hypoxic and/or ischemic brain damage. In this study, we investigated the effect of arginine vasopressin (AVP) on hypoxia/hypoglycemia-induced impairment of dopamine release from striatal slices. Striatal slices were incubated in hypoxia-/hypoglycemia-inducing medium with or without AVP (0.01-1.0 microM) for 20 min. After 1-3 h of washout in normal medium, high K(+)-evoked dopamine release from the slices were examined. Hypoxia/hypoglycemia-induced decrease of striatal dopamine release was reversed by the removal of Ca2+ in the medium, but not by VP1- or VP2-receptor antagonist. In contrast, AVP potentiated the hypoxia/hypoglycemia-induced decrease of dopamine release in the striatum. This AVP-induced deterioration of the striatal response was antagonized by VP2 receptor antagonist, but not by VP1 receptor antagonist. The present results suggest that AVP may play a facilitatory role in hypoxia/hypoglycemia-induced dopamine release deficit mediated through the activation of VP2 receptor.