Elsevier

Brain Research

Volume 633, Issues 1–2, 7 January 1994, Pages 91-96
Brain Research

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

https://doi.org/10.1016/0006-8993(94)91526-1Get rights and content

Abstract

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 μM) 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.

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Cited by (3)

  • Arginine-vasopressin in nucleus of the tractus solitarius induces hyperglycemia and brain glucose retention

    2001, Brain Research
    Citation Excerpt :

    Arginine-vasopressin antagonist microinjections alone produced a small but significant reduction in brain A–V glucose difference, in contrast to the increases observed after AVP injections into the NTS. This effect could, perhaps, be explained by the antagonist preventing action of endogenous AVP [39], but the possibility that the VP1-A could act as an inverse agonist by reducing the constitutive activity, might also be considered [48]. The changes in circulating glucose were not caused by peripheral effects of AVP.

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