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.
Original language | English |
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Pages (from-to) | 91-96 |
Number of pages | 6 |
Journal | Brain Research |
Volume | 633 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 1994 Jan 7 |
Externally published | Yes |
Keywords
- Brain slice
- Dopamine release
- Hypoxia/hypoglycemia
- Ischemia
- Striatum
- Vasopressin
ASJC Scopus subject areas
- Neuroscience(all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology