We investigated the effects of vasopressin-related neuropeptides on the hypoxia/hypoglycemia (ischemia)-induced decrease of the CA1 potential presynaptic elicited by stimulation of Schaffer collaterals in rat hippocampal slices. Treatment with arginine-vasopressin (AVP) potentiated the ischemic decrease of the CA1 presynaptic potential. In contrast, a V1 receptor antagonist produced a dose-dependent neuroprotective effect, whereas a V2 receptor antagonist had no effect. The AVP-induced decrease of the CA1 presynaptic potential was completely blocked by simultaneous application of the V1 receptor antagonist. Because AVP4-9 is regarded as the major proteoplytic product of AVP in the rat brain, we examined its effect on the ischemic decrease of the CA1 presynaptic potential. Treatment with AVP4-9 produced a more marked reduction of the potential than treatment with AVP itself. The present study demonstrates that stimulation of the V1 receptor has a detrimental effect on the development of ihe ischemic damage whereas V1 receptor blockade has a neuroprotective effect, suggesting that AVP may potentiate ischemic neuronal deficits via V1 receptor stimulation.
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