Reduction of arginine vasopressin binding sites in mouse lateral septum by treatment with 6-hydroxydopamine.

The neuropeptide arginine vasopressin modulates neuroadaptive processes, including memory consolidation and functional tolerance to ethanol, by actions at CNS V1 receptors. Noradrenergic systems play a role in these actions of the peptide. To assess whether vasopressin may act presynaptically on catecholamine neurons, vasopressin receptors were measured by quantitative autoradiography in the lateral septum, an area that is innervated by catecholaminergic neurons and has a high density of V1 receptors, of control and 6-hydroxydopamine-treated mice. Vasopressin receptors were distributed non-uniformly throughout the lateral septum, with greater binding in the more caudal regions. Treatment with 6-hydroxydopamine lowered septal catecholamine levels and vasopressin binding, with a greater effect on binding in the intermediate and caudal portions of the lateral septum. Pretreatment with desmethylimipramine reversed the depletion of norepinephrine, and attenuated the effect of 6-hydroxydopamine on vasopressin binding in the intermediate region, but was less effective in the caudal region of the lateral septum. The results suggest that a portion of septal vasopressin receptors are localized on the terminals of noradrenergic and, possibly, dopaminergic neurons, consistent with the hypothesis that certain neuroadaptive responses to vasopressin could be mediated by modulation of neurotransmitter release. In contrast to the results with 6-hydroxydopamine, treatment of mice with 5,7-dihydroxytryptamine, to destroy serotonergic terminals, did not alter vasopressin binding in the lateral septum.