Decreased norepinephrine in the ventral lamina terminalis region is associated with angiotensin II drinking response deficits following local 6-hydroxydopamine injections.

Previous studies have demonstrated that punctate injections of 6-hydroxydopamine (6-OHDA) into structures along the ventral lamina terminalis reduce drinking responses elicited by angiotensin II (ANG II). The purpose of the present study was to extend these findings by quantifying the catecholamine depletions that are associated with the drinking response deficits. Male Sprague-Dawley rats were given injections of 6-OHDA into the median preoptic nucleus (MnPO) and the organum vasculosum of the lamina terminalis (OVLT) after pretreatment with pargyline. Controls were injected with vehicle and a third group received 6-OHDA after pretreatment with desmethylimipramine (DMI). All subjects were tested for drinking responses to centrally injected ANG II and carbachol. Changes in catecholamine content of the MnPO, OVLT, supraoptic nucleus, paraventricular nucleus, caudate and cortex were determined using HPLC with electrochemical detection after behavioral testing. Only rats injected with 6-OHDA without DMI pretreatment showed a significant reduction in ANG II-induced drinking responses. This behavioral deficit was associated with a significant norepinephrine decrease in the ventral lamina terminalis region. All 3 groups showed comparable drinking responses to carbachol. These data support the hypothesis that noradrenergic innervation of the ventral lamina terminalis region is necessary for ANG II-induced drinking responses.