Vasopressin preferentially depresses excitatory over inhibitory synaptic transmission in the rat supraoptic nucleus in vitro

Endogenous arginine-vasopressin (AVP) in the supraoptic nucleus is known to decrease the firing rate of some supraoptic nucleus neurones. To determine a possible mechanism by which this locally released AVP produces this chan ge in neuronal excitability, we investigated the effects of AVP on evoked e xcitatory (e.p.s.c.) and inhibitory post-synaptic (i.p.s.c.) responses reco rded in magnocellular neurones in a hypothalamic slice preparation, using t he perforated-patch recording technique. Our data show that AVP produces a dose-dependent decrease in the evoked e.p.s.c. in about 80% of magnocellula r neurones tested with an estimated EC50 of about 0.9 mu M. The maximum dec rease in e.p.s.c. amplitude was about 31% of control and was obtained with an AVP concentration of 2 mu M. The AVP-induced synaptic depression was blo cked by Manning Compound (MC), a non-selective antagonist of oxytocin (OXT) and vasopressin (AVP) receptors, but not by a selective OXT receptor antag onist. It was not mimicked by desmopressin (ddAVP), a V2-receptor subtype a gonist. By contrast, AVP used at the same concentration (2 mu M), had no gl obal effect on pharmacologically isolated i.p.s.c.s in the majority of magn ocellular neurones tested. These results show that AVP acts in the supraopt ic nucleus to reduce excitatory synaptic transmission to magnocellular neur ones by activating a non-OXT receptor, presumably the V1 receptor subtype.