INFLUENCE OF PENTOBARBITAL AND URETHANE ON RELEASE FROM MAGNOCELLULAR NEURONS

We examined the responses of vasopressin-neurons (VP-neurons) and oxytocin-neurons (OT-neurons) to acute salt-loading in a group of conscious rats (CON, n = 8) and rats under sodium pentobarbital (NEM, 50 mg/kg, i.p., n = 8) or urethane (URE, 1.6 g/kg, i.p. n = 8) anesthesia. Fifteen minutes following the induction of anesthesia, sodium pentobarbital produced an increase in basal plasma osmolality (Posm, 290 +/- 2 to 296 +/- 3 mosm/kg H2O, P < 0.007) while urethane did not change basal Posm (287 +/- to 289 +/- mosm/kg H2O). Neither anesthetic agent resulted in any significant changes in basal plasma levels of vasopressin-associated neurophysin (VP-RNP) and oxytocin-associated neurophysin (OT-RNP). In response to intravenous infusion of 18% saline, all three groups of rats had similar rises in Posm. The slopes of the relationship between the rise in plasma VP-RNP and the rise in Posm were markedly reduced in both groups of anesthetized animals compared to that observed for conscious animals (CON = 2.54 +/- 0.5; NEM = 1.22 +/- 0.18; URE = 1. 17 +/- 0.24 fmol.ml-1.mosm-1.kg H2O-1 p < 0.0126). The slopes of the relationship between the rise in plasma OT-RNP and the rise in Posm were not significantly (p < 0.4478) different between the CON group and the NEM group, while the slope for the URE group was significantly (p < 0.05) smaller than that for the CON group (CON = 10.9 +/- 1.5; NEM = 9.3 +/- 1.5; URE = 6.3 +/- 0.7 fmol.ml-1.mosm-1.kg H2O-1). Our data suggest that anesthesia induced by either sodium pentobarbital or urethane significantly reduces the responsiveness of VP-neurons to acute salt loading, but the responsiveness of OT-neurons is lowered by urethane only. It implies that the action of urethane on OT-neurons, and perhaps also on VP-neurons, might be mediated by a mechanism different from that of sodium pentobarbital. Barbiturates are known to reduce the activity at glutamate receptors and also to enhance the activity at gamma-aminobutyric acid (GABA) receptors. GABA reportedly is involved in the osmotic release of both OT-neurons and VP-neurons. Therefore, the absence of an effect by pentobarbital on OT-neurons, in addition to its inhibitory influence on VP-neurons, suggests that GABA receptors do not play a predominant role in the actions barbiturates have on die osmotic responsiveness of VP-neurons. Our data might also imply that there is a relative scarcity of glutamate receptors on OT-neurons.