The vasopressin-induced excitation of hypoglossal and facial motoneurons in young rats is mediated by V1a but not V1b receptors, and is independent of intracellular calcium signalling

As a hormone, vasopressin binds to three distinct receptors: V1a and V1b receptors, which induce phospholipase‐Cβ (PLCβ) activation and Ca2+ mobilization; and V2 receptors, which are coupled to adenylyl cyclase. V1a and V1b receptors are also present in neurons. In particular, hypoglossal (XII) and facial (VII) motoneurons are excited following vasopressin‐V1a receptor binding. The aim of the present study was double: (i) to determine whether V1b receptors contribute to the excitatory effect of vasopressin in XII and VII motoneurons; and (ii) to establish whether the action of vasopressin on motoneurons is mediated by Ca2+ signalling. Patch‐clamp recordings were performed in brainstem slices of young rats. Vasopressin depolarized the membrane or generated an inward current. By contrast, [1‐deamino‐4‐cyclohexylalanine] arginine vasopressin (d[Cha4]AVP), a V1b agonist, had no effect. The action of vasopressin was suppressed by Phaa‐d‐Tyr(Et)‐Phe‐Gln‐Asn‐Lys‐Pro‐Arg‐NH2, a V1a antagonist, but not by SSR149415, a V1b antagonist. Thus, the vasopressin‐induced excitation of brainstem motoneurons was exclusively mediated by V1a receptors. Light microscopic autoradiography failed to detect V1b binding sites in the facial nucleus. In motoneurons loaded with GTP‐γ‐S, a non‐hydrolysable analogue of GTP, the effect of vasopressin was suppressed, indicating that neuronal V1a receptors are G‐protein‐coupled. Intracellular Ca2+ chelation suppressed a Ca2+‐activated potassium current, but did not affect the vasopressin‐evoked current. H7 and GF109203, inhibitors of protein kinase C, were without effect on the vasopressin‐induced excitation. U73122 and D609, PLCβ inhibitors, were also without effect. Thus, excitation of brainstem motoneurons by V1a receptor activation is probably mediated by a second messenger distinct from that associated with peripheral V1a receptors.