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Title

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

Authors
Reymond-Marron, I.
Published in European Journal of Neuroscience. 2006, vol. 24, no. 6, p. 1565-1574
Abstract As a hormone, vasopressin binds to three distinct receptors: V1a and V1b receptors, which induce phospholipase-Cbeta (PLCbeta) 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-gamma-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, PLCbeta 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.
Keywords AnimalsAnimals, NewbornArginine Vasopressin/analogs & derivatives/pharmacologyAutoradiography/methodsBrain Stem/cytologyCalcium Signaling/physiologyExcitatory Amino Acid Agonists/pharmacologyFacial Nerve/ physiologyHypoglossal Nerve/ physiologyMembrane Potentials/drug effects/physiology/radiation effectsMotor Neurons/ drug effects/physiologyOligopeptides/pharmacologyOxytocin/analogs & derivatives/pharmacologyPatch-Clamp Techniques/methodsProtein Binding/drug effects/physiologyRatsRats, Sprague-DawleyReceptors, Vasopressin/agonists/antagonists & inhibitors/ physiologyVasopressins/ pharmacologyAlpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/pharmacology
Stable URL http://archive-ouverte.unige.ch/unige:10422
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PMID: 17004920
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