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-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.
Reymond-Marron
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I
Department of Basic Neurosciences, University Medical Center, CH-1211 Geneva 4, Switzerland.
Tribollet
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E
Raggenbass
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M
D000818:Animals; D000831:Animals, Newborn; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000031:analogs & derivatives / Q000494:pharmacology; D001345:Autoradiography / Q000379:methods; D001933:Brain Stem / Q000166:cytology; D020013:Calcium Signaling / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D005154:Facial Nerve / Q000502:physiology*; D007002:Hypoglossal Nerve / Q000502:physiology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D009046:Motor Neurons / Q000187:drug effects* / Q000502:physiology; D009842:Oligopeptides / Q000494:pharmacology; D010121:Oxytocin / Q000031:analogs & derivatives / Q000494:pharmacology; D018408:Patch-Clamp Techniques / Q000379:methods; D011485:Protein Binding / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017483:Receptors, Vasopressin / Q000819:agonists / Q000502:physiology*; D014667:Vasopressins / Q000494:pharmacology*; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / Q000494:pharmacology
D065092:Antidiuretic Hormone Receptor Antagonists; D018690:Excitatory Amino Acid Agonists; D009842:Oligopeptides; D017483:Receptors, Vasopressin; C469699:argipressin, dCha(4)-; C515868:phenylacetyl-O-ethyltyrosyl-phenylalanyl-glutaminyl-asparagyl-lysyl-prolyl-argininamide; D014667:Vasopressins; D001127:Arginine Vasopressin; C033683:oxytocin, tri-Gly-; D010121:Oxytocin; D018350:alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid