Effect of vasopressin on the input-output properties of rat facial motoneurons.
Vasopressin can directly excite facial motoneurons in young rats and mice. It acts by generating a persistent inward current, which is Na(+)-dependent, tetrodotoxin-insensitive and voltage-gated. This peptide-evoked current is unaffected by Ca(++) or K(+) channel blockade and is modulated by extracellular divalent cations. In the present work, we determined how vasopressin alters the input-output properties of facial motoneurons. Whole-cell recordings were obtained from these neurons in the current clamp mode, in brainstem slices of young rats. Repetitive firing was evoked by injecting depolarizing current pulses. Steady-state frequency-current (f-I) relationships were constructed and the effect of vasopressin on these relationships was studied. We found that vasopressin caused a parallel shift to the left of the cell steady-state f-I relationship. This effect persisted in the presence of blockers of K(+) or Ca(++) channels. The peptide effect was distinct from that brought about by Ca(++) channel suppression or by apamin, a blocker of the mAHP. These latter manipulations resulted in an increase in the slope of the steady-state f-I relationship. We conclude that the vasopressin-induced modification of the input-output properties of facial motoneurons is probably exclusively caused by the sodium-dependent, voltage-modulated inward current elicited by the peptide, rather than being due to indirect effects of the peptide on Ca(++) channels, K(+) channels or Ca(++)-dependent K(+) channels. Computer simulation, based on a simple model of facial motoneurons, indicates that the introduction of a conductance having the properties of the vasopressin-dependent conductance can entirely account for the observed peptide-induced shift of the f-I relationship.
Pierson
P
P
Department of Physiology, University Medical Center, 1 rue Michel-Servet, CH-1211 Geneva 4, Switzerland.
Tribollet
E
E
Raggenbass
M
M
D000465:Algorithms; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D003198:Computer Simulation; D004594:Electrophysiology; D005152:Facial Muscles / Q000187:drug effects / Q000294:innervation*; D066298:In Vitro Techniques; D009046:Motor Neurons / Q000187:drug effects*; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014667:Vasopressins / Q000494:pharmacology*
D002121:Calcium Channel Blockers; D026902:Potassium Channel Blockers; D014667:Vasopressins