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 alter s the input-output properties of facial motoneurons. Whole-cell recordings were obtained from these neurons in the current clamp mode, in brainstem sl ices of young rats. Repetitive firing was evoked by injecting depolarizing current pulses. Steady-state frequency-current (f-l) relationships were con structed and the effect of vasopressin on these relationships was studied. We found that vasopressin caused a parallel shift to the left of the cell s teady-state f-l relationship. This effect persisted in the presence of bloc kers of K+ or Ca++ channels. The peptide effect was distinct from that brou ght 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 stea dy-state f-l relationship. We conclude that the vasopressin-induced modific ation of the input-output properties of facial motoneurons is probably excl usively caused by the sodium-dependent, voltage-modulated inward current el icited by the peptide, rather than being due to indirect effects of the pep tide on Ca++ channels, K+ channels or Ca++-dependent K+ channels. Computer simulation, based on a simple model of facial motoneurons, indicates that t he introduction of a conductance having the properties of the vasopressin-d ependent conductance can entirely account for the observed peptide-induced shift of the f-l relationship.