{'fraction_non_alphanumeric': 0.033787465940054495, 'fraction_numerical': 0.0, 'mean_word_length': 5.700729927007299, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
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.