alpha(1)-adrenergic receptor-induced slow rhythmicity in nonrespiratory cervical motoneurons of neonatal rat spinal cord

Previous studies have reported that the alpha(1)-adrenergic system can acti vate spinal rhythm generators belonging to the central respiratory network. In order to analyse alpha(1)-adrenergic effects on both cranial and spinal motoneuronal activity, phenylephrine (1-800 mu m) was applied to in vitro preparations of neonatal rat brainstem-spinal cord. High concentration of p henylephrine superfusion exerted multiple effects on spinal cervical output s (C2-C6), consisting of a lengthening of respiratory period and an increas e in inspiratory burst duration. Furthermore, in 55% of cases a slow motor rhythm recorded from the same spinal outputs was superimposed on the inspir atory activity. However, this phenylephrine-induced slow motor rhythm gener ated at the spinal level was observed neither in inspiratory cranial nerves (glossopharyngeal, vagal and hypoglossal outputs) nor in phrenic nerves. W hole-cell patch-clamp recordings were carried out on cervical motoneurons ( C4-C5), to determine first which motoneurons were involved in this slow rhy thm, and secondly the cellular events underlying direct phenylephrine effec ts on motoneurons. In all types of motoneurons (inspiratory and nonrespirat ory) phenylephrine induced a prolonged depolarization with an increase in n euronal excitability. However, only nonrespiratory motoneurons showed addit ional rhythmic membrane depolarizations (with spiking) occurring in phase w ith the slow motor rhythm recorded from the ventral root. Furthermore the t onic depolarization produced in all motoneurons results from an inward curr ent [which persists in the presence of tetrodotoxin (TTX)] associated with a decrease in neuron input conductance, with a reversal potential varying a s a Nernstian function of extracellular K+ concentration. Our results indic ate that the alpha(1)-adrenoceptor activation: (i) affects both the central respiratory command (i.e. respiratory period and inspiratory burst duratio n) and spinal inspiratory outputs; (ii) induces slow spinal motor rhythmici ty, which is unlikely to be related to the respiratory system; and (iii), i ncreases motoneuronal excitability, probably through a decrease in postsyna ptic leak K+ conductance.