Pontine neurones: electrophysiological evidence of mediating carotid baroreceptor inputs to supraoptic neurones in rats.

Effects of pressure stimulation of the isolated carotid sinus, of occlusion of the common carotid artery and of tail pinching on the discharge activity of dorsal pontine area neurones and antidromically identified supraoptic neurosecretory neurones were studied in male rats anaesthetized with urethane. Electrical stimulation of the supraoptic nucleus (SON) produced antidromically conducted action potentials in a small number (24/384) of the units recorded in the dorsal pontine area. Pressure pulse stimulation of the isolated carotid sinus inhibited and carotid occlusion facilitated discharge activity in some of the tested dorsal pontine area neurones. In these responsive pontine neurones a transient excitation of grouped discharges was occasionally observed to concur with a small, spontaneous depression of the arterial blood pressure. Tail pinching excited some of these pontine neurones. Histological examination revealed that these responsive neurones were located in the dorsal pontine area close, but ventral and lateral, to the locus coeruleus. Electrical stimulation of the dorsal pons evoked a synaptically mediated excitation in 20 and inhibition in the other seven of the 52 SON units which were identified antidromically after stimulation of the pituitary stalk. Pressure stimulation of the isolated carotid sinus evoked an inhibition of discharge activity in some of th SON units which were excited by dorsal pontine area stimulation. All of the six tested units which showed inhibition after dorsal pontine area stimulation were unresponsive to pressure stimulation. Based on these data, it was concluded that at least some of the neurones which mediate carotid baroreceptor inputs to SON neurosecretory neurones are located in the dorsal pontine area close, but ventral and lateral, to the locus coeruleus and that these dorsal pontine area neurones also mediate converging synaptic inputs originating from somatic pain receptors.