RESPONSES OF ELECTROPHYSIOLOGICALLY IDENTIFIED RAT PARAVENTRICULAR NEURONS TO CHOLECYSTOKININ AND OTHER STIMULI

Extracellular recordings were carried out in the paraventricular nucleus of halothane-anesthetized male rats. Responses of neurons identified by antidromic criteria with projections to the nucleus tractus solitarius or to the ventral lateral medulla were compared to those of neurohypophysial neurons following alterations in blood pressure and osmolarity, hemorrhage and after intravenous injection of cholecystokinin. Neurohypophysial neurons displayed the well-described responses to blood pressure for putative vasopressin neurons and increases in excitability after cholecystokinin for putative oxytocin neurons. Twenty per cent of the ventral lateral medulla-projecting neurons were responsive to cardiovascular perturbations, with these displaying reduced activity after either decreases or increases in blood pressure. None of nine neurons projecting to the ventral lateral medulla responded to i.v. cholecystokinin. Two of 20 nucleus tractus solitarius-projecting neurons showed reduced activity after cholecystokinin and none increased their firing rate. Nitroprusside-induced hypotension was associated with reduced activity in 10% of this population. Three neurons displayed axon projections to both pituitary and medulla; two of these which projected to the nucleus tractus solitarius were activated by cholecystokinin. We conclude that some of the paraventricular nucleus neurons projecting to the medulla respond to recognized cardiovascular stimuli for neurohypophysial neurons, but neurons in these populations are generally unresponsive to cholecystokinin. The former group of neurons may act to coordinate autonomic and endocrine responses to cardiovascular perturbation; however, there may be other stimuli; such as cholecystokinin, which act only on one of the populations of paraventricular nucleus neurons. Furthermore, many neurons in the descending pathways may respond to stimuli not presently associated with activation of magnocellular neurons.