Forebrain contribution to sympathetic nerve discharge in anesthetized cats

Abstract

We tested the hypothesis that the forebrain is responsible for a component of basal sympathetic nerve discharge (SND) in the anesthetized cat. For this purpose integrated postganglionic inferior cardiac SND and blood pressure were measured before and after serial transections of the midbrain at stereotaxic planes A3 and AP0. In the first series of experiments on baroreceptor-denervated cats anesthetized with alpha-chloralose, A3 transection significantly reduced SND to 62 +/- 7% of control. Blood pressure was reduced 33 +/- 4 mmHg. SND and frontal-parietal cortical activity were temporally related prior to A3 transection in many of these animals. Recovery of SND and blood pressure to control levels occurred within 30 min after A3 transection. A second midbrain transection at AP0 failed to affect SND and blood pressure at this time. This observation suggests that the effects of A3 transection were due to the loss of a component of SND of forebrain origin rather than to generalized trauma. The effects of A3 transection were not attributable to cataleptic anesthesia with alpha-chloralose, since SND and blood pressure were significantly reduced by midbrain transection in baroreceptor-denervated cats anesthetized with diallylbarbiturate-urethan. A3 transection also reduced SND and blood pressure in some baroreceptor-innervated cats. Finally, medial diencephalic ablation prevented the effects of A3 transection. We conclude that the forebrain is responsible for a significant component of sympathetic tone in anesthetized cats. Recovery from the loss of this component, however, occurs rapidly even in animals deprived of their compensatory baroreceptor reflex mechanisms.