AJP - Regulatory, Integrative and Comparative Physiology, Vol 252, Issue 4 645-R652, Copyright © 1987 by American Physiological Society
Forebrain contribution to sympathetic nerve discharge in anesthetized cats
Z. S. Huang, G. L. Gebber, S. M. Barman and K. J. Varner
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.
