Effect of lesion of a5 and a7 brainstem noradrenergic areas or transection of brainstem pathways on sympathoadrenal activity in rats during immobilization stress.

Both A5 and A7 brainstem noradrenergic cell groups innervate dorsal horns of the spinal cord. Moreover, A5 cell group directly innervates sympathetic preganglionic neurons. Thus, A5 and A7 noradrenergic neurons could modulate the sympathoadrenal system (SAS) activity. We investigated the role of A5 and A7 noradrenergic cell groups in regulation of the SAS activity under control and stressful conditions. We evaluated the effect of electrolytical lesions of A5 or A7 cell groups and also the effect of bilateral brainstem cuts interrupting brainstem pathways on tyrosine hydroxylase gene expression in A5 and A7 areas and on the SAS activity measured by plasma epinephrine and norepinephrine levels. We have found that immobilization stress increases activity of the A5 and A7 brainstem areas and also levels of the gene expression of tyrosine hydroxylase, the rate-limiting catecholamine biosynthetic enzyme. Immobilization of sham-operated and brainstem pathways transected or A5 or A7 lesioned animals induced a similar, highly significant increase in plasma epinephrine and norepinephrine levels in both sham-operated and A5 or A7 destroyed or transected groups. Our data suggest that both A5 and A7 noradrenergic cell groups are activated during immobilization stress. However, transection of brainstem pathways innervating A5 and A7 neurons or lesion of A5 or A7 cell groups is not sufficient enough for changes in immobilization stress-induced activation of the SAS. We suggest that neither A5 and A7 noradrenergic neurons nor the transected brainstem pathways represent structures crucial for an activation of the SAS during immobilization stress. We hypothesize that during regulation of the stress response, various areas and pathways are involved and the elimination just one of them might be compensated by the remained intact areas and pathways.