Neuronal inputs from the forebrain and the brainstem to sympathetic preganglionic neurons in the spinal cord were investigated by the transneuronal retrograde tracing technique using pseudorabies virus in intact and brainstem-lesioned rats. After unilateral subcutaneous viral inoculations into the hind limb of intact rats, infected neurons were then visualized by immunostaining. At 3.5 days after inoculation, infected neurons appeared in the thoracic (T10) intermediolateral (IML) cell column. On the 4th day, infected neurons were present in the C1, A5, A6, A7 catecholamine cell groups and the rostral ventromedial medulla (RVMM). On the 5th day, viral labeling was seen in the hypothalamic paraventricular and arcuate nuclei and the lateral hypothalamic area. In all of these nuclei, the infected cells appeared bilaterally. However, the appearance of virus-labeled cells in these nuclei was unilateral following unilateral coronal sections between the medulla and the spinal cord (depending on the side of hemisection, but not on the site of virus inoculation). Midsagittal sections throughout the entire medulla oblongata did not alter the topographical pattern of virus-infected neurons in the forebrain or the brainstem. These findings indicate that descending fibers to the spinal neurons may not cross over in the lower brainstem but that they decussate within the spinal cord.
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.
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