Immunohistochemical modifications of vasoactive neuropeptides and excitatory amino acids in the nervous tissue of the Mongolian gerbil after transient cerebral ischemia.

Modifications in the tissue concentration of vasoactive peptides (Endothelin, Calcitonin Gene Related Peptide, Atrial Natriuretic Peptide) and excitatory amino acids (glutamate, aspartate) were found in the nervous tissue of Mongolian gerbils after transient cerebral ischemia which was induced by unilateral occlusion of the common carotid artery for 30 min 4 h. In fact, immunostaining for these peptides was more intense in the ischemic tissue: the greatest increases of tissue immunoreactivity were observed for Endothelin; smaller differences were found for Calcitonin Gene Related Peptide and Atrial Natriuretic Peptide. Immunostaining for Neuropeptide Y, another vasoactive neuropeptide, was virtually unchanged. Infarct areas, when present, contained numerous Endothelin-immunoreactive cell bodies. On the contrary, the same areas were completely void of glutamate- or aspartate-immunostained neurons, normally present in the correspondent regions of the control tissue. The present results suggest that severe cerebral ischemia is paralleled by an unbalance of local vasoactive factors. The predominance of vasoconstrictor action of Endothelin might play a major role in the irreversible damage, together with the excitotoxic effect of the extracellular accumulation of excitatory amino acids, probably due to a leakage from neuronal cell somata, as suggested by the disappearance of glutamate- or aspartate-immunostained neurons.