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Immunohistochemical modifications of vasoactiveneuropeptides and excitatory amino acids in the nervoustissue of the mongolian gerbil after transient cerebralischemia
Author(s) -
Giuffrida Rosario,
Malatino Lorenzo S.,
Bellomo Maria,
Sapienza Salvatore
Publication year - 1999
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/s0736-5748(98)00089-6
Subject(s) - gerbil , calcitonin gene related peptide , neuropeptide , vasoactive intestinal peptide , immunostaining , glutamate receptor , medicine , endocrinology , neuropeptide y receptor , biology , endothelin receptor , ischemia , chemistry , immunohistochemistry , biochemistry , receptor
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 transientcerebral ischemia which was induced by unilateral occlusion of the common carotid artery for 30min–4 h. In fact, immunostaining for these peptides was more intense in the ischemic tissue : thegreatest increases of tissue immunoreactivity were observed for Endothelin ; smaller differenceswere found for Calcitonin Gene Related Peptide and Atrial Natriuretic Peptide. Immunostainingfor Neuropeptide Y, another vasoactive neuropeptide, was virtually unchanged. Infarct areas,when present, contained numerous Endothelin‐immunoreactive cell bodies. On the contrary, thesame areas were completely void of glutamate‐ or aspartate‐immunostained neurons, normallypresent in the correspondent regions of the control tissue. The present results suggest that severecerebral ischemia is paralleled by an unbalance of local vasoactive factors. The predominance ofvasoconstrictor action of Endothelin might play a major role in the irreversible damage, togetherwith the excitotoxic effect of the extracellular accumulation of excitatory amino acids, probablydue to a leakage from neuronal cell somata, as suggested by the disappearance of glutamate‐ oraspartate‐immunostained neurons.