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

Citation
R. Giuffrida et al., Immunohistochemical modifications of vasoactive neuropeptides and excitatory amino acids in the nervous tissue of the mongolian gerbil after transient cerebral ischemia, INT J DEV N, 17(2), 1999, pp. 99-107
Citations number
46
Categorie Soggetti
Neurosciences & Behavoir
Journal title
INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
ISSN journal
07365748 → ACNP
Volume
17
Issue
2
Year of publication
1999
Pages
99 - 107
Database
ISI
SICI code
0736-5748(199904)17:2<99:IMOVNA>2.0.ZU;2-O
Abstract
Modifications in the tissue concentration of vasoactive peptides (Endotheli n, Calcitonin Gene Related Peptide, Atrial Natriuretic Peptide) and excitat ory amino acids (glutamate, aspartate) were Found in the nervous tissue of Mongolian gerbils after transient cerebral ischemia which was induced by un ilateral occlusion of the common carotid artery for 30 min-4 h. In fact. im munostaining for these peptides was more intense in the ischemic tissue: th e greatest increases of tissue immunoreactivity were observed for Endotheli n; smaller differences sere Found for Calcitonin Gene Related peptide and A trial Natriuretic Peptide. Immunostaining for Neuropeptide Y, another vasoa ctive neuropeptide. was virtually unchanged. Infarct areas, when present, c ontained numerous Endothelin-immunoreactive cell bodies. On the contrary, t he same areas were completely void of glutamate or aspartate-immunostained neurons, normally present in the correspondent regions of the control tissu e. The present results suggest that severe cerebral ischemia is paralleled by an unbalance of local vasoactive factors. The predominance of vasoconstr ictor action of Endothelin might play a major role in the irreversible dama ge, together with the excitotoxic effect of the extracellular accumulation of excitatory amino acids, probably due to a leakage from neuronal cell som ata, as suggested by the disappearance of glulamate- or aspartate-immunosta ined neurons. (C) 1999 ISDN. Published by Elsevier Science Ltd. All rights reserved.