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NMDA receptor mediated changes in IGF‐II gene expression in the rat brain after injury and the possible role of nitric oxide
Author(s) -
Giannakopoulou M.,
Mansour M.,
Kazanis E.,
Bozas E.,
Philpipidis H.,
Stylianopoulou F.
Publication year - 2000
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.0305-1846.2000.00286.x
Subject(s) - nmda receptor , endocrinology , hippocampal formation , medicine , receptor , messenger rna , traumatic brain injury , nitric oxide , glutamate receptor , chemistry , biology , gene , biochemistry , psychiatry
This study was undertaken in order to investigate the role of insulin‐like growth factor (IGF)‐II, c‐fos, N‐methyl‐ D ‐aspartate (NMDA) receptors, and nNOS in the cellular processes following a penetrating brain injury. IGF‐II mRNA levels, as determined by Northern analysis, were decreased at 4, 8, and 24 h after brain injury, in the lesioned, compared to the contralateral intact hemisphere. Forty‐eight and 72 h after the injury, there was no difference between the lesioned and the contralateral intact hemisphere in IGF‐II mRNA levels. c‐fos mRNA levels followed a parallel, but opposite course: They were increased at 4, 8 and 24 h after the injury, while at 48 and 72 h c‐fos mRNA levels in the lesioned hemisphere did not differ from those in the intact. Administration of MK‐801 reversed the injury‐induced decrease in IGF‐II mRNA levels. Administration of MK‐801 resulted in an increase in IGF‐II mRNA in both the intact and the lesioned hemispheres. Brain injury resulted in an increase in nNOS immunopositive cells in the hippocampal formation, which was detectable at 4 and 12, but not 48 h after the injury. These results suggest that IGF‐II, c‐fos, NMDA receptors and nNOS are involved in the cellular responses to brain injury.