Impairment of Fos protein formation in the rat infarct borderzone by MK-801, but not by NBQX
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Impairment of Fos protein formation in the rat infarct borderzone by MK-801, but not by NBQX. / Christensen, Thomas; Jørgensen, M B; Diemer, Nils Henrik.
In: Acta Neurologica Scandinavica, Vol. 87, No. 6, 1993, p. 510-515.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Impairment of Fos protein formation in the rat infarct borderzone by MK-801, but not by NBQX
AU - Christensen, Thomas
AU - Jørgensen, M B
AU - Diemer, Nils Henrik
PY - 1993
Y1 - 1993
N2 - In the present immunocytochemical study, we investigated the mechanism of Fos protein induction and the regional distribution of the Fos protein in brains of spontaneously hypertensive rats subjected to 2 h of permanent middle cerebral artery occlusion (MCAO). Rats were administered either saline or a glutamate receptor antagonist; the non-competitive NMDA receptor antagonist MK-801 or the AMPA receptor antagonist NBQX which are known to be able to reduce infarct size in MCA occluded rats. The saline treated rats showed presence of Fos protein in nerve cell nuclei throughout the cortical and striatal infarct borderzone, but no staining in the infarct core or contralateral hemisphere. MK-801 almost totally abolished this expression of Fos protein whereas NBQX had no significant effect on Fos protein expression. It is suggested that the Fos protein induction is due to repeated spreading depressions mediated by NMDA receptors in the infarct borderzone, and that Fos protein due to its persistence in the tissue can be used as a histochemical marker of borderzone tissue at risk for eventually becoming recruited in the infarct.
AB - In the present immunocytochemical study, we investigated the mechanism of Fos protein induction and the regional distribution of the Fos protein in brains of spontaneously hypertensive rats subjected to 2 h of permanent middle cerebral artery occlusion (MCAO). Rats were administered either saline or a glutamate receptor antagonist; the non-competitive NMDA receptor antagonist MK-801 or the AMPA receptor antagonist NBQX which are known to be able to reduce infarct size in MCA occluded rats. The saline treated rats showed presence of Fos protein in nerve cell nuclei throughout the cortical and striatal infarct borderzone, but no staining in the infarct core or contralateral hemisphere. MK-801 almost totally abolished this expression of Fos protein whereas NBQX had no significant effect on Fos protein expression. It is suggested that the Fos protein induction is due to repeated spreading depressions mediated by NMDA receptors in the infarct borderzone, and that Fos protein due to its persistence in the tissue can be used as a histochemical marker of borderzone tissue at risk for eventually becoming recruited in the infarct.
KW - Animals
KW - Cerebral Cortex
KW - Cerebral Infarction
KW - Corpus Striatum
KW - Cortical Spreading Depression
KW - Dizocilpine Maleate
KW - Energy Metabolism
KW - Gene Expression Regulation
KW - Male
KW - Neurons
KW - Proto-Oncogene Proteins c-fos
KW - Quinoxalines
KW - Rats
KW - Rats, Inbred SHR
KW - Receptors, N-Methyl-D-Aspartate
M3 - Journal article
C2 - 8356885
VL - 87
SP - 510
EP - 515
JO - Acta Neurologica Scandinavica
JF - Acta Neurologica Scandinavica
SN - 0001-6314
IS - 6
ER -
ID: 272524