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Spreading depression‐induced preconditioning in the mouse cortex: differential changes in the protein expression of ionotropic nicotinic acetylcholine and glutamate receptors
Author(s) -
Chazot P. L.,
Godukhin O. V.,
McDonald A.,
Obrenovitch T. P.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2002.01240.x
Subject(s) - ionotropic effect , glutamate receptor , ionotropic glutamate receptor , nicotinic agonist , ampa receptor , acetylcholine receptor , nmda receptor , nicotinic acetylcholine receptor , chemistry , neuroprotection , neuroscience , protein subunit , long term depression , cortical spreading depression , cerebral cortex , cortex (anatomy) , receptor , pharmacology , biology , biochemistry , medicine , gene , migraine
Preconditioning of the cerebral cortex was induced in mice by repeated cortical spreading depression (CSD), and the major ionotropic glutamate (GluRs) and nicotinic acetylcholine receptor (nAChRs) subunits were compared by quantitative immunoblotting between sham‐ and preconditioned cortex, 24 h after treatment. A 30% reduction in α‐amino‐3‐hydroxy‐5‐methyl‐4‐iso‐ xazolepropionate (AMPA) GluR1 and 2 subunit immunoreactivities was observed in the preconditioned cortex ( p < 0.03), but there was no significant change in the NMDA receptor subunits, NR1, NR2A and NR2B. A 12–15‐fold increase in α7 nAChR subunit expression following in vivo CSD ( p < 0.001) was by far the most remarkable change associated with preconditioning. In contrast, the α4 nAChR subunit was not altered. These data point to the α7 nAChR as a potential new target for neuroprotection because preconditioning increases consistently the tolerance of the brain to acute insults such as ischaemia. These data complement recent studies implicating α7 nAChR overexpression in the amelioration of chronic neuropathologies, notably Alzheimer's disease (AD).