Abstract

We previously reported that a late onset reduction of muscarinic acetylcholine receptors (LORMAR) occurs in the gerbil hippocampus after 5 min of transient ischemia. This reduction begins as late as 7 days post-ischemia and accompanies the accumulation of glia, but is subsequent to completion of the disappearance of CA1 pyramidal cells. In the present study, we showed that this LORMAR was prevented by daily post-ischemic administration of the immunosuppressant cyclosporin A (CsA). The effectiveness of CsA against the LORMAR indicates that an immune mechanism may be involved in the progressive brain damage occurring after transient ischemia.

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