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Microinjection to the cerebellum of the glutamatergic agonist, kainate, creates glutamatergic excito\u2010toxicity characteristic of focal stroke, head injury or alcoholism. Inherited protection and prior exercise were both accompanied by higher cerebellar expression levels of the Kir6.1 ATP\u2010dependent potassium channel in adjacent Bergmann glia, and voltage\u2010gated KVbeta2 and cyclic nucleotide\u2010gated cation HCN1 channels in basket cells. Sedentary FVB\/N and exercised C57BL\/6 mice both expressed higher levels of these cation channels compared to sedentary C57BL\/6 mice, and were both found to be less sensitive to glutamate toxicity. Moreover, blocking ATP\u2010dependent potassium channels with Glibenclamide enhanced kainate\u2010induced cell death in cerebellar slices from the resilient sedentary FVB\/N mice. Furthermore, exercise increased the number of acetylcholinesterase\u2010positive fibres in the molecular layer, reduced cerebellar cytokine levels and suppressed serum acetylcholinesterase activity, suggesting anti\u2010inflammatory protection by enhanced cholinergic signalling. Our findings demonstrate for the first time that routine exercise and specific genetic backgrounds confer protection from cerebellar glutamatergic damages by similar molecular mechanisms, including elevated expression of cation channels. In addition, our findings highlight the involvement of the cholinergic anti\u2010inflammatory pathway in insult\u2010inducible cerebellar processes. These mechanisms are likely to play similar roles in other brain regions and injuries as well, opening new venues for targeted research efforts.<\/jats:p>","DOI":"10.1111\/j.1582-4934.2011.01331.x","type":"journal-article","created":{"date-parts":[[2011,4,20]],"date-time":"2011-04-20T16:21:18Z","timestamp":1303316478000},"page":"555-568","source":"Crossref","is-referenced-by-count":8,"title":["Similar cation channels mediate protection from cerebellar exitotoxicity by exercise and 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