Calc~ ton~ nietllnte~ treruotoxicity: relatlorrship to specific clmtwel types~ ttd role bt isclro~ ric tfanmqe’, has made a frequent-citation list, although I know that this circumstance is as much a reflection of generally burgeoning interest in excltotoxicity and hypoxicischemic neuronal cell death, as of any merits of the article itself. The revlew also enjoyed the beneflt I+ being positioned within a superb special issue on Ca2+ and rieuronal excitability, edited by Richard Miller, and 1 suspect that more than a few readers stumbled across It by chance while looking at one of the other excellent articles In the issue. The review summarized evidence that excess entry of Caz+, and consequent neuronal-cell CaZ+ overload, is a key early step in the Injury induced by excess exposure to glutamate In the hypoxic-ischemic