CEREBELLAR granule cells (CGC) undergo massive DNA fragmentation, an apoptotic marker, in 8-day-old rat cerebellum.In vitro, they survive in the presence of depolarizing concentrations of KCl. Bisindolylmaleimide, a specific PKC inhibitor, blocks CGC apoptosisin vitro. Here I show that PKC δ, which has been involved in apoptosis in different cell lines, is constitutively cleaved in CGC, suggesting that its catalytic subunit is activeper se. Moreover, KCl deprivation induces cyclin D1 expression and accumulation in nuclei. This process is blocked by bisindolylmaleimide. A model is proposed where, in the absence of survival signals, activated PKC δ induces cyclin D1 expression and accumulation in the nucleus, which subsequently, would lead to an aborted cell cycle and apoptosis.