Adrenal corticosteroid hormones modulate voltage-gated calcium currents in rat CA1 hippocampal neurons. In the present whole-cell recording study we examined whether calcium currents in dentate granule cells are also under control of corticosteroids. In a first series of experiments, in which the calcium chelator BAPTA was added to the recording solution, the amplitude of calcium currents induced by a voltage step to −10 mV was found to be enhanced shortly (1 or 2 days) after adrenalectomy compared to sham operation. No enhancement was seen when adrenalectomized animals received a low dose of corticosterone in the drinking water. By contrast, 3 or 7 days after adrenalectomy calcium current amplitude was decreased. Starting 3 days after adrenalectomy, some of the granule cells underwent apoptosis. This caused a bias in the recorded cell population towards relatively apoptosis-resistant cells, suggesting that restricted calcium influx may be a key feature of cells withstanding the apoptotic route. In accordance, cells from a small percentage (≈ 20%) of animals that resisted apoptosis after adrenalectomy also displayed small calcium currents. In a second series without BAPTA, thus focusing on the endogenous calcium-buffering capacity, we found that the time constant for the decay of the calcium current was decreased after adrenalectomy, probably due to enhanced calcium-dependent inactivation of the current. The data indicate that cellular calcium current characteristics of dentate granule cells are altered after adrenalectomy and that the alterations may in part determine the vulnerability to undergo apoptosis.