Adrenal corticosteroid hormones modulate voltage-gated calcium currents in
rat CAI hippocampal neurons. In the present whole-cell recording study we e
xamined whether calcium currents in dentate granule cells are also under co
ntrol of corticosteroids. In a first series of experiments, in which the ca
lcium 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 enhanc
ed 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 adrena
lectomy calcium current amplitude was decreased. Starting 3 days after adre
nalectomy, some of the granule cells underwent apoptosis. This caused a bia
s in the recorded cell population towards relatively apoptosis-resistant ce
lls, suggesting that restricted calcium influx may be a key feature of cell
s withstanding the apoptotic route. In accordance, cells from a small perce
ntage (approximate to 20%) of animals that resisted apoptosis after adrenal
ectomy also displayed small calcium currents. In a second series without BA
PTA, thus focusing on the endogenous calcium-buffering capacity, we found t
hat the time constant for the decay of the calcium current was decreased af
ter adrenalectomy, probably due to enhanced calcium-dependent inactivation
of the current. The data indicate that cellular calcium current characteris
tics of dentate granule cells are altered after adrenalectomy and that the
alterations may in part determine the vulnerability to undergo apoptosis.