Abstract
Corticosterone activates two types of intracellular receptors in the rodent brain: the high affinity mineralocorticoid receptor (MR) and lower affinity glucocorticoid receptor (GR). These receptors act as transcriptional regulators and mediate slow changes in neuronal activity in a region-dependent manner. For example, in CA1 pyramidal cells, corticosterone slowly changes Ca(2+) currents and glutamate transmission but dentate granule cells appear to be resistant. Recent studies have shown that corticosteroids also exert rapid MR-dependent, nongenomic effects on hippocampal CA1 cells [e.g. increasing the frequency of miniature excitatory postsynaptic currents (mEPSCs)]. In the present study, we investigated whether dentate granule cells are also resistant to the rapid effects of corticosterone. We found that, comparable to the CA1 area, corticosterone quickly and reversibly increases mEPSC frequency but not amplitude of dentate cells. This effect did not require protein synthesis and displayed the pharmacological profile of an MR- rather than GR-dependent event. These data support the hypothesis that, unlike the slow gene-mediated effects of corticosterone, rapid hormonal actions are quite similar for CA1 and dentate cells.
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