Consequences of corricosteroid receptor activation on voltage-dependent Na+ conductances were studied in acutely dissociated CA1 hippocampal neurons. This preparation was selected because of the compact electrotonic properties of dissociated neurons, allowing reliable voltage-clamp of the large and fast Na+ currents. The Na+ currents were studied in (i) neurons of adrenalectomized animals (no steroid receptors occupied), (ii) neurons from tissue of adrenalectomized rats treated in vitro with corticosterone and the glucocorticoid receptor antagonist RU38486 (selectively occupying the mineralocorticoid receptor), (iii) corticosterone-treated neurons of adrenalectomized animals (occupying both the mineralocorticoid and glucocorticoid receptors) and (iv) neurons of sham-operated animals. Activation and steady-state inactivation properties of the Na+ current recorded in neurons of adrenalectomized animals were slightly shifted (3-5 mV) to hyperpolarized potentials as compared to the Na+ currents from neurons of the other experimental groups. Furthermore, the removal from inactivation of the Na+ current in the group of neurons of adrenalectomized animals was relatively slow. Although small, these effects could influence neuronal properties like action potential generation and accommodation. Under the present experimental conditions, no apparent differences were seen between cells with predominant mineralocorticoid receptor activation and cells where both mineralocorticoid and glucocorticoid receptors were occupied. In contrast to Na+ currents, voltage-dependent Ca2+ currents displayed no steroid-dependent shifts in voltage-dependent properties. However, Ca2+ current amplitudes were increased by similar to 160% in CA1 neurons of adrenalectomized animals as compared to Ca2+ currents from neurons of the other experimental groups.
We conclude that corticosteroid receptor activation affects various properties of voltage-dependent Na+ and Ca2+ conductances in CA1 neurons, indicating that the steroid receptors are involved in the modulation of neuronal excitability in these cells. (C) 1997 IBRO.