Corticosteroids influence the action potential firing pattern of hippocampal subfield CA3 pyramidal cells

Corticosteroids regulate gene expression through the activation of mineralocorticoid and glucocorticoid receptors. The hippocampus contains the highest density of mineralocorticoid and glucocorticoid receptors in the central nervous system. The modulation of neuron excitability by corticosteroids in hippocampal subfield CA1 is well documented. However, it is not known whether corticosteroids produce different effects across the various hippocampal subfields. Therefore, we used intracellular recording techniques to examine the actions of chronic corticosteroid treatment (2 weeks) on the electrophysiological properties of rat hippocampal subfield CA3 pyramidal cells. The treatment groups used in this investigation were: adrenalectomy (ADX), selective mineralocorticoid receptor activation with aldosterone (ALD), mineralocorticoid and glucocorticoid receptor activation with high levels of corticosterone (HCT), and SHAM. Corticosteroid treatment altered the percentage of nonburst and burst firing neurons. The percentages of nonbursting cells were 74 and 62% in tissue from ADX and HCT animals compared to 42 and 41% in ALD and SHAM animals, respectively. The corticosteroid-induced effect on the ratio of nonbursting to bursting cells does not appear to be secondary to changes in the cell's membrane input resistance, resting potential, time constant, action potential, slow-or fast-afterhyperpolarizing potential properties. Based on these results we conclude that corticosteroids are important for maintaining the ratio of nonburst and burst firing pyramidal neurons in subfield CA3. These novel results are distinct from those previously reported for subfield CA1, suggesting that corticosteroids have different effects across hippocampal subfields.