Corticosteroids regulate gene expression through the activation of min
eralocorticoid and glucocorticoid receptors. The hippocampus contains
the highest density of mineralocorticoid and glucocorticoid receptors
in the central nervous system. The modulation of neuron excitability b
y corticosteroids in hippocampal subfield CA1 is well documented. Howe
ver, it is not known whether corticosteroids produce different effects
across the various hippocampal subfields. Therefore, we used intracel
lular recording techniques to examine the actions of chronic corticost
eroid treatment (2 weeks) on the electrophysiological properties of ra
t hippocampal subfield CA3 pyramidal cells. The treatment groups used
in this investigation were: adrenalectomy (ADX), selective mineralocor
ticoid receptor activation with aldosterone (ALD), mineralocorticoid a
nd glucocorticoid receptor activation with high levels of corticostero
ne (HCT), and SHAM. Corticosteroid treatment altered the percentage of
nonburst and burst firing neurons. The percentages of nonbursting cel
ls were 74 and 62% in tissue from ADX and HCT animals compared to 42 a
nd 41% in ALD and SHAM animals, respectively. The corticosteroid-induc
ed effect on the ratio of nonbursting to bursting cells does not appea
r to be secondary to changes in the cell's membrane input resistance,
resting potential, time constant, action potential, slow-or fast-after
hyperpolarizing potential properties. Based on these results we conclu
de that corticosteroids are important for maintaining the ratio of non
burst 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 hippocam
pal subfields.