The Acute Anticonvulsant Effects of Deoxycorticosterone in Developing Rats: Role of Metabolites and Mineralocorticoid-Receptor Responses

    November 2005 in “ Epilepsia ”
    Heather E. Edwards, Sutha Vimal, W. McIntyre Burnham
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    Studysummary This study suggests that the anticonvulsant effects of deoxycorticosterone in young rats may be mediated by its metabolites and interactions with multiple receptors, including mineralocorticoid and progesterone receptors. Our plain-language summary of this paper — not a Tressless recommendation.
    The study investigated the acute anticonvulsant effects of deoxycorticosterone (DOC) in 15-day-old rats, focusing on the role of its metabolites and mineralocorticoid-receptor responses. The results indicated that agonists of mineralocorticoid receptors increased the latency to seizures and sometimes completely suppressed them. Spironolactone, a mineralocorticoid-receptor antagonist, blocked the anticonvulsant effects of a nonsedating dose of DOC, suggesting the involvement of these receptors. Finasteride, which inhibits DOC metabolism, partially blocked DOC's protective effects, indicating the contribution of metabolites. Metabolites like dihydrodeoxycorticosterone and tetrahydrodeoxycorticosterone, which modulate the GABAA receptor, also blocked seizures. The findings suggested that both DOC and its metabolites contributed to anticonvulsant effects through interactions with various receptors.
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