Dehydroepiandrosterone reversibly blocks GABA-induced currents, behaving as an allosteric antagonist of the GABAA receptor in cultured neurons from ventral mesencephalon. [1] Dehydroepiandrosterone (DHEA) protects primary hippocampal cultures from embryonic day 18 (E18) embryos against NMDA-induced toxicity, DHEAS also reduces NMDA-induced toxicity. DHEA (100 nM) protects cultured neurons against the neurotoxic actions of either AMPA (25 mM) or kainic acid (1 mM) as well. [2] Dehydroepiandrosterone (DHEA) increases the length of neurites containing the axonal marker Tau-1 in primary cultures of mouse embryonic neocortical neurons, and the incidence of varicosities and basket-like process formations in a dose-dependent fashion. Dehydroepiandrosterone (DHEA) rapidly increases free intracellular calcium via activation of N-methyl-D-aspartate (NMDA) receptors. [3] Dehydroepiandrosterone with H874Y stimulates a 3- to 8-fold greater response than with wild type AR and at 100 nM the response is similar with the LNCaP mutant in the androgen-dependent human prostate cancer xenograft CWR22 and LNCaP cells. [4]