Figure 2.

Summary of known and potential mechanisms of neuroactive steroids. 3β-OH inhibits postsynaptic T-channels without having a direct effect on postsynaptic GABA_A receptors. In addition to postsynaptic potentiation of GABA_A, both CDNC24 and alphaxalone presynaptically reduce spontaneous GABA release, thus decreasing GABA content in the synaptic cleft. In addition to its effect on postsynaptic GABA_A receptors and reduction in presynaptic GABA release in the synaptic cleft, alphaxalone also simultaneously blocks postsynaptic T-channels. Additionally, based on the well-known abilities of steroid compounds to pass cellular membranes, there is a possibility that the explanation for the absence of cell death in neurons lies in their direct or indirect interactions with membrane-bound, intracellular, and nuclear receptors, either as agonists or antagonists. These targets, as well other potential targets on the presynaptic terminal, remain unknown.