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Seminiferous tubules contain a cytoplasmic androgen receptor similar to the receptors in the epididymis and ventral prostate. The presence of a cytoplasmic receptor indicates that androgens maintain spermatogenesis by a direct action on certain types of cells within the seminiferous tubule. The Sertoli cell appears to be one of the cell types containing androgen receptors and the receptor might also be present in spermatogonia, primary spermatocytes, or peritubular cells. The Sertoli cell is stimulated by FSH to produce an androgen-binding protein which may serve to increase the accumulation of androgen in the seminiferous epithelium and make it available for binding by intracellular androgen receptors. This may be a way in which FSH enhances the action of androgen on spermatogenesis. Androgens act on the Sertoli cell to increase its response to FSH. This action of androgens on the Sertoli cell results in increased production of androgen-binding protein and may enhance the production of other substances which exert trophic effects on spermatogenesis.

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Previous studies of plasma taurine concentrations in epileptics have yielded equivocal results. We measured plasma and urinary taurine in 41 epileptic and 68 control subjects and found plasma concentrations among epileptics to be comparable in general to those of controls, but that two or three classes of plasma taurine concentrations, possibly genetically regulated, occur in both epileptic and control subjects. Our previous studies and data from the present study on taurine excretion revealed three excretion classes under genetic control. The principal finding is that epileptics include disproportionate numbers of low excretors (high reabsorbers), who are presumptive homozygotes for the allele effecting higher reabsorption. If confirmed, these findings suggest that the transport of taurine, rather than absolute taurine concentration, may explain the efficacy of taurine administration in some epileptics but not in others. The locus involved may be one component in the polygenic diathesis to the idiopathic epilepsies.

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