Abstract

Three questions were asked in an attempt to understand how testosterone (T) concentration in the veins of the remaining testis can double within 24 h after hemicastration in the mature rat without a change in plasma luteinizing hormone (LH) levels. These three questions (and their answers) were: 1) Can the testicular hemicastration response occur in hypophysectomized rats? Answer, No. 2) Does LH binding to the testis increase after hemicastration? Answer, No. 3) Is there a neural route to the testis alternate to the superior spermatic plexi? Answer, Yes, apparently there is, since hemivasectomy contralateral to the excised testis partially suppressed the testicular hemicastration response (150.4 +/- 13.2 ng/ml in hemicastrated, sham- hemivasectomized rats [n = 18] vs. 109.4 +/- 11.6 ng/ml in hemicastrated, hemivasectomized rats [n = 18], P less than 0.026). It was concluded that LH was probably necessary to the testicular hemicastration response but that its presence did not provide a mechanism. The response was mediated at least partly through the inferior spermatic nerves associated with the vas deferens. A possible reason, although highly speculative, for failure to previously block the testicular hemicastration response by bilateral denervation of the superior spermatic plexi (Mock and Frankel , 1982) was that during the 12-wk interval between denervation and hemicastration, testicular innervation functionally transferred from the superior spermatic to the inferior spermatic nerves.

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