Previous anatomical studies suggest that androgen regulates synapse elimination in the androgen-sensitive levator ani(LA) muscle of the rat. Androgen treatment beginning on postnatal day 7 (P7) prevents some of the normal loss of multiaxonal innervation in this muscle. The present study used physiological techniques to measure the number and size of LA motor units during the synapse elimination period in muscles from normals, and castrates treated with either testosterone propionate or oil. The number of increments in LA twitch tension as nerve stimulation intensity increased, a measure of the number of motor units, was the same at the end (P28) of synapse elimination as near the beginning (P7) of this process. This result indicates that motoneuronal cell death does not contribute to synapse elimination in the LA. Moreover, androgen during this period did not influence the number of LA motor units. In contrast, between P7 and P28, there was a dramatic decline in the size of LA motor units, as indicated by a decrease in the percentage of twitch or tetanus tension of individual motor units relative to the maximal twitch or tetanus tension of the whole muscle. In addition, androgen treatment of castrated males during this period prevented some of the normal decline in the size of LA motor units. Estimates of the number of inputs per LA muscle fiber derived from the number of LA motor units and their average size indicate that androgen maintains polyneuronal innervation in the LA muscle. This finding supports previous anatomical studies suggesting that androgen can prevent synapse elimination in this muscle. The strength of LA synapses was also examined by measuring the tetanus: twitch ratio of individual motor units and by measuring the safety margin of LA synapses. Both measurements indicated that the average strength of LA synapses increases during synapse elimination. Moreover, androgen appeared to spare synapses from elimination without increasing their strength, since androgen-treated muscles generally had larger motor units but the same mean tetanus:twitch ratio and safety margins as untreated LA muscles except at P28, when synapses in androgen-treated LA muscles had appreciably lower safety margins than normal. These results suggest that androgen regulates synapse elimination through a mechanism(s) independent of synaptic strength.

Seasonal variation in prepubertal penile growth has not previously been studied. The present study assessed the influence of daylength and androgens on penile development in the Siberian hamster (Phodopus sungorus). Adult penile masses were achieved at 18 and 8 weeks of age in hamsters maintained from birth under short (10 h light:14 h dark) versus long (14 h light:10 h dark) daylengths, respectively. Insulin-like growth factor I concentrations, previously implicated in penile growth, did not differ between hamsters maintained in short versus long daylengths. Gonadectomized juvenile males maintained in short and long daylengths and administered testosterone attained adult penile masses well in advance of untreated gonad-intact males maintained in short daylengths. Hamsters from both photoperiods, castrated as juveniles and first treated with testosterone in adulthood, also achieved adult penile masses. The photoinhibited gonad is insufficient to promote penile growth, and prepubertal gonadal secretions during short daylengths are not necessary for eventual penile development. Among young born near the end of the mating season, onset of neuroendocrine refractoriness to short daylengths at about 100 days of age and subsequent gonadal development induces growth in all reproductive tissues. Timing of puberty and increased androgen secretion controlled by daylength are the primary determinants of postnatal penile growth, which may also be affected by prenatal and early postnatal organizational actions of androgens.

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