Altered sympathetic-salivary gland development: delayed response to postnatal castration.

These studies defined the normal and hormonally altered development of activity for tyrosine hydroxylase (T-OH), the rate-limiting enzyme in catecholamine biosynthesis (Levitt et al., 1965), and choline acetyltransferase activity (CAT) in the male rat superior cervical ganglion (SCG). Additionally, salivary gland weight was monitored. Two distinct developmental plateaus for postsynaptic T-OH activity exist. The first plateau represents the prepubertal level, which is significantly lower than the second postpubertal plateau. In contrast, presynaptic CAT activity displayed only a single plateau, commencing at approximately 45 days of age. The effects of postnatal castration (at 10 or 11 days of age) on the submandibular gland and T-OH activity were delayed until after puberty. No change in T-OH activity was seen at two and four post-operative weeks between control and castrated animals; however, T-OH activity was significantly less in castrated animals at 12 and 16 post-operative weeks. Testosterone replacement reversed the effect of castration on T-OH activity. Conversely, CAT activity in the SCG was unchanged by postnatal castration for at least 16 post-operative weeks, the longest time point studied. The failure of castrated animals to display the normal developmental increase in T-OH activity following puberty was comparable with the effect of castration on the development of submandibular salivary gland weight. These results suggest that in postpubertal male rats, development of T-OH activity in the superior cervical ganglion is influenced by testosterone. The parallel effects of castration on submandibular gland weight imply that testosterone regulates T-OH activity via an indirect mechanism. In contrast to noradrenergic enzyme activity and target tissue size, the ontogeny of presynaptic CAT activity appears to be insensitive to testosterone levels.