Gonadal hormone regulation of neurotransmitter synthesizing enzymes in the developing hypogastric ganglion.

The effects of postnatal castration at 10-11 days of age were examined in the sympathetic hypogastric ganglion (HG). Assays for choline acetyltransferase (ChAT) activity, a biochemical marker for presynaptic cholinergic maturation, and the activity of tyrosine hydroxylase (T-OH), the rate limiting enzyme in postsynaptic catecholamine biosynthesis and an index of noradrenergic development, were employed to monitor HG ontogeny. After 1 postoperative week ChAT activity and T-OH activity were significantly reduced in castrated animals as compared to sham operated controls. Over the 12 week postoperative observation period T-OH activity never varied significantly from the day 10 precastration value; thus, by 12 postoperative weeks T-OH activity in the castrated animals was 3% of the control value. In contrast, ChAT activity and total ganglion protein continued to mature in the castrated animals, but at diminished rates, so that by 12 postoperative weeks both indices were approximately 40% of the control values. Testosterone replacement therapy restored both ChAT and T-OH activities to control levels. Additionally, testosterone replacement restored the control level of activity for DOPA decarboxylase, a catecholamine synthetic enzyme which is differentially regulated from T-OH. The failure of enzyme activities to develop normally subsequent to castration on postnatal day 10 suggests that testosterone regulates the postorganizational maturation of postsynaptic noradrenergic enzyme activities and presynaptic ChAT activity.