The major pelvic ganglion: androgen control of postnatal development

Abstract

Previously we reported the effects of postnatal castration on the postorganizational development of the sympathetic hypogastric ganglion (Hamill and Guernsey, 1983; Melvin and Hamill, 1986). "Postorganization" implies an activational role for gonadal hormones, in contrast to the permanent organizing effects that occur perinatally. We now report results that suggest that the major pelvic ganglion (PG), a mixed parasympathetic and sympathetic ganglion, is similarly regulated by testosterone during development. Choline acetyltransferase (CAT) and tyrosine hydroxylase (T-OH) activities were used to examine normal PG ontogeny. The normal development of these biochemical indices occurs primarily after day 10. Postnatal castration at 10-11 d of age completely prevented the postorganizational developmental increase of T-OH activity. At 12 postoperative weeks T-OH activity in castrates was approximately 6% that of the control animals (control, 2880 +/- 127 pmol/ganglion X hr; castrated, 161 +/- 16 pmol/ganglion X hr; p less than 0.001). In fact, by only 1 postoperative week, T-OH activity was already significantly reduced in castrated animals (control, 480 +/- 69 pmol/ganglion X hr; castrated, 179 +/- 6 pmol/ganglion X hr; p less than 0.001). CAT activity and total ganglion protein were also significantly reduced by 1 postoperative week. In contrast to T-OH activity, however, these indices continued to develop at diminished rates. By 12 postoperative weeks CAT activity and total ganglion protein in castrates were 30 and 50% of control values, respectively, resulting in a significant developmental abnormality in CAT-specific activity. Testosterone replacement reversed the castration-induced developmental deficits of T-OH and CAT activities.(ABSTRACT TRUNCATED AT 250 WORDS)

Age-Associated Remodeling of Thymopoiesis: Role for Gonadal Hormones and Catecholamines

“…However, since both testosterone [314] and E2 [315,316] have direct regulatory influences on TH gene expression, the changes in thymic NA level may reflect a reduction in the nerve fiber level of NA, as well. In keeping with this notion are data showing that TH activity in the pelvic [317] and hypogastric ganglion [318] during postnatal development of male rats rises in parallel with the testosterone plasma level (which reaches adult levels around the age of 60 days) [319] , and those showing that in female rats the estrous cycle-, pregnancy-and ovariectomy-related hormonal changes coincide with alterations in the TH level in the superior cervical ganglion [320] . Accordingly, it may be supposed that withdrawal of gonadal steroids can affect the thymic NA levels by reducing the density of sympathetic innervation and/or by decreasing TH gene expression, and thereby NA synthesis.…”

Translational Perspective on the Role of Testosterone in Sexual Function and Dysfunction

“…Delayed testosterone administration can restore soma size but not the number of neurites or tyrosine hydroxylase activity [102]. If castration occurs 10–11 days following birth, there is a large decrease in sympathetic neurons, a slight decrease in parasympathetic neurons and immediate or delayed testosterone supplementation can prevent the decline in soma size, neuron number and sympathetic and parasympathetic input [104]. These data suggest that testosterone plays an important role in PG development at late gestation and in the early postnatal period after birth.…”

Androgen-specific critical periods for the organization of the major pelvic ganglion

“…Previous studies indicate that the PG is sensitive to hormonal manipulations. Tyrosine hydroxylase (T-OH) activity, an index of noradrenergic sympathetic development (Black and Geen, 1973), DOPA decarboxylase (DDC) activity, and choline acetyltransferase (CAT) activity, a cholinergic developmental marker, are significantly reduced by postnatal castration at day 10-l 1 (Melvin and Hamill, 1987). Testosterone replacement completely restored all maturational deficits produced by postnatal castration (Melvin and Hamill, 1987).…”

“…Tyrosine hydroxylase (T-OH), DOPA decarboxylase, and choline acetyltransferase (CAT) activities are significantly reduced by postnatal castration on day 10-l 1, while testosterone replacement therapy reversed all developmental enzyme activity deficits (Melvin and Hamill, 1987).…”