Hypogastric ganglion perinatal development: evidence for androgen specificity via androgen receptors.
The hypogastric ganglion (HG) has previously been shown to be sensitive to both the organizational and activational influences of testosterone. The current investigations examined whether testosterone exerts similar effects prenatally, whether these events are specifically controlled by androgen, and whether androgens might directly masculinize the HG. Prenatal treatment with an anti-androgen, flutamide, resulted in significant decreases in the adult levels of tyrosine hydroxylase (TH) activity, an index of postsynaptic noradrenergic ontogeny, and choline acetyltransferase (ChAT) activity, a marker for presynaptic terminal formation. In addition, testosterone propionate and dihydrotestosterone benzoate reversed the effects of neonatal castration on the development of TH and ChAT activities. In contrast estradiol benzoate was unable to restore enzyme activities. To determine whether the above observations might be produced by direct effects on the HG, androgen cytosol receptor characteristics were studied. Competition and saturation analyses demonstrate that the affinity and specificity of the androgen cytosol receptor in the HG are similar to that displayed in the pituitary, which has previously been shown to contain androgen receptors. These results suggest that the adult levels of TH and ChAT activities are organized during prenatal and early postnatal development. In addition, the organization of the HG appears to be androgen specific. The presence of cytosol androgen receptors suggests that the organizational effects of androgens are possibly induced by a direct mechanism.
Melvin
J E
JE
Monroe Community Hospital, Rochester, NY.
Hamill
R W
RW
D000320:Adrenergic Fibers / Q000378:metabolism / Q000502:physiology; D000818:Animals; D002795:Choline O-Acetyltransferase / Q000378:metabolism*; D002799:Cholinergic Fibers / Q000378:metabolism / Q000502:physiology; D005260:Female; D005485:Flutamide / Q000494:pharmacology; D007001:Hypogastric Plexus / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism; D008297:Male; D009919:Orchiectomy; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains; D011944:Receptors, Androgen / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D013739:Testosterone / Q000494:pharmacology / Q000502:physiology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism*
D011944:Receptors, Androgen; D013739:Testosterone; D005485:Flutamide; D014446:Tyrosine 3-Monooxygenase; D002795:Choline O-Acetyltransferase