Organizational role of testosterone on the biochemical and morphological development of the hypogastric ganglion.
Previous reports have demonstrated that after postnatal day 10 testosterone influences hypogastric ganglion (HG) development by 'activating' morphological and biochemical indices. We now report an 'organizational' influence on the developing HG during the first 10 postnatal days. To investigate the organizational effects of testosterone, male rats were castrated within 12 h of birth. Testosterone replacement therapy initiated following castration maintained the normal number of neurons in the HG. Conversely, delayed replacement therapy starting at day 10 or vehicle treatment only, resulted in a significant decrease in neuron number. Castration also produced a significant decrease in somal and nuclear cross-sectional areas. Testosterone replacement, whether initiated immediately or if delayed until day 10, restored somal and nuclear cross-sectional areas to normal. Tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT) activities were sensitive to both testosterone dosage and the time of administration. Testosterone decanoate administered subsequent to castration was not able to completely reverse the enzyme activity deficits, while delayed replacement therapy was even less effective in restoring enzyme activities. In contrast, higher doses of testosterone completely reversed enzyme activity deficits, and in fact produced a significant increase in TH activity. Again, delayed testosterone replacement did not fully restore deficits in enzyme activity. In summary, the hormonal environment during the first 10 days of life is critical for the organization of HG cell number; in contrast, nuclear and cell size appear to be dependent on testosterone for activation. TH and ChAT activities also appear to be organized during this dose- and time-dependent developmental period.
Melvin
J E
JE
Monroe Community Hospital, Rochester, NY.
McNeill
T H
TH
Hervonen
A
A
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; D004305:Dose-Response Relationship, Drug; D007001:Hypogastric Plexus / Q000166:cytology / Q000187:drug effects / Q000254:growth & development*; D008297:Male; D009919:Orchiectomy; D051381:Rats; D011919:Rats, Inbred Strains; D013739:Testosterone / Q000494:pharmacology / Q000502:physiology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism*
D013739:Testosterone; D014446:Tyrosine 3-Monooxygenase; D002795:Choline O-Acetyltransferase