Rw. Rhees et al., EFFECTS OF PRENATAL TESTOSTERONE ON SEXUAL-BEHAVIOR, REPRODUCTIVE MORPHOLOGY AND LH-SECRETION IN THE FEMALE RAT, Developmental neuroscience, 19(5), 1997, pp. 430-437
Sexual differentiation of many brain structures and functions is depen
dent on levels of testosterone (T) or its metabolites during certain '
sensitive' developmental periods. If T is present during these perinat
al periods, masculinization and defeminization of sexual behavior occu
r; also, reproductive physiology, and central nervous system morpholog
y and function are altered. The purpose of the present study was to ch
aracterize the influence of T at specific prenatal developmental inter
vals on offspring reproductive morphology? physiology, locomotor activ
ity and sexual behavior during postnatal development. To avoid complic
ations induced by endogenous testicular activity, only females were ex
amined. Free T was used because of its relative short half-life, so th
at the effects induced by its administration on a specific gestational
day (GD) could be evaluated. Pregnant rats received a single subcutan
eous injection of either sesame oil (controls) or 5 mg of T on GD 16,
17, 18, 19, 20, 21, or 22. Female offspring of pregnant rats exposed t
o T displayed significant alterations in morphology and behavior. The
anogenital distance, measured at ?5 days postbirth, was significantly
increased if T was administered on GD 16, 17 or 18. T treatment on GD
16 or each day thereafter through GD 20 significantly delayed the norm
al occurrence of vaginal opening (controls at 37.5 days vs. T treatmen
t which ranged from 38.5 to 41.4 days). Abnormal vaginal morphology (e
nlarged clitoris) was also observed when T was injected during a simil
ar prenatal interval (i.e. GD 16 to GD 22). Furthermore, prenatal T tr
eatment on GD 18 (and each day thereafter), until GD 22 significantly
decreased lordotic behavior compared to control values. However, expos
ure to T, on any prenatal GD did not alter the animals' ability to exh
ibit an induced luteinizing hormone (LH) surge. These results suggest
that the onset for altered reproductive morphology occurs at least as
early as GD 16, whereas the onset of sexual behavior sensitivity occur
s precisely at GD 18, and that the normal pattern of adult LH release
in females is not altered by prenatal androgen treatment using this sp
ecific paradigm.