Neonatal testosterone masculinizes sexual behavior without affecting the morphology of the dorsal preoptic/anterior hypothalamic area of female ferrets.

We examined whether testosterone (T) administered to female ferrets neonatally--a treatment known to enhance masculine coital capacity--induces formation of the sexually dimorphic male nucleus in the dorsal preoptic/anterior hypothalamic area (MN-POA/AH), and/or sensitizes dorsal POA/AH neurons to the stimulatory effect of later androgen treatment on somal dimensions. In males, the MN-POA/AH was present in all subjects, and exposure to androgen following castration at postnatal day 56 (P56) increased both MN-POA/AH volume as well as mean somal areas of MN-POA/AH neurons relative to oil-treated controls. Females given androgen from P5 to P20 and for one month beginning after ovariectomy on P56 failed to develop the MN-POA/AH, but displayed high levels of masculine sexual behavior. Somal areas of dorsal POA/AH neurons in females that received either T or a control neonatally did not increase following androgen treatment at P56. Thus, the correlation that exists between somal enlargement of dorsal POA/AH neurons and masculine sexual behavior in androgen-treated males is not found in behaviorally masculinized females. Masculine coital ability does not appear related to aspects of dorsal POA/AH morphology, supporting data from a previous study in which lesions of the MN-POA/AH caused negligible deficits in masculine sexual behavior of adult male ferrets.