Steroid-dependent plasticity in the medial amygdala

Behavioral sex differences have traditionally been thought to arise from gonadal steroids during a neonatal sensitive period. However, it is possible to sex-reverse certain behaviors by reversing the levels of circulating androgen in adult males and females. These results suggest that the sexually dimorphic substrates of sex behavior are subject to a high degree of plasticity, even in adulthood. I have found that circulating androgen exerts a trophic effect on the Nissl-stained morphology of an important nucleus in the control of sex behavior, namely, the posterodorsal subnucleus of the medial amygdala. First, sex-reversing the level of circulating androgen reversed the sex difference in soma size and regional volume of the posterodorsal subnucleus of the medial amygdala in adult rats. Interestingly, activation of both androgen and estrogen receptors was necessary for the post-castration maintenance of a masculine phenotype in terms of posterodorsal subnucleus of the medial amygdala cell size, whereas only estrogen receptor activity was necessary to maintain a masculine posterodorsal subnucleus of the medial amygdala volume. Then, we showed that seasonal variation in androgen was correlated with morphologic plasticity in the posterodorsal subnucleus of the medial amygdala of the Siberian hamster. However, if the experimental males were housed with females, their posterodorsal subnucleus of the medial amygdalas failed to regress in response to winter-like short daylengths. Furthermore, when male hamsters were castrated and treated with testosterone, the posterodorsal subnucleus of the medial amygdala responded to the hormone only if the animals were in summer-like photoperiods. Overall, these findings indicate that circulating androgens are critical for the maintenance of greater posterodorsal subnucleus of the medial amygdala regional volumes and soma sizes, and that environmental variables can regulate testosterone secretion and responsiveness.