Testosterone regulates the density of dendritic spines in the male preoptic area.

Male-typical behavior is dependent on testosterone. Castrated males gradually stop mating and engaging in sexual behaviors. Castrates treated with testosterone regain motivation and sex behaviors over time. Although this effect is well characterized, the specific mechanisms by which testosterone treatment recovers sexual behaviors remain unknown. The medial preoptic area (MPOA) is a likely site for testosterone's action on copulation. The integrity of the area is essential for the expression of male sex behavior; and the MPOA is densely populated with receptors for gonadal steroids. Moreover testosterone appears to regulate synaptic efficacy in the MPOA. Exposure to sexually relevant stimuli stimulates the MPOA but only in the presence of circulating testosterone. Sites afferent to the area respond to similar exposure independent of the hormonal milieu suggesting that testosterone mediates communication between the MPOA and its afferents. The protracted time course suggests that the effects of steroidal manipulation are mediated by structural changes. The present experiment evaluated this hypothesis by comparing dendritic spine density among Syrian hamsters that were castrated, castrated and treated with testosterone, or were left gonadally intact. Brains were sectioned and stained using the rapid Golgi stain protocol (FD Neurotechnologies, Baltimore), and the spine density, dendrite length, and the number of branches were compared among groups. Intact and testosterone replaced animals had more spines and greater spine density but did not differ in dendrite length and branching from castrated animals. These results suggest that existing dendrites increase the number of spines available for synapse formation but do not extend their dendrites in response to testosterone treatment.