Evaluation of the involvement of the androgen receptor in motivated behaviour using male rats carrying the testicular feminization mutation

Androgen insensitive male rats carrying the Testicular Feminization mutation (TFM), a genetic mutation in the androgen receptor, have observed to display sexual performance abnormalities. The nature of this deficit has not been fully described, but androgens and estrogens are important in mediating sexual behaviour in normal (wild type; WT) males. This dissertation examined pre-copulatory behaviours (appetitive) and re-examined sexual performance (consumatory), as well as anxiety levels, in order to determine the contribution of this mutation to these behaviours. A re-examination of sexual behaviour in the TFMs confirmed previous studies showing that these mutants display decreased intromissions and few ejaculations; regions within the brain important for mating displayed male like activation patterns. The accessory olfactory bulbs, important for pheromone mediated sexual behaviour, revealed the TFMs did not display morphological abnormalities, but the activation of this region was different than the WT males. An analysis of partner preference and the latency to achieve mounts did not reveal any abnormalities in sexual motivation. However, an examination of 50 kHz ultrasonic vocalizations (USVs), a precopulatory behaviour important for enhancement of feminine receptivity, revealed the TFMs displayed far fewer USVs than WT males. The expression of Foxp2, a protein linked to USV production in mice, did not differ between TFMs and WT males, however, a sex difference was found in that both groups contained higher optical densities (suggesting higher protein content) than females. Estrogen receptor alpha levels were feminized in certain regions of the TFM brain important for sexual behaviour. In terms of anxiety levels, TFMs displayed masculine levels, but displayed abnormal motor activity. Overall, the data support the conclusion that some appetitive and consumatory sexual behaviours are affected by the androgen receptor (TFM) mutation, and these abnormalities may directly or indirectly contribute to the inability of the TFMs to display sexual behaviour.