Elsevier

Hormones and Behavior

Volume 43, Issue 2, February 2003, Pages 336-346
Hormones and Behavior

Regular article
Both estrogen receptors and androgen receptors contribute to testosterone-induced changes in the morphology of the medial amygdala and sexual arousal in male rats

https://doi.org/10.1016/S0018-506X(02)00047-8Get rights and content

Abstract

In male rats, a steroid-sensitive circuit in the forebrain regulates mating behavior. The masculine phenotype in one component of the circuit, the posterodorsal nucleus of the medial amygdala (MePD), depends on the level of circulating androgens in the adult. To investigate which gonadal steroid receptor(s) mediate sexual arousal and MePD plasticity, adult male rats were castrated and given Silastic capsules containing the nonaromatizable androgen 5α-dihydrotestosterone (DHT), 17β-estradiol (E2), both steroids, or nothing. A fifth group was sham-castrated and treated with blank capsules. DHT treatment was necessary and sufficient to maintain the expression of noncontact penile erections and ultrasonic vocalizations in castrates. E2 had no significant effect on these measures. Both DHT and E2 increased olfactory investigation (“nosepokes”) during the noncontact penile erection test. E2, but not DHT, maintained intromission patterns, while either steroid, alone or in combination, maintained ejaculatory behavior. Regional volume and cell soma size of the MePD both decreased following castration. Additionally, MePD cell size was lateralized, with left hemisphere neurons larger than those on the right, an effect that appeared independent of steroid manipulations. DHT and E2 each maintained neuronal soma size. E2 maintained MePD regional volume more effectively in the left MePD than in the right, which may have been due to a greater sensitivity of the left to both castration and hormone treatment. Thus, both androgen receptors and estrogen receptors appear to participate in sexual behaviors that may be mediated by the MePD in adult rats, and both receptors contribute to the steroid-regulated structural plasticity in this brain region.

Section snippets

Animals and surgery

Forty-nine adult male Long-Evans rats (Harlan) were selected from a pool of 60 for their display of at least two ejaculations during a preoperative copulation test. Animals were housed in standard rat cages (27 × 49 × 20 cm) with food and water freely available. Animals in different treatment conditions were distributed evenly among the cages, such that each treatment group received equivalent housing and social stimulation. Lights in the colony were set to a 12:12 schedule, with lights off at

Body, brain, and seminal vesicle weights

Animal body weights were the same at the onset of the experiment and, as expected, untreated castrates gained less weight than did sham-operated controls (P = 0.002). Among the castrates, E2 treatment, also as expected (Wade, 1972), caused the animals to gain less weight during the experiment (P = 0.01), but DHT had no effect on body weight (P = 0.6; Table 1), and there was no statistical interaction of the two steroids on this measure. Although the mean brain weight of sham castrates was less

Discussion

The overall objective of this work was to determine which gonadal steroid receptor is responsible for the steroid-dependent plasticity in the MePD of adult rats. In a former study, we found that after 30 days, blank-treated castrates had significantly smaller MePD regional volumes and somata than did sham castrates. Testosterone treatment was able to prevent the reductions in volume and soma size in castrate males, and significantly increased somal and volume measures in adult females (Cooke et

Conclusion

Interconnections between the MeA and other sexually dimorphic circuits appear to underlie the expression of male sexual behavior in rodents (Newman, 1999). Having previously found that the morphology of one subnucleus of the circuit, the MePD, was dependent upon circulating testosterone in adulthood, we now report that stimulation of both ARs and ERs appears to be required for testosterone to maintain MePD morphology fully. Furthermore, both androgenic and estrogenic stimulation appears to be

Acknowledgements

NIH NS045195 and NIH MH58703 grants supported this research. The authors thank the reviewers for their thoughtful comments on the manuscript. We also thank B.D. Sachs for advice on the construction of the NCE chamber, which was made by Ted Claire. R. Sethi provided assistance with histology.

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