GENETIC-DIFFERENCES IN FEMALE HOUSE MICE IN AGGRESSIVE RESPONSE TO SEX STEROID-HORMONE TREATMENT

Citation
Jc. Compaan et al., GENETIC-DIFFERENCES IN FEMALE HOUSE MICE IN AGGRESSIVE RESPONSE TO SEX STEROID-HORMONE TREATMENT, Physiology & behavior, 54(5), 1993, pp. 899-902
Citations number
38
Categorie Soggetti
Behavioral Sciences",Physiology
Journal title
ISSN journal
00319384
Volume
54
Issue
5
Year of publication
1993
Pages
899 - 902
Database
ISI
SICI code
0031-9384(1993)54:5<899:GIFHMI>2.0.ZU;2-8
Abstract
Male mice, genetically selected for aggression, characterized by short attack latency (SAL) or long attack latency (LAL), differ on several testosterone (T)-related parameters during ontogeny and adult age. The variation in aggressive behavior at adult age may be due to differenc es in degree of androgenization prenatally. When exposed to T at prena tal, neonatal, and/or adult age, nonlactating females also display int raspecific fighting behavior. In the present study, we investigated in females of the SAL and LAL selection lines, whether the differentiati on of aggression involves processes similar to ones seen in males. The refore, we injected females with testosterone propionate (TP) or vehic le on the day of birth, treated them after ovariectomy at adult age wi th T, estradiol (E), or vehicle, and tested their aggressive response. We found that neonatally vehicle-treated SAL females show a higher ag gressive response to chronic T treatment at adult age than LAL females receiving the same treatment. Females of both selection lines treated with vehicle or E as adults were not aggressive. Neonatal TP treatmen t did not influence the adult T sensitivity and difference between sel ection lines in response to T at adult age. However, neonatally TP-tre ated SAL females showed aggressive behavior when treated with E at adu lt age, whereas LAL females failed to do so. These results suggest a g enetic difference in susceptibility to T and E, which plays a major ro le prenatally, in organizing the development of sex steroid-dependent neural systems.