| Abstract: | The role played by the neonatal 5-hydroxytryptamine (5HT) system in the organization and sexual differentiation of adult agonistic behavior was investigated in rats. Focus was on the 5HT2 receptor subtype, which has been demonstrated to be involved in agonism control in the adult. 5HT2 activity was experimentally manipulated by administration of a specific agonist 1-(2, 5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI)] or antagonist (ritanserin) during the second week of life, when serotonin is known to concur to anatomical and behavioral sexual differentiation. Interactions between early 5HT2 activity, genetic sex, and neonatal circulating testosterone (T) were studied by administering the ligands to males, females, and androgenized females. At adulthood, the animals were tested for both aspects of agonism, i. e., aggression and defense, in a 20-min confrontation with an unfamiliar conspecific of the same sex, age, body weight, and social experience. Neonatal administration of the 5HT2 antagonist ritanserin increased aggression independently of sex; it also increased defense, but this effect was confined to males. The agonist DOI had no effect on aggression, but enhanced defense in males and androgenized females, with an effect which depended therefore more on neonatal T than genetic sex. Females appeared in general less sensitive to neonatal 5HT2 manipulation than both androgenized females and males; this suggests that neonatal T is crucial for experimental modifications of neonatal 5HT2 activity to have any consistent effect on adult agonistic behavior. On the other hand, effects observed in males and androgenized females were dependent on the behavior considered and the drug administered. This was especially evident for defense, enhanced by ritanserin in males only, and in both males and androgenized females by DOI. Neonatal 5HT2 activity seems therefore to play a role in the modulation of adult agonistic behaviors, which depends on the behavior considered and is under multiple control of genetic sex and hormonal neonatal substrate. © 1994 Wiley-Liss, Inc. |
