Research ReportActivation of ERK1/2 is required for normal response of isosexual social interactions in male rats

- Isosexual social interaction induces rapidly pERK expression in the MOE related brain.
- After olfactory deprivation, the rat′ social interaction reduced.
- Treatment with SL327 significantly increases the rats′ social interaction, while the expression of pERK is suppressed.

Previous studies have indicated involvement of the mitogen-activated protein kinase (MAPK) pathway in heterosexual interactions among rats. Very few studies, however, have focused its role in isosexual social interactions. We studied the male rat′s isosexual social interactional behavior using (i) the three-chambered social interaction box and (ii) phosphorylated extracellular signal-regulated kinase 1 and 2 (pERK1/2) to localize the brain regions that are activated during isosexual behavior. When faced with the social target side of the box versus the inanimate side, all rats preferred the social target side. Within 10 min, isosexual social interactions induced a rapid increase in pERK1/2 expression in the brain, especially the main olfactory epithelial (MOE)-related brain regions. After ZnSO4-induced olfactory deprivation, rats showed no preference for either the social target or inanimate side, with a concomitant decrease in pERK1/2 expression in MOE-related brain regions. Additionally, to determine the role of pERK1/2 in isosexual social interactional behavior, rats were injected intraperitoneally with SL327 (30 mg/kg, a MAPK kinase inhibitor). Although SL327 dramatically down-regulated expression of brain pERK1/2, experimental animals also spent significantly more time in the social target side. These results indicate that (i) A brief interacting with a male partner induced rapidly phosphorylated ERK1/2 in the rat′s brain. (ii) Destroy the function of MOE abolished the rats′ isosexual social interactional behavior. (iii) Suppressed the phosphorylated ERK1/2 in the rats′ brain disrupt their normal social behaviour.