Pavel Osten and his colleagues at Cold Spring Harbor Laboratory in New York studied mouse brain circuits that mediate social and other innate behaviors, such as aggression and sexual behaviors. The researchers used a novel method called serial two-photon tomography and computational whole-brain analysis of the induction of the immediate early gene c-FOS, one of a class of genes induced by neuronal activity and a molecular marker of neuronal activation.
This method allowed the group to map and study brain circuits mediating behaviors in non-mutant ‘wild-type’ mice. It also allowed them to study brain circuit deficits that may underlie abnormal social and other complex behaviors in genetic mouse models of autism, including mice with deletion or duplication of the 16p11.2 chromosomal region.
Motivated by a clinical observation suggesting that fever-evoked brain activation has a positive effect in children with autism, Osten and his team studied the mechanisms of body temperature regulation and fever response in 16p11.2 deletion mice.
The group discovered that 16p11.2 deletion mice have lower-than-normal baseline body temperatures during the day and show an exacerbated fever response in response to injection of a bacterial toxin. The findings suggest that brain regions known to regulate temperature and mediate fever response may have altered functions in mice with the deletion.
