Fetal environment: Transplanting BTBR fetuses into a typical mouse strain improves the social behaviors of BTBR mice, which are often used to model autism.  

Exposure to immune factors during gestation may account for the social deficits seen in a mouse model of autism, according to a study published 15 May in the Journal of Neuroimmunology¹. Fetuses of a normal mouse strain develop the same social deficits when exposed to the immune factors.

Studies in the past few years have hinted at a connection between inflammation during pregnancy and the risk of having a child with autism. For example, antibodies that attack fetal brain proteins are more common in mothers of children with autism than in controls. What’s more, injecting these antibodies into pregnant mice alters the brains and behavior of the mouse pups, studies have found.

In a 2011 study, researchers found high levels of some immune molecules in the brains of BTBR mice, a strain with behaviors that resemble the symptoms of autism. In particular, these mice show little interest in interacting with other mice and display many repetitive and obsessive behaviors. 

In the new study, the same team purified antibodies from the blood of BTBR mice. They injected the antibodies into pregnant B6 mice, which are socially normal, six times during their pregnancy.

The offspring of these B6 mice are less social than those of B6 mice injected with either B6 antibodies or with a salt solution, the study found.

The researchers also transplanted BTBR fetuses into B6 mice on gestational day three, and B6 fetuses into BTBR mice. To control for the stress of the transplant, they moved another set of B6 fetuses into B6 mice.

Gestation in a B6 mother improves the sociability of BTBR mice, whereas developing in a BTBR mother lessens the sociability of B6 mice, the study found. Transplanting to a mother of the same strain has no effect.

References:

1: Zhang Y. et al. J. Neuroimmunol. 258, 51-60 (2013) PubMed