Zhong et al. (2019) : Autism and CRH-PVN

Zhong, S., Zhang, S., Fan, X., Wu, Q., Yan, L., Dong, J., & Li, L. (2019). Paraventricular nucleus corticotrophin-releasing hormone neurons mediate social behavioral deficits in a mouse model of autism. Translational Psychiatry, 9(1), 26. doi: 10.1038/s41398-019-0385-1 can you expand on findings in this paper

The study by Zhong et al. (2019) aimed to investigate the role of CRH-PVN neurons in social behavior deficits in a mouse model of ASD. The researchers used a mouse model that had a mutation in the SHANK3 gene, which is a gene that has been strongly associated with ASD in humans.

The authors found that mice with the SHANK3 mutation had alterations in the activity of CRH-PVN neurons compared to wild-type mice. Specifically, they found that the SHANK3 mutant mice had decreased activity of CRH-PVN neurons during social interaction compared to wild-type mice. They also found that optogenetic stimulation of CRH-PVN neurons in the SHANK3 mutant mice rescued social interaction deficits, suggesting that the deficits were due to the altered activity of these neurons.

The authors further showed that the social behavior deficits in the SHANK3 mutant mice were mediated by the CRH-PVN system. They found that infusion of a CRH antagonist into the PVN of the SHANK3 mutant mice improved social interaction deficits, while infusion of CRH into the PVN of wild-type mice impaired social interaction.

Overall, these findings suggest that alterations in the activity of CRH-PVN neurons may contribute to social behavior deficits in ASD. The study highlights the potential of targeting the CRH-PVN system as a therapeutic approach for ASD.