Information sharing within a social network is key to behavioral flexibility-Lessons from mice tested under seminaturalistic conditions.

Being part of a social structure offers chances for social learning vital for survival and reproduction. Nevertheless, studying the neural mechanisms of social learning under laboratory conditions remains challenging. To investigate the impact of socially transmitted information about rewards on individual behavior, we used Eco-HAB, an automated system monitoring the voluntary behavior of group-housed mice under seminaturalistic conditions.

Mutation in the mitochondrial chaperone TRAP1 leads to autism with more severe symptoms in males.

There is increasing evidence of mitochondrial dysfunction in autism spectrum disorders (ASD), but the causal relationships are unclear. In an ASD patient whose identical twin was unaffected, we identified a postzygotic mosaic mutation p.Q639* in the TRAP1 gene, which encodes a mitochondrial chaperone of the HSP90 family.

Optogenetic and chemogenetic approaches reveal differences in neuronal circuits that mediate initiation and maintenance of social interaction.

For social interaction to be successful, two conditions must be met: the motivation to initiate it and the ability to maintain it. This study uses both optogenetic and chemogenetic approaches to reveal the specific neural pathways that selectively influence those two social interaction components.

Astrocytic β-catenin signaling via TCF7L2 regulates synapse development and social behavior.

The Wnt/β-catenin pathway contains multiple high-confidence risk genes that are linked to neurodevelopmental disorders, including autism spectrum disorder. However, its ubiquitous roles across brain cell types and developmental stages have made it challenging to define its impact on neural circuit development and behavior. Here, we show that TCF7L2, which is a key transcriptional effector of the Wnt/β-catenin pathway, plays a cell-autonomous role in postnatal astrocyte maturation and impacts adult social behavior.

Glycogen phosphorylase inhibition improves cognitive function of aged mice.

Inhibition of glycogen breakdown blocks memory formation in young animals, but it stimulates the maintenance of the long-term potentiation, a cellular mechanism of memory formation, in hippocampal slices of old animals. Here, we report that a 2-week treatment with glycogen phosphorylase inhibitor BAY U6751 alleviated memory deficits and stimulated neuroplasticity in old mice. Using the 2-Novel Object Recognition and Novel Object Location tests, we discovered that the prolonged intraperitoneal administration of BAY U6751 improved memory formation in old mice.