Astrocytic neuroligin 3 regulates social memory and synaptic plasticity through adenosine signaling in male mice

Rui Dang, An Liu (), Yu Zhou, Xingcan Li, Miao Wu, Kun Cao, Yanghong Meng, Haiwang Zhang, Guangming Gan, Wei Xie () and Zhengping Jia ()
Additional contact information
Rui Dang: Southeast University
An Liu: Southeast University
Yu Zhou: Southeast University
Xingcan Li: Southeast University
Miao Wu: Southeast University
Kun Cao: Southeast University
Yanghong Meng: 555 University Ave.
Haiwang Zhang: 555 University Ave.
Guangming Gan: Southeast University
Wei Xie: Southeast University
Zhengping Jia: 555 University Ave.

Nature Communications, 2024, vol. 15, issue 1, 1-22

Abstract: Abstract Social memory impairment is a key symptom of many brain disorders, but its underlying mechanisms remain unclear. Neuroligins (NLGs) are a family of cell adhesion molecules essential for synapse development and function and their dysfunctions are linked to neurodevelopmental and neuropsychiatric disorders, including autism and schizophrenia. Although NLGs are extensively studied in neurons, their role in glial cells is poorly understood. Here we show that astrocytic deletion of NLG3 in the ventral hippocampus of adult male mice impairs social memory, attenuates astrocytic Ca2+ signals, enhances the expression of EAAT2 and prevents long-term potentiation, and these impairments are rescued by increasing astrocyte activity, reducing EAAT2 function or enhancing adenosine/A2a receptor signaling. This study has revealed an important role of NLG3 in astrocyte function, glutamate homeostasis and social memory and identified the glutamate transporter and adenosine signaling pathway as potential therapeutic strategies to treat brain disorders.

Date: 2024
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DOI: 10.1038/s41467-024-52974-3

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