Neuroligin 2 regulates absence seizures and behavioral arrests through GABAergic transmission within the thalamocortical circuitry

Feng Cao, Jackie J. Liu, Susan Zhou, Miguel A. Cortez, O. Carter Snead, Jing Han () and Zhengping Jia ()
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Feng Cao: The Hospital for Sick Children
Jackie J. Liu: The Hospital for Sick Children
Susan Zhou: The Hospital for Sick Children
Miguel A. Cortez: The Hospital for Sick Children
O. Carter Snead: The Hospital for Sick Children
Jing Han: Shaanxi Normal University
Zhengping Jia: The Hospital for Sick Children

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract Epilepsy and autism spectrum disorders (ASD) are two distinct brain disorders but have a high rate of co-occurrence, suggesting shared pathogenic mechanisms. Neuroligins are cell adhesion molecules important in synaptic function and ASD, but their role in epilepsy remains unknown. In this study, we show that Neuroligin 2 (NLG2) knockout mice exhibit abnormal spike and wave discharges (SWDs) and behavioral arrests characteristic of absence seizures. The anti-absence seizure drug ethosuximide blocks SWDs and rescues behavioral arrests and social memory impairment in the knockout mice. Restoring GABAergic transmission either by optogenetic activation of the thalamic reticular nucleus (nRT) presynaptic terminals or postsynaptic NLG2 expression in the thalamic neurons reduces the SWDs and behavioral arrests in the knockout mice. These results indicate that NLG2-mediated GABAergic transmission at the nRT-thalamic circuit represents a common mechanism underlying both epileptic seizures and ASD.

Date: 2020
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DOI: 10.1038/s41467-020-17560-3

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