![]() The prevalence of epileptic seizures in autistic individuals is particularly striking 9. In addition to these symptoms, ASD also exhibit high rates of comorbidity with other abnormalities such as increased seizures, depression, anxiety, and sleep problems 4, 5, 6, 7, 8. These results indicate that NLG2-mediated GABAergic transmission at the nRT-thalamic circuit represents a common mechanism underlying both epileptic seizures and ASD.Īutism spectrum disorders (ASD) are a class of life-long neurodevelopmental disorders characterized by deficits in social behavior and communication, repetitive behaviors, and restricted interests 1, 2, 3. 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. The anti-absence seizure drug ethosuximide blocks SWDs and rescues behavioral arrests and social memory impairment in the knockout mice. 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. Neuroligins are cell adhesion molecules important in synaptic function and ASD, but their role in epilepsy remains unknown. Epilepsy and autism spectrum disorders (ASD) are two distinct brain disorders but have a high rate of co-occurrence, suggesting shared pathogenic mechanisms. ![]()
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