Repressing lateral septum neurons that disable sociability in an autism mouse model

Social deficits cause poor clinical outcome in neuropsychiatric diseases, and treatments are lacking. The researchers looked at the downstream of oxytocin and vasopressin for targets alleviating social deficits in a mouse model. 

The researchers identified a population of neurons activated in the lateral septum on the termination of social contacts that fail to disengage in experimental autism.

These are somatostatin neurons expressing oxytocin receptors coupled to GABA-B signaling, which are inhibited via GABA-A channels by vasopressin-excited GABA neurons. Loss of oxytocin or vasopressin signaling recapitulated the disease phenotype.

Suppressing the activity or signaling of these somatostatin neurons or receptor signaling alleviated social deficits of disease models by increasing the duration of contacts with mates and strangers. 

 
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https://www.cell.com/cell-reports-medicine/fulltext/S2666-3791(24)00528-7
https://sciencemission.com/Neuropeptide-therapeutics-to-repress-lateral-septum-neurons-that-disable-sociability-in-an-autism-mouse-model