Activity-driven synaptic translocation of LGI1 controls excitatory neurotransmission
Cuhadar et al. find that the abundance of LGI1 at the presynaptic surface controls glutamatergic transmission. Synaptic surface LGI1 increases with neuronal activity but is reduced by patient-derived autoantibodies against LGI1. Results support the role of LGI1 in the control of synaptic transmission and its causal role in epilepsy.