Neuroligin-2-dependent adhesion defines a molecular checkpoint for inhibitory synaptic plasticity - PubMed
2 days ago
- #hippocampus
- #synaptic plasticity
- #neuroligin-2
- Neuroligin-2 (Nlgn2) is identified as a critical mediator of inhibitory long-term potentiation (iLTP) in hippocampal CA1 pyramidal cells.
- Nlgn2-neurexin binding is essential for maintaining NMDA-induced iLTP, with disruption blocking gephyrin clustering and Nlgn2 recruitment to GABAergic synapses.
- A 10-minute post-induction window is crucial for Nlgn2-neurexin adhesion to consolidate iLTP.
- Optogenetic experiments show NMDA-induced iLTP at somatostatin (SST) and parvalbumin (PV) inputs depends on Nlgn2.
- High-frequency stimulation paired with postsynaptic depolarization triggers heterosynaptic iLTP at SST→PC synapses, requiring Nlgn2-neurexin interaction for consolidation.
- Disruption of Nlgn2-neurexin adhesion may contribute to E/I imbalance in neurodevelopmental and psychiatric disorders like epilepsy, autism, and schizophrenia.