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Neuroligin-2-Dependent Adhesion Defines a Molecular Checkpoint for Inhibitory Synaptic Plasticity.

Anna Lech1,2, Grzegorz Wiera3, Jerzy W Mozrzymas1

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The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|March 9, 2026
PubMed
Summary

Neuroligin-2 is essential for inhibitory long-term potentiation (iLTP) in the hippocampus. Blocking neuroligin-2-neurexin interactions disrupts iLTP consolidation within a narrow window, impacting brain E/I balance.

Keywords:
GABAgephyriniLTPinhibitory plasticityinhibitory synapseneuroligin-2

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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular and Cellular Neuroscience

Background:

  • Maintaining excitation-inhibition (E/I) balance is critical for cortical circuit function.
  • Long-term regulation of inhibitory synaptic strength is less understood than excitatory plasticity.
  • Neuroligin-2 (Nlgn2) is implicated in inhibitory synapse formation and function.

Purpose of the Study:

  • To identify the role of neuroligin-2 (Nlgn2) in inhibitory long-term potentiation (iLTP) in hippocampal CA1 pyramidal cells.
  • To investigate the necessity of Nlgn2-neurexin interactions for iLTP induction and consolidation.
  • To elucidate the temporal requirements of Nlgn2-neurexin binding for inhibitory plasticity.

Main Methods:

  • Whole-cell recordings in mouse hippocampal slices.
  • Application of neurolide-2, a synthetic peptide targeting Nlgn2-neurexin binding.
  • Immunostaining for Nlgn2 and gephyrin.
  • Optogenetic manipulation of specific inhibitory inputs (SST and PV).
  • High-frequency stimulation paired with postsynaptic depolarization.

Main Results:

  • Nlgn2-neurexin interaction is required for NMDA-induced iLTP maintenance, blocking gephyrin clustering and Nlgn2 recruitment.
  • NMDA-induced enlargement of synaptic Nlgn2 clusters in CA1 stratum oriens was abolished by neurolide-2.
  • A critical 10-minute post-induction window exists for Nlgn2-neurexin adhesion in iLTP consolidation.
  • NMDA-induced iLTP at both somatostatin (SST) and parvalbumin (PV) inputs depends on Nlgn2.
  • Heterosynaptic iLTP at SST→PC synapses failed to consolidate when Nlgn2-neurexin interaction was blocked, while excitatory LTP and PV inhibition remained intact.

Conclusions:

  • Perisynaptic Nlgn2-neurexin adhesion is an activity-dependent mechanism essential for inhibitory plasticity consolidation.
  • This mechanism is input-specific and dependent on the induction protocol.
  • Disruption of Nlgn2-neurexin interactions may contribute to E/I imbalance in neurological disorders.