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Significance Brain function requires high-fidelity transmission of information between individual brain cells at synapses, physical contacts that contain a specialized machinery for passing and receiving signals. Synaptic cell adhesion proteins form physical bridges between neurons and are critical for fine-tuning synaptic properties. Because of their roles in synaptic transmission, mutations in these proteins contribute to a wide range of neuropsychiatric diseases. Here, we study the role of two synaptic cell adhesion proteins, LRRTM1 and LRRTM2, in signaling at excitatory synapses utilizing a conditional knockout mouse line. Genetically deleting these proteins in mature neurons dramatically impairs basal synaptic transmission and disrupts long-term potentiation, a prominent form of synaptic plasticity that is critical for learning and memory.

Deletion of LRRTM1 and LRRTM2 in adult mice impairs basal AMPA receptor transmission and LTP in hippocampal CA1 pyramidal neurons