Neurobeachin regulates neurotransmitter receptor trafficking to synapses

Author:

Nair Ramya1,Lauks Juliane22,Jung SangYong1,Cooke Nancy E.3,de Wit Heidi2,Brose Nils1,Kilimann Manfred W.4,Verhage Matthijs22,Rhee JeongSeop1

Affiliation:

1. Department of Molecular Neurobiology, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany

2. Department of Functional Genomics and Department of Clinical Genetics, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, Vrije Universiteit and Vrije Universiteit Medical Center, 1081 HV Amsterdam, Netherlands

3. Department of Genetics and Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104

4. Department of Neuroscience, Uppsala University, 75124 Uppsala, Sweden

Abstract

The surface density of neurotransmitter receptors at synapses is a key determinant of synaptic efficacy. Synaptic receptor accumulation is regulated by the transport, postsynaptic anchoring, and turnover of receptors, involving multiple trafficking, sorting, motor, and scaffold proteins. We found that neurons lacking the BEACH (beige-Chediak/Higashi) domain protein Neurobeachin (Nbea) had strongly reduced synaptic responses caused by a reduction in surface levels of glutamate and GABAA receptors. In the absence of Nbea, immature AMPA receptors accumulated early in the biosynthetic pathway, and mature N-methyl-d-aspartate, kainate, and GABAA receptors did not reach the synapse, whereas maturation and surface expression of other membrane proteins, synapse formation, and presynaptic function were unaffected. These data show that Nbea regulates synaptic transmission under basal conditions by targeting neurotransmitter receptors to synapses.

Publisher

Rockefeller University Press

Subject

Cell Biology

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