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Neurobeachin and the Kinesin KIF21B Are Critical for Endocytic Recycling of NMDA Receptors and Regulate Social Behavior.

Abstract：

:Autism spectrum disorders (ASDs) are associated with mutations affecting synaptic components, including GluN2B-NMDA receptors (NMDARs) and neurobeachin (NBEA). NBEA participates in biosynthetic pathways to regulate synapse receptor targeting, synaptic function, cognition, and social behavior. However, the role of NBEA-mediated transport in specific trafficking routes is unclear. Here, we highlight an additional function for NBEA in the local delivery and surface re-insertion of synaptic receptors in mouse neurons. NBEA dynamically interacts with Rab4-positive recycling endosomes, transiently enters spines in an activity-dependent manner, and regulates GluN2B-NMDAR recycling. Furthermore, we show that the microtubule growth inhibitor kinesin KIF21B constrains NBEA dynamics and is present in the NBEA-recycling endosome-NMDAR complex. Notably, Kif21b knockout decreases NMDAR surface expression and alters social behavior in mice, consistent with reported social deficits in Nbea mutants. The influence of NBEA-KIF21B interactions on GluN2B-NMDAR local recycling may be relevant to mechanisms underlying ASD etiology.

journal_name

Cell Rep

journal_title

Cell reports

authors

Gromova KV,Muhia M,Rothammer N,Gee CE,Thies E,Schaefer I,Kress S,Kilimann MW,Shevchuk O,Oertner TG,Kneussel M

doi

10.1016/j.celrep.2018.04.112

subject

Has Abstract

pub_date

2018-05-29 00:00:00

pages

2705-2717

issue

9

issn

2211-1247

pii

S2211-1247(18)30712-5

journal_volume

23

pub_type

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