AMPA receptor trafficking and synaptic plasticity require SQSTM1/p62 (Hippocampus, 2009, doi:10.1002/hipo.20528)

報告日期: 2009/05/15
報告時間: 16:00/16:50
報告學生: 賀豫君
講評老師: 簡伯武
附件下載:

http://basicmed.med.ncku.edu.tw/admin/up_img/980515-2.pdf

AMPA receptor trafficking and synaptic plasticity require SQSTM1/p62

Hippocampus (2009) 19:392-406

 

Speaker: Yu-Chun Ho (賀豫君)

Commentator: Dr. Po-Wu Gean (簡伯武老師)

Date: 2009/5/15 16:00-16:50

Place: Room 602

 

Abstract:

    AMPA-type glutamate receptors (AMPARs) are responsible for most excitatory synaptic transmission in the brain, and their trafficking to and away from synapses is an important mechanism underlying synaptic plasticity. AMPAR trafficking to the surface is primarily regulated by certain receptor associated proteins and receptor phosphorylation. Recently, a new phosphorylation site at S818 of GluR1 (a subunit of the AMPAR) has been identified for PKC. However, the role of this phosphorylation in AMPAR trafficking is not yet fully understood. Using coimmunoprecipitation and Western blotting, the authors discovered that Sequestosome 1 (SQSTM1)/p62, a scaffold protein for the atypical PKC (aPKC), interacts with GluR1 intracellular loop L2-3 through its ZZ-type zinc finger domain. Furthermore, p62 deficient mice displayed impaired hippocampal CA1 long-term potentiation (LTP), as well as diminished surface expression and S818 phosphorylation of GluR1. Altogether, these results propose that p62 interaction and aPKC phosphorylation act together to mediate AMPAR trafficking and LTP in the hippocampus.

 

References:

1.     Jiang, J. et al. (2007) Neurosignals 15:266-282.

2.     Boehm, J. et al. (2006) Neuron 51:213-225.