[Molecular mechanisms for AMPA receptor trafficking]

Nihon Shinkei Seishin Yakurigaku Zasshi. 2008 Jun;28(3):131-4.
[Article in Japanese]

Abstract

Finely tuned synaptic transmission in the brain provides the molecular basis for learning and memory. The misregulation of synaptic transmission is involved in the pathogenesis of various neurological disorders like epilepsy. AMPA-typed glutamate receptors (AMPARs) mediate the most prominent form of excitatory neurotransmission in the brain. Dynamic regulation of AMPARs is thought to be a primary mechanism for controlling synaptic strength. We have analyzed the molecular mechanism for AMPAR-trafficking and function by focusing on PSD-95, a major postsynaptic scaffolding protein. Here, we review the novel regulatory mechanisms of AMPARs by 1) the PSD-95 palmitoylating enzyme, which determines the position of PSD-95 at postsynapses, and 2) the epilepsy related ligand/receptor, LGI1/ADAM22, identified as the PSD-95-interacting protein.

Publication types

  • Review

MeSH terms

  • ADAM Proteins / physiology
  • Animals
  • Calcium Channels / physiology
  • Disks Large Homolog 4 Protein
  • Epilepsy / etiology
  • Guanylate Kinases
  • Intracellular Signaling Peptides and Proteins / physiology
  • Lipoylation
  • Membrane Proteins / physiology
  • Mice
  • Nerve Tissue Proteins / physiology
  • Proteins / physiology
  • Receptors, AMPA / metabolism*
  • Synaptic Membranes / metabolism
  • Synaptic Transmission

Substances

  • Cacng2 protein, mouse
  • Calcium Channels
  • Disks Large Homolog 4 Protein
  • Dlg4 protein, mouse
  • Intracellular Signaling Peptides and Proteins
  • Lgi1 protein, mouse
  • Membrane Proteins
  • Nerve Tissue Proteins
  • Proteins
  • Receptors, AMPA
  • Guanylate Kinases
  • ADAM Proteins
  • Adam22 protein, mouse