Hippocampal LTD expression involves a pool of AMPARs regulated by the NSF-GluR2 interaction

Neuron. 1999 Oct;24(2):389-99. doi: 10.1016/s0896-6273(00)80852-1.

Abstract

We investigated whether the interaction between the N-ethyl-maleimide-sensitive fusion protein (NSF) and the AMPA receptor (AMPAR) subunit GluR2 is involved in synaptic plasticity in the CA1 region of the hippocampus. Blockade of the NSF-GluR2 interaction by a specific peptide (pep2m) introduced into neurons prevented homosynaptic, de novo long-term depression (LTD). Moreover, saturation of LTD prevented the pep2m-induced reduction in AMPAR-mediated excitatory postsynaptic currents (EPSCs). Minimal stimulation experiments indicated that both pep2m action and LTD were due to changes in quantal size and quantal content but were not associated with changes in AMPAR single-channel conductance or EPSC kinetics. These results suggest that there is a pool of AMPARs dependent on the NSF-GluR2 interaction and that LTD expression involves the removal of these receptors from synapses.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Carrier Proteins / metabolism*
  • Electrophysiology
  • Hippocampus / physiology*
  • In Vitro Techniques
  • Long-Term Potentiation / drug effects
  • Long-Term Potentiation / physiology*
  • N-Ethylmaleimide-Sensitive Proteins
  • Peptides / pharmacology
  • Rats
  • Receptors, AMPA / metabolism*
  • Vesicular Transport Proteins*

Substances

  • Carrier Proteins
  • Peptides
  • Receptors, AMPA
  • Vesicular Transport Proteins
  • N-Ethylmaleimide-Sensitive Proteins
  • Nsf protein, rat
  • glutamate receptor ionotropic, AMPA 2