TrkB as a potential synaptic and behavioral tag

J Neurosci. 2011 Aug 17;31(33):11762-71. doi: 10.1523/JNEUROSCI.2707-11.2011.

Abstract

Late-phase long-term potentiation (L-LTP), a cellular model for long-term memory (LTM), requires de novo protein synthesis. An attractive hypothesis for synapse specificity of long-term memory is "synaptic tagging": synaptic activity generates a tag, which "captures" the PRPs (plasticity-related proteins) derived outside of synapses. Here we provide evidence that TrkB, the receptor of BDNF (brain-derived neurotrophic factor), may serve as a "synaptic tag." TrkB is transiently activated by weak theta-burst stimulation (TBS) that induces only early-phase LTP (E-LTP). This TrkB activation is independent of protein synthesis, and confined to stimulated synapses. Induction of L-LTP by strong stimulation in one synaptic pathway converts weak TBS-induced E-LTP to L-LTP in a second, independent pathway. Transient inhibition of TrkB around the time of weak TBS to the second pathway diminished L-LTP in that pathway without affecting the first one. Behaviorally, weak training, which induces short-term memory (STM) but not LTM, can be consolidated into LTM by exposing animals to novel but not familiar environment 1 h before training. Inhibition of TrkB during STM training blocked such consolidation. These results suggest TrkB as a potential tag for synapse-specific expression of L-LTP and LTM.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Intramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Avoidance Learning / physiology
  • Cells, Cultured
  • Gene Knock-In Techniques
  • Hippocampus / physiology
  • Humans
  • Long-Term Potentiation / physiology*
  • Male
  • Memory, Long-Term / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Random Allocation
  • Receptor, trkB / genetics*
  • Receptor, trkB / metabolism*
  • Synapses / genetics*
  • Synapses / metabolism*

Substances

  • Receptor, trkB