A tropomyosin-related kinase B ligand is required for ERK activation, long-term synaptic facilitation, and long-term memory in Aplysia

Shiv K. Sharma, Carolyn M. Sherff, Shara Stough, Vickie Hsuan, Thomas J. Carew

Research output: Contribution to journalArticle

Abstract

BDNF, which acts through tropomyosin-related kinase B (TrkB) receptors during mammalian development also enhances long-term synaptic facilitation (LTF) in adult Aplysia. Because LTF is a substrate for long-term memory (LTM) in Aplysia, we examined the requirement of a secreted TrkB ligand in LTM formation at molecular, synaptic, and behavioral levels. Using an extracellular fusion protein that sequesters secreted TrkB ligands, we show that TrkB function is required for serotonin-induced activation of extracellular signal-regulated kinase, tail nerve shock-induced LTF in the CNS, and tail shock-induced LTM but is not necessary for short-term synaptic facilitation or short-term memory. These results show that a secreted growth factor, acting through a TrkB signaling cascade, is critical for the induction of long-lasting plasticity and memory formation in Aplysia.

Original languageEnglish (US)
Pages (from-to)14206-14210
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume103
Issue number38
DOIs
StatePublished - Sep 19 2006

Keywords

  • Growth factor
  • Molecular signaling
  • Sensitization

ASJC Scopus subject areas

  • General

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