Serotonin-induced regulation of the actin network for learning-related synaptic growth requires Cdc42, N-WASP, and PAK in Aplysia sensory neurons

Hiroshi Udo, Iksung Jin, Joung Hun Kim, Hsiu Ling Li, Trisha Youn, Robert D. Hawkins, Eric R. Kandel, Craig H. Bailey

Research output: Contribution to journalArticlepeer-review

91 Citations (Scopus)

Abstract

Application of Clostridium difficile toxin B, an inhibitor of the Rho family of GTPases, at the Aplysia sensory to motor neuron synapse blocks long-term facilitation and the associated growth of new sensory neuron varicosities induced by repeated pulses of serotonin (5-HT). We have isolated cDNAs encoding Aplysia Rho, Rac, and Cdc42 and found that Rho and Rac had no effect but that overexpression in sensory neurons of a dominant-negative mutant of ApCdc42 or the CRIB domains of its downstream effectors PAK and N-WASP selectively reduces the long-term changes in synaptic strength and structure. FRET analysis indicates that 5-HT activates ApCdc42 in a subset of varicosities contacting the postsynaptic motor neuron and that this activation is dependent on the PI3K and PLC signaling pathways. The 5-HT-induced activation of ApCdc42 initiates reorganization of the presynaptic actin network leading to the outgrowth of filopodia, some of which are morphological precursors for the learning-related formation of new sensory neuron varicosities.

Original languageEnglish
Pages (from-to)887-901
Number of pages15
JournalNeuron
Volume45
Issue number6
DOIs
Publication statusPublished - Mar 24 2005

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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