A New Component in Synaptic Plasticity: Upregulation of Kinesin in the Neurons of the Gill-Withdrawal Reflex

Sathyanarayanan V. Puthanveettil, Francisco J. Monje, Maria Concetta Miniaci, Yun Beom Choi, Kevin A. Karl, Eugene Khandros, Mary Ann Gawinowicz, Michael P. Sheetz, Eric R. Kandel

Research output: Contribution to journalArticle

61 Scopus citations

Abstract

To explore how gene products, required for the initiation of synaptic growth, move from the cell body of the sensory neuron to its presynaptic terminals, and from the cell body of the motor neuron to its postsynaptic dendritic spines, we have investigated the anterograde transport machinery in both the sensory and motor neurons of the gill-withdrawal reflex of Aplysia. We found that the induction of long-term facilitation (LTF) by repeated applications of serotonin, a modulatory transmitter released during learning in Aplysia, requires upregulation of kinesin heavy chain (KHC) in both pre- and postsynaptic neurons. Indeed, upregulation of KHC in the presynaptic neurons alone is sufficient for the induction of LTF. However, KHC is not required for the persistence of LTF. Thus, in addition to transcriptional activation in the nucleus and local protein synthesis at the synapse, our studies have identified a third component critical for long-term learning-related plasticity: the coordinated upregulation of kinesin-mediated transport.

Original languageEnglish (US)
Pages (from-to)960-973
Number of pages14
JournalCell
Volume135
Issue number5
DOIs
StatePublished - Nov 28 2008

Keywords

  • CELLBIO
  • MOLNEURO
  • PROTEINS

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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