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TRPM7 is required within zebrafish sensory neurons for the activation of touch-evoked escape behaviors

  • Sean E. Low
  • , Kimberly Amburgey
  • , Eric Horstick
  • , Jeremy Linsley
  • , Shawn M. Sprague
  • , Wilson W. Cui
  • , Weibin Zhou
  • , Hiromi Hirata
  • , Louis Saint-Amant
  • , Richard I. Hume
  • , John Y. Kuwada

Research output: Contribution to journalArticlepeer-review

52 Scopus citations

Abstract

Mutations in the gene encoding TRPM7(trpm7), a member of the Transient Receptor Potential (TRP) superfamily of cation channels that possesses an enzymatically active kinase at its C terminus, cause the touch-unresponsive zebrafish mutant touchdown. We identified and characterized a new allele of touchdown, as well as two previously reported alleles, and found that all three alleles harbor mutations that abolish channel activity. Through the selective restoration of TRPM7 expression in sensory neurons, we found that TRPM7's kinase activity and selectivity for divalent cations over monovalent cations were dispensable for touch-evoked activation of escape behaviors in zebrafish. Additional characterization revealed that sensory neurons were present and capable of responding to tactile stimuli in touchdown mutants, indicating that TRPM7 is not required for sensory neuron survival or mechanosensation. Finally, exposure to elevated concentrations of divalent cations was found to restore touch-evoked behaviors in touchdown mutants. Collectively, these findings are consistent with a role for zebrafish TRPM7 within sensory neurons in the modulation of neurotransmitter release at central synapses, similar to that proposed for mammalian TRPM7 at peripheral synapses.

Original languageEnglish
Pages (from-to)11633-11644
Number of pages12
JournalJournal of Neuroscience
Volume31
Issue number32
DOIs
StatePublished - 10 Aug 2011
Externally publishedYes

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