Activation of a TRPC3-dependent cation current through the neurotrophin BDNF

Neuron. 1999 Sep;24(1):261-73. doi: 10.1016/s0896-6273(00)80838-7.


Nonvoltage-gated cation currents, which are activated following stimulation of phospholipase C (PLC), appear to be major modes for Ca2+ and Na+ entry in mammalian cells. The TRPC channels may mediate some of these conductances since their expression in vitro leads to PLC-dependent cation influx. We found that the TRPC3 protein was highly enriched in neurons of the central nervous system (CNS). The temporal and spatial distribution of TRPC3 paralleled that of the neurotrophin receptor TrkB. Activation of TrkB by brain-derived nerve growth factor (BDNF) led to production of a PLC-dependent, nonselective cation conductance in pontine neurons. Evidence is provided that TRPC3 contributes to this current in vivo. Thus, activation of TrkB and PLC leads to a TRPC3-dependent cation influx in CNS neurons.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Brain-Derived Neurotrophic Factor / pharmacology*
  • Cations
  • Cell Line
  • Cerebral Cortex / chemistry
  • Cerebral Cortex / embryology
  • Cerebral Cortex / growth & development
  • Electric Conductivity*
  • Humans
  • Ion Channels / analysis
  • Ion Channels / genetics
  • Ion Channels / physiology*
  • Neurons / physiology
  • Pons / physiology
  • Rats
  • Receptor, trkB / analysis
  • Receptor, trkB / physiology
  • TRPC Cation Channels
  • Tissue Distribution
  • Transfection
  • Type C Phospholipases / metabolism


  • Brain-Derived Neurotrophic Factor
  • Cations
  • Ion Channels
  • TRPC Cation Channels
  • TRPC3 cation channel
  • Receptor, trkB
  • Type C Phospholipases