Differential nociceptive responses in mice lacking the alpha(1B) subunit of N-type Ca(2+) channels

Neuroreport. 2001 Aug 8;12(11):2423-7. doi: 10.1097/00001756-200108080-00027.


The role of N-type Ca(2+) channels in nociceptive transmission was examined in genetically engineered mice lacking the alpha(1B) subunit of N-type channels and in their heterozygote and wild-type littermates. In alpha(1B)-deficient mice, N-type channel activities in dorsal root ganglion neurons and spinal synaptoneurosomes were eliminated without compensation by other types of voltage-dependent Ca(2+) channels. The alpha(1B)-deficient mice showed a diminution in the phase 2 nociceptive responses more extensively than in the phase 1 nociceptive responses of the formalin test. The alpha(1B)-deficient mice exhibited significantly increased thermal nociceptive thresholds in the hot plate test, but failed to increase mechanical nociceptive thresholds in the tail pinch test. These results suggest a crucial role of N-type channels in nociceptive transmission, especially for persistent pain like phase 2 of the formalin test and for nociception induced by thermal stimuli.

MeSH terms

  • Animals
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels, N-Type / genetics*
  • Ganglia, Spinal / physiology*
  • Hot Temperature
  • Male
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Mice
  • Mice, Knockout
  • Nimodipine / pharmacology
  • Nociceptors / physiology*
  • Pain Threshold / physiology*
  • Patch-Clamp Techniques
  • Physical Stimulation
  • Posterior Horn Cells / physiology
  • Synaptic Transmission / drug effects
  • Synaptic Transmission / physiology
  • omega-Agatoxin IVA / pharmacology
  • omega-Conotoxin GVIA / pharmacology


  • Calcium Channel Blockers
  • Calcium Channels, N-Type
  • omega-Agatoxin IVA
  • Nimodipine
  • omega-Conotoxin GVIA