Altered nociceptive response in mice deficient in the α1B subunit of the voltage-dependent calcium channel

Chanki Kim, Kisun Jun, Taehoon Lee, Sung Sook Kim, Maureen W. McEnery, Hemin Chin, Hyung Lae Kim, Joo Min Park, Dong Kwan Kim, Sung Jun Jung, Jun Kim, Hee Sup Shin

Research output: Contribution to journalArticlepeer-review

157 Scopus citations

Abstract

Calcium influx through N-type calcium channels mediates synaptic transmission at numerous central synapses and transduces nociceptive information in the spinal dorsal horn. However, the precise role of N-type calcium channels in pain perception is not fully elucidated. To address this issue, we generated and analyzed knockout mice for α1B, the pore-forming subunit of the N-type calcium channel. Homozygous mutants are viable, fertile, and show normal motor coordination. In small-diameter dorsal root ganglion neurons from mutants the density of calcium channel currents is significantly reduced, which can be accounted for by the abolition of N-type currents. We performed several pain-related behavioral tests using the mutant mice. α1B-Deficient mice show reduced response to mechanical stimuli in the von Frey test and increased tail flick latency in response to radiant heat, indicating altered spinal reflexes. However, pain response in the hot plate test is normal. In the formalin paw test, the mutant mice exhibit significantly attenuated response in Phase 2, but normal pain behaviors in Phase 1. The response to visceral inflammatory pain caused by acetic acid is also reduced in α1B knockout mice. These results suggest that the α1B subunit of N-type calcium channel plays a major role in pain perception by acting at the spinal level, but not at the supraspinal level.

Original languageEnglish
Pages (from-to)235-245
Number of pages11
JournalMolecular and Cellular Neuroscience
Volume18
Issue number2
DOIs
StatePublished - 2001

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