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Thalamic Control of Visceral Nociception Mediated by T-Type Ca2+ Channels

Science, 3 October 2003
Vol. 302, Issue 5642, p. 117-119
DOI: 10.1126/science.1088886

Thalamic Control of Visceral Nociception Mediated by T-Type Ca2+ Channels

  1. Daesoo Kim,
  2. Donghyun Park,
  3. Soonwook Choi,
  4. Sukchan Lee,
  5. Minjeong Sun,
  6. Chanki Kim,
  7. Hee-Sup Shin*
  1. National Creative Research Initiative Center for Calcium and Learning, Korea Institutes of Science and Technology, Seoul 136-791, Korea.
  1. * To whom correspondence should be addressed. E-mail: shin{at}kist.re.kr

Abstract

Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking α1G T-type Ca2+ channels show hyperalgesia to visceral pain. Thalamic infusion of a T-type blocker induced similar hyperalgesia in wild-type mice. In response to visceral pain, the ventroposterolateral thalamic neurons evokeda surge of single spikes, which then slowly decayed as T type–dependent burst spikes gradually increased. In α1G-deficient neurons, the single-spike response persisted without burst spikes. These results indicate that T-type Ca2+ channels underlie an antinociceptive mechanism operating in the thalamus andsupport the idea that burst firing plays a critical role in sensory gating in the thalamus.

  • Received for publication 7 July 2003.
  • Accepted for publication 19 August 2003.

Citation:

D. Kim, D. Park, S. Choi, S. Lee, M. Sun, C. Kim, and H.-S. Shin, Thalamic Control of Visceral Nociception Mediated by T-Type Ca2+ Channels. Science 302, 117-119 (2003).

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