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Science 3 October 2003:
Vol. 302. no. 5642, pp. 117 - 119
DOI: 10.1126/science.1088886
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Reports

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

Daesoo Kim, Donghyun Park, Soonwook Choi, Sukchan Lee, Minjeong Sun, Chanki Kim, Hee-Sup Shin*

Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking {alpha}1G 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 {alpha}1G-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.

National Creative Research Initiative Center for Calcium and Learning, Korea Institutes of Science and Technology, Seoul 136-791, Korea.

* To whom correspondence should be addressed. E-mail: shin{at}kist.re.kr

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