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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

Science, 2003 Oct 3 , 302, 117-9

Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking alpha1G 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 alpha1G-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.

http://www.ncbi.nlm.nih.gov/pubmed/14526084