Thalamic control of visceral nociception mediated by T-type Ca2+ channels

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Sensations from viscera, like fullness, easilybecomepainful if the stimulus persists. Mice lacking1GT-typeCa2channelsshowhyperalgesia 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 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.
Publisher
American Association for the Advancement of Science
Issue Date
2003-10
Citation

Science, Vol.302

URI
http://hdl.handle.net/10203/25024
Appears in Collection
BS-Journal Papers(저널논문)

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