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