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

Abstract

Sensations from viscera, like fullness, easilybecomepainful if the stimulus persists. Micelacking1GT-typeCa2channelsshowhyperalgesia to visceral pain. Thalamic infusionof a T-type blocker induced similar hyperalgesia in wild-type mice. In response tovisceral pain, the ventroposterolateral thalamic neurons evokeda surge of single spikes,which then slowly decayed as T type–dependent burst spikes gradually increased. In1G-deficient neurons, the single-spike response persisted without burst spikes. Theseresults indicate that T-type Ca2 channels underlie an antinociceptive mechanismoperating in the thalamus andsupport the idea that burst firing plays a critical role insensory gating in the thalamus.