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

Abstract

Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking alpha1GT-typeCa(2+) 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 evoked a 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 and support the idea that burst. ring plays a critical role in sensory gating in the thalamus.