Thalamic Control of Visceral Nociception Mediated by T-Type Ca 2+ Channels

Abstract

Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking α1G T-type Ca 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 evokeda surge of single spikes, which then slowly decayed as T type–dependent burst spikes gradually increased. In α1G-deficient neurons, the single-spike response persisted without burst spikes. These results indicate that T-type Ca ²⁺ 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.