Thalamic Control of Visceral Nociception Mediated by T-Type Ca²⁺ Channels.

THALAMUS; NERVOUS system; NEURONS; CELLS; BRAIN; HYPERALGESIA

Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking α1G T-type Ca[sup 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 α1G-deficient neurons, the single-spike response persisted without burst spikes. These results indicate that T-type Ca[sup 2+] channels underlie an antinociceptive mechanism operating in the thalamus and support the idea that burst firing plays a critical role in sensory gating in the thalamus. [ABSTRACT FROM AUTHOR]

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