Thalamic control of visceral nociception mediated by T-type Ca2+ channels.
Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking alpha1G T-type Ca2+ 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 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 andsupport the idea that burst firing plays a critical role in sensory gating in the thalamus.
Kim
Daesoo
D
National Creative Research Initiative Center for Calcium and Learning, Korea Institutes of Science and Technology, Seoul 136-791, Korea.
Park
Donghyun
D
Choi
Soonwook
S
Lee
Sukchan
S
Sun
Minjeong
M
Kim
Chanki
C
Shin
Hee-Sup
HS
D015746:Abdominal Pain / Q000503:physiopathology; D019342:Acetic Acid / Q000494:pharmacology; D000200:Action Potentials; D000704:Analysis of Variance; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020747:Calcium Channels, T-Type / Q000235:genetics / Q000502:physiology*; D005260:Female; D008278:Magnesium Sulfate / Q000494:pharmacology; D008297:Male; D020748:Mibefradil / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation; D009474:Neurons / Q000502:physiology; D010146:Pain / Q000503:physiopathology*; D010147:Pain Measurement; D020651:Ventral Thalamic Nuclei / Q000502:physiology*; D014781:Viscera
C498197:Cacna1g protein, mouse; D002121:Calcium Channel Blockers; D020747:Calcium Channels, T-Type; D020748:Mibefradil; D008278:Magnesium Sulfate; D019342:Acetic Acid