Thalamic control of visceral nociception mediated by T-type Ca2+ channels
Thalamic control of visceral nociception mediated by T-type Ca2+ channels
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DOI：
10.1126/science.1088886
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发表时间：
2003-10-03
期刊：
影响因子：
56.9
通讯作者：
Shin, HS
中科院分区：
文献类型：
--
作者：
Kim, D;Park, D;Shin, HS
来自内脏的感觉，如饱腹感，如果刺激持续下去，很容易变得疼痛。缺乏α 1GT型Ca（2+）通道的小鼠表现出对内脏痛的痛觉过敏。在野生型小鼠中，T型阻断剂的丘脑输注诱导了类似的痛觉过敏。内脏痛时，丘脑腹后外侧区神经元诱发单棘波的激增，然后随着T型依赖的爆发性棘波逐渐增加而缓慢衰减。在alpha1G缺陷的神经元，单棘波反应持续没有爆发尖峰。这些结果表明，T型钙通道的基础上的抗伤害性机制在丘脑中运作，并支持的想法，爆发。环在丘脑的感觉门控中起关键作用。
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.