Kim, Daesoo Park, Donghyun Choi, Soonwook Lee, Sukchan Sun, Minjeong Kim, Chanki Shin, Hee-Sup 2024-01-21T08:09:15Z 2024-01-21T08:09:15Z 2021-09-03 2003-10 0036-8075 https://pubs.kist.re.kr/handle/201004/138197 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. English American Association for the Advancement of Science Thalamic control of visceral nociception mediated by T-type Ca2+ channels Article 10.1126/science.1088886 1 Science, v.302, no.5642, pp.117 - 119 Science 302 5642 117 119 N scie scopus 000185678500049 2-s2.0-0141642208 Multidisciplinary Sciences Science & Technology - Other Topics Article NEURONS BURST RESPONSES PATHWAY NUCLEUS RATS THALAMOCORTICAL RELAY CALCIUM CHANNELS DORSAL COLUMN SPINAL-CORD