| First Author | Kim D | Year | 2003 |
| Journal | Science | Volume | 302 |
| Issue | 5642 | Pages | 117-9 |
| PubMed ID | 14526084 | Mgi Jnum | J:256598 |
| Mgi Id | MGI:6116201 | Doi | 10.1126/science.1088886 |
| Citation | Kim D, et al. (2003) Thalamic control of visceral nociception mediated by T-type Ca2+ channels. Science 302(5642):117-9 |
| abstractText | 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. |
