AI Article Synopsis
- * A study found that introducing a blocker for T-type channels into the thalamus of normal (wild-type) mice resulted in increased sensitivity to pain similar to that seen in the alpha1G-deficient mice.
- * The findings suggest that T-type calcium channels play an important role in reducing pain in the thalamus, and they help in controlling sensory information by contrasting the patterns of nerve firing, indicating that burst firing is crucial for managing sensory input effectively.
Article Abstract
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.
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| http://dx.doi.org/10.1126/science.1088886 | DOI Listing |
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