期刊
JOURNAL OF NEUROSCIENCE
卷 41, 期 39, 页码 8210-8219出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1104-21.2021
关键词
crossover inhibition; in vivo calcium imaging; injury; spinal cord; thermosensation
资金
- Whitehall Foundation
- Terman Scholarship
- Firmenich Scholarship
- National Institutes of Health [R21 NS101407]
Different types of tissue injury, such as inflammatory and neuropathic conditions, cause modality-specific alterations on temperature perception. The study shows that injury-induced sensitization to temperature stimuli is encoded by patterned neuronal activities in the CNS, with a push-pull mechanism in processing cold and heat inputs. Additionally, chemotherapy medication oxaliplatin can rapidly change spinal responses to cooling and heating stimuli.
Different types of tissue injury, such as inflammatory and neuropathic conditions, cause modality-specific alternations on temperature perception. There are profound changes in peripheral sensory neurons after injury, but how patterned neuronal activities in the CNS encode injury-induced sensitization to temperature stimuli is largely unknown. Using in vivo calcium imaging and mouse genetics, we show that formalin- and prostaglandin E2-induced inflammation dramatically increase spinal responses to heating and decrease responses to cooling in male and female mice. The reduction of cold response is largely eliminated on ablation of TRPV1-expressing primary sensory neurons, indicating a crossover inhibition of cold response from the hyperactive heat inputs in the spinal cord. Interestingly, chemotherapy medication oxaliplatin can rapidly increase spinal responses to cooling and suppress responses to heating. Together, our results suggest a push-pull mechanism in processing cold and heat inputs and reveal a synergic mechanism to shift thermosensation after injury.
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