| First Author | Tran M | Year | 2020 |
| Journal | J Comp Neurol | Volume | 528 |
| Issue | 10 | Pages | 1629-1643 |
| PubMed ID | 31872868 | Mgi Jnum | J:296270 |
| Mgi Id | MGI:6438274 | Doi | 10.1002/cne.24847 |
| Citation | Tran M, et al. (2020) Ablation of spinal cord estrogen receptor alpha-expressing interneurons reduces chemically induced modalities of pain and itch. J Comp Neurol 528(10):1629-1643 |
| abstractText | Estrogens are presumed to underlie, at least in part, the greater pain sensitivity and chronic pain prevalence that women experience compared to men. Although previous studies revealed populations of estrogen receptor-expressing neurons in primary afferents and in superficial dorsal horn neurons, there is little to no information as to the contribution of these neurons to the generation of acute and chronic pain. Here we molecularly characterized neurons in the mouse superficial spinal cord dorsal horn that express estrogen receptor alpha (ERalpha) and explored the behavioral consequences of their ablation. We found that spinal ERalpha-positive neurons are largely excitatory interneurons and many coexpress substance P, a marker for a discrete subset of nociceptive, excitatory interneurons. After viral, caspase-mediated ablation of spinal ERalpha-expressing cells, we observed a significant decrease in the first phase of the formalin test, but in male mice only. ERalpha-expressing neuron-ablation also reduced pruritogen-induced scratching in both male and female mice. There were no ablation-related changes in mechanical or heat withdrawal thresholds or in capsaicin-induced nocifensive behavior. In chronic pain models, we found no change in Complete Freund's adjuvant-induced thermal or mechanical hypersensitivity, or in partial sciatic nerve injury-induced mechanical allodynia. We conclude that ERalpha labels a subpopulation of excitatory interneurons that are specifically involved in chemically evoked persistent pain and pruritogen-induced itch. |
