| First Author | Barik A | Year | 2021 |
| Journal | Elife | Volume | 10 |
| PubMed ID | 33591273 | Mgi Jnum | J:316084 |
| Mgi Id | MGI:6808181 | Doi | 10.7554/eLife.61135 |
| Citation | Barik A, et al. (2021) A spinoparabrachial circuit defined by Tacr1 expression drives pain. Elife 10:e61135 |
| abstractText | Painful stimuli evoke a mixture of sensations, negative emotions and behaviors. These myriad effects are thought to be produced by parallel ascending circuits working in combination. Here, we describe a pathway from spinal cord to brain for ongoing pain. Activation of a subset of spinal neurons expressing Tacr1 evokes a full repertoire of somatotopically directed pain-related behaviors in the absence of noxious input. Tacr1 projection neurons (expressing NKR1) target a tiny cluster of neurons in the superior lateral parabrachial nucleus (PBN-SL). We show that these neurons, which also express Tacr1 (PBN-SL(Tacr1)), are responsive to sustained but not acute noxious stimuli. Activation of PBN-SL(Tacr1) neurons alone did not trigger pain responses but instead served to dramatically heighten nocifensive behaviors and suppress itch. Remarkably, mice with silenced PBN-SL(Tacr1) neurons ignored long-lasting noxious stimuli. Together, these data reveal new details about this spinoparabrachial pathway and its key role in the sensation of ongoing pain. |
