Parabrachial Calca neurons drive nociplasticity
Summary: Pain that persists beyond the time required for tissue healing and pain that arises in the absence of tissue injury, collectively referred to as nociplastic pain, are poorly understood phenomena mediated by plasticity within the central nervous system. The parabrachial nucleus (PBN) is a hu...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2024-04-01
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| Series: | Cell Reports |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2211124724003851 |
| _version_ | 1797219300775297024 |
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| author | Logan F. Condon Ying Yu Sekun Park Feng Cao Jordan L. Pauli Tyler S. Nelson Richard D. Palmiter |
| author_facet | Logan F. Condon Ying Yu Sekun Park Feng Cao Jordan L. Pauli Tyler S. Nelson Richard D. Palmiter |
| author_sort | Logan F. Condon |
| collection | DOAJ |
| description | Summary: Pain that persists beyond the time required for tissue healing and pain that arises in the absence of tissue injury, collectively referred to as nociplastic pain, are poorly understood phenomena mediated by plasticity within the central nervous system. The parabrachial nucleus (PBN) is a hub that relays aversive sensory information and appears to play a role in nociplasticity. Here, by preventing PBN Calca neurons from releasing neurotransmitters, we demonstrate that activation of Calca neurons is necessary for the manifestation and maintenance of chronic pain. Additionally, by directly stimulating Calca neurons, we demonstrate that Calca neuron activity is sufficient to drive nociplasticity. Aversive stimuli of multiple sensory modalities, such as exposure to nitroglycerin, cisplatin, or lithium chloride, can drive nociplasticity in a Calca-neuron-dependent manner. Aversive events drive nociplasticity in Calca neurons in the form of increased activity and excitability; however, neuroplasticity also appears to occur in downstream circuitry. |
| first_indexed | 2024-04-24T12:31:28Z |
| format | Article |
| id | doaj.art-2619f8d0afdd4ff5be1a9441d2dc0550 |
| institution | Directory Open Access Journal |
| issn | 2211-1247 |
| language | English |
| last_indexed | 2024-04-24T12:31:28Z |
| publishDate | 2024-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Cell Reports |
| spelling | doaj.art-2619f8d0afdd4ff5be1a9441d2dc05502024-04-08T04:08:17ZengElsevierCell Reports2211-12472024-04-01434114057Parabrachial Calca neurons drive nociplasticityLogan F. Condon0Ying Yu1Sekun Park2Feng Cao3Jordan L. Pauli4Tyler S. Nelson5Richard D. Palmiter6Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA; Departments of Biochemistry and Genome Sciences, University of Washington, Seattle, WA 98195, USA; Graduate Program in Neuroscience, University of Washington, Seattle, WA 98195, USA; Medical Scientist Training Program, University of Washington, Seattle, WA 98195, USAHoward Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA; Departments of Biochemistry and Genome Sciences, University of Washington, Seattle, WA 98195, USAHoward Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA; Departments of Biochemistry and Genome Sciences, University of Washington, Seattle, WA 98195, USAHoward Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA; Departments of Biochemistry and Genome Sciences, University of Washington, Seattle, WA 98195, USAHoward Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA; Departments of Biochemistry and Genome Sciences, University of Washington, Seattle, WA 98195, USADepartment of Pharmacology and Therapeutics, College of Medicine, University of Florida, Gainesville, FL 32610, USAHoward Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA; Departments of Biochemistry and Genome Sciences, University of Washington, Seattle, WA 98195, USA; Graduate Program in Neuroscience, University of Washington, Seattle, WA 98195, USA; Corresponding authorSummary: Pain that persists beyond the time required for tissue healing and pain that arises in the absence of tissue injury, collectively referred to as nociplastic pain, are poorly understood phenomena mediated by plasticity within the central nervous system. The parabrachial nucleus (PBN) is a hub that relays aversive sensory information and appears to play a role in nociplasticity. Here, by preventing PBN Calca neurons from releasing neurotransmitters, we demonstrate that activation of Calca neurons is necessary for the manifestation and maintenance of chronic pain. Additionally, by directly stimulating Calca neurons, we demonstrate that Calca neuron activity is sufficient to drive nociplasticity. Aversive stimuli of multiple sensory modalities, such as exposure to nitroglycerin, cisplatin, or lithium chloride, can drive nociplasticity in a Calca-neuron-dependent manner. Aversive events drive nociplasticity in Calca neurons in the form of increased activity and excitability; however, neuroplasticity also appears to occur in downstream circuitry.http://www.sciencedirect.com/science/article/pii/S2211124724003851CP: NeuroscienceCP: Cell biology |
| spellingShingle | Logan F. Condon Ying Yu Sekun Park Feng Cao Jordan L. Pauli Tyler S. Nelson Richard D. Palmiter Parabrachial Calca neurons drive nociplasticity Cell Reports CP: Neuroscience CP: Cell biology |
| title | Parabrachial Calca neurons drive nociplasticity |
| title_full | Parabrachial Calca neurons drive nociplasticity |
| title_fullStr | Parabrachial Calca neurons drive nociplasticity |
| title_full_unstemmed | Parabrachial Calca neurons drive nociplasticity |
| title_short | Parabrachial Calca neurons drive nociplasticity |
| title_sort | parabrachial calca neurons drive nociplasticity |
| topic | CP: Neuroscience CP: Cell biology |
| url | http://www.sciencedirect.com/science/article/pii/S2211124724003851 |
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