Tonic inhibition of chronic pain by neuropeptide Y
| Autor: | Renee R. Donahue, Gregory Corder, Soma C. Bose, Bradley K. Taylor, Brian Solway |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
medicine.medical_specialty
Pain Arginine Synaptic Transmission Mice Internal medicine mental disorders medicine Animals Neuropeptide Y Receptor Mice Knockout Multidisciplinary Behavior Animal Chemistry Nociceptors Nerve injury Benzazepines Biological Sciences Neuropeptide Y receptor Spinal cord humanities Receptors Neuropeptide Y Posterior Horn Cells Allodynia medicine.anatomical_structure Endocrinology Nociception Gene Expression Regulation Hyperalgesia Chronic Disease Nociceptor medicine.symptom Proto-Oncogene Proteins c-fos |
| Zdroj: | Proceedings of the National Academy of Sciences of the United States of America. 108(17) |
| ISSN: | 1091-6490 |
| Popis: | Dramatically up-regulated in the dorsal horn of the mammalian spinal cord following inflammation or nerve injury, neuropeptide Y (NPY) is poised to regulate the transmission of sensory signals. We found that doxycycline-induced conditional in vivo ( Npy tet/tet ) knockdown of NPY produced rapid, reversible, and repeatable increases in the intensity and duration of tactile and thermal hypersensitivity. Remarkably, when allowed to resolve for several weeks, behavioral hypersensitivity could be dramatically reinstated with NPY knockdown or intrathecal administration of Y1 or Y2 receptor antagonists. In addition, Y2 antagonism increased dorsal horn expression of Fos and phosphorylated form of extracellular signal-related kinase. Taken together, these data establish spinal NPY receptor systems as an endogenous braking mechanism that exerts a tonic, long-lasting, broad-spectrum inhibitory control of spinal nociceptive transmission, thus impeding the transition from acute to chronic pain. NPY and its receptors appear to be part of a mechanism whereby mammals naturally recover from the hyperalgesia associated with inflammation or nerve injury. |
| Databáze: | OpenAIRE |
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