Active role of the central amygdala in widespread mechanical sensitization in rats with facial inflammatory pain
| Autor: | Fusao Kato, Mariko Sugimoto, Ryota Tokunaga, Manami Yajima, Yukari Takahashi, Yae K. Sugimura |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
Male
Pain Threshold medicine.medical_specialty Inflammation von Frey filament test Amygdala Mechanical allodynia Adeno-associated virus Facial Pain Internal medicine Medicine Premovement neuronal activity Animals Rats Wistar Sensitization Neurons Designer receptor exclusively activated by a designer drug GABAergic neurons business.industry Central nucleus of the amygdala Central Amygdaloid Nucleus Chronic pain Central sensitization medicine.disease Rats Anesthesiology and Pain Medicine medicine.anatomical_structure Nociception Endocrinology Neurology nervous system Latent orofacial formalin model VGAT-cre rat Body region Neurology (clinical) Clozapine-N-Oxide medicine.symptom Amygdala lateralization business Latent inflammatory pain psychological phenomena and processes Research Paper Calcitonin gene–related peptide receptor |
| Zdroj: | Pain |
| ISSN: | 1872-6623 0304-3959 |
| Popis: | Supplemental Digital Content is Available in the Text. Activity of gamma-aminobutyric acid-ergic neurons in the right-side central amygdala determines ectopic mechanical allodynia in the bilateral hind limbs in rats with orofacial inflammation. Widespread or ectopic sensitization is a hallmark symptom of chronic pain, characterized by aberrantly enhanced pain sensitivity in multiple body regions remote from the site of original injury or inflammation. The central mechanism underlying widespread sensitization remains unidentified. The central nucleus of the amygdala (also called the central amygdala, CeA) is well situated for this role because it receives nociceptive information from diverse body sites and modulates pain sensitivity in various body regions. In this study, we examined the role of the CeA in a novel model of ectopic sensitization of rats. Injection of formalin into the left upper lip resulted in latent bilateral sensitization in the hind paw lasting >13 days in male Wistar rats. Chemogenetic inhibition of gamma–aminobutyric acid-ergic neurons or blockade of calcitonin gene-related peptide receptors in the right CeA, but not in the left, significantly attenuated this sensitization. Furthermore, chemogenetic excitation of gamma-aminobutyric acid-ergic neurons in the right CeA induced de novo bilateral hind paw sensitization in the rats without inflammation. These results indicate that the CeA neuronal activity determines hind paw tactile sensitivity in rats with remote inflammatory pain. They also suggest that the hind paw sensitization used in a large number of preclinical studies might not be simply a sign of the pain at the site of injury but rather a representation of the augmented CeA activity resulting from inflammation/pain in any part of the body or from activities of other brain regions, which has an active role of promoting defensive/protective behaviors to avoid further bodily damage. |
| Databáze: | OpenAIRE |
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