Substantial role of locus coeruleus-noradrenergic activation and capsaicin-insensitive primary afferent fibers in bee venom's anti-inflammatory effect
| Autor: | Alvin J. Beitz, Seuk Yun Kang, Kee-Won Kim, Ho Jae Han, Yeon Hee Ryu, Hyejung Lee, Sun Mi Choi, Jang Hern Lee, Seo Yeon Yoon, Hyun-Woo Kim, Dae Hyun Roh, Young Bae Kwon |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Leukocyte migration
medicine.medical_specialty Resiniferatoxin Anti-Inflammatory Agents Gene Expression Hindlimb Biology Functional Laterality chemistry.chemical_compound Mice Norepinephrine Adrenergic Agents Internal medicine medicine Leukocytes Animals Drug Interactions Oxidopamine Denervation Inflammation Mice Inbred ICR General Neuroscience Zymosan General Medicine Bee Venoms Disease Models Animal Endocrinology Oncogene Proteins v-fos chemistry Capsaicin Anesthesia Catecholamine Locus coeruleus Locus Coeruleus Diterpenes Sciatic Neuropathy Idazoxan medicine.drug |
| Zdroj: | Neuroscience research. 55(2) |
| ISSN: | 0168-0102 |
| Popis: | Several lines of evidence indicate significant interactions between the immune and nervous systems. Our recent study reveals that 'bee venom (BV) induced anti-inflammatory effect' (BVAI) was produced by sympathetic preganglionic neuronal activation and subsequent adrenomedullary catecholamine release in a zymosan-induced inflammation model. However, the specific peripheral input and the supraspinal neuronal systems that are involved in this BVAI remain to be defined. Here we show that subcutaneous BV injection into left hind limb significantly reduces zymosan-induced leukocyte migration and that this effect is completely inhibited by denervation of the left sciatic nerve. This BVAI was not affected by the destruction of capsaicin-sensitive primary afferent fibers using either neonatal capsaicin or resiniferatoxin (RTX) pretreatment. BV injection into the left hind limb significantly increased Fos expression in the contralateral locus coeruleus (LC) in non-inflamed mice. In zymosan-inflamed mice, BV injection produced a further increase in LC Fos expression as compared with non-inflamed mice. This BV-induced Fos increase in the LC was not affected by RTX pretreatment. Pharmacological blockage of central noradrenergic activity by either central chemical sympathectomy (i.c.v. 6-hydroxydopamine) or alpha2 adrenoceptor antagonism (i.c.v. idazoxan) completely blocked BVAI. Taken together, these results suggest that BVAI is mediated by peripheral activation of capsaicin-insensitive primary afferent fibers and subsequent central noradrenergic activation including the LC. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect