Sección de Neurofarmacología y Neurociencias, Instituto de Investigaciones Clínicas "Dr. Américo Negrette", Facultad de Medicina, Universidad del Zulia, Apartado Postal 23, Maracaibo 4001-A, Venezuela.
Sección de Neurofarmacología y Neurociencias, Instituto de Investigaciones Clínicas "Dr. Américo Negrette", Facultad de Medicina, Universidad del Zulia, Apartado Postal 23, Maracaibo 4001-A, Venezuela.
Brain Res Bull. 2014 Jan;100:61-9. doi: 10.1016/j.brainresbull.2013.11.003. Epub 2013 Dec 4.
Although it is widely known that immunological, hormonal and nociceptive mechanisms are altered by exposure to repeated stress, the interplaying roles of each function in the development of post-stress hyperalgesia are not completely clear. Thus, we wanted to establish how interleukin 1-beta (IL-1β), corticosterone and microglia interact to contribute in the development of hyperalgesia following repeated forced swim. Rats were subjected to either forced swim, sham swim or non-conditioned. Each group was then treated with minocycline, ketoconazole, or saline. Thermal nociception was measured via the hot plate test, before and after the behavioral conditioning, whereas blood and lumbar spinal cord tissue samples were obtained at the end of the protocol. Serum levels of corticosterone, spinal tissue concentration of IL-1β and spinal OX-42 labeling (microglial marker) were determined. Rats exposed to forced swim stress developed thermal hyperalgesia along with elevated spinal tissue IL-1β, increased OX-42 labeling and relatively diminished serum corticosterone. Pre-treatment with minocycline and ketoconazole prevented the development of thermal hyperalgesia and the increase in IL-1β, without significantly modifying serum corticosterone. These results suggest that the development of forced swim-induced thermal hyperalgesia requires the simultaneous presence of increased spinal IL-1β, microglial activation, and relatively decreased serum corticosterone.
虽然人们普遍知道，暴露于反复的应激会改变免疫、激素和伤害性感受机制，但每种功能在应激后痛觉过敏发展中的相互作用尚不完全清楚。因此，我们想确定白细胞介素 1-β（IL-1β）、皮质酮和小胶质细胞如何相互作用，以促成重复强迫游泳后的痛觉过敏。将大鼠置于强迫游泳、假游泳或非条件化中。然后，每组分别用米诺环素、酮康唑或生理盐水处理。在行为训练前后，通过热板试验测量热痛觉，在方案结束时获得血液和腰脊髓组织样本。测定血清皮质酮、脊髓组织中 IL-1β 和脊髓 OX-42 标记（小胶质细胞标记物）的浓度。暴露于强迫游泳应激的大鼠出现热痛觉过敏，同时脊髓组织中 IL-1β 升高、OX-42 标记增加和血清皮质酮相对减少。米诺环素和酮康唑预处理可预防热痛觉过敏和 IL-1β 增加，而对血清皮质酮无显著影响。这些结果表明，强迫游泳诱导的热痛觉过敏的发展需要同时存在脊髓 IL-1β 增加、小胶质细胞激活和血清皮质酮相对减少。
