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The long-lasting sensitization of primary afferent nociceptors induced by inflammation involves prostanoid and dopaminergic systems in mice

机译:炎症诱导的初级传入伤害者的长期敏化涉及小鼠前列腺和多巴胺能系统

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In recent years, evidence that sensitization of primary afferent nociceptors is an important event associated with chronic pain has been accumulating. The present study aimed to evaluate the participation of the prostaglandin and sympathetic components in the long-lasting sensitization of nociceptors induced by acute inflammation in mice. The intraplantar administration of carrageenan (100 ??g) enhanced the nociceptive response to a small dose of PGE2 (9 ng/paw) or dopamine (3 ??g/paw) up to 30 days later. This long-lasting sensitization is dependent on dopaminergic and prostanoid systems, since the pre-treatment with chlorpromazine (3 ??g/paw) or indomethacin (100 ??g/paw), but not local (6 ??g/paw) or systemic (6 mg/kg) treatment with morphine, prevented its development. In agreement with this idea, the previous intraplantar administration of hyperalgesic doses of PGE 2 or dopamine also induced long-lasting sensitization, which was fully prevented by pretreatment with EP4 and D1 antagonists, respectively. In summary, the present work described in mice a long-lasting sensitization of nociceptors, initiated by an acute inflammatory stimulation and dependent on dopaminergic and prostanoid systems. The present data represent new insights on the mechanisms of peripheral sensitization that could contribute to establish the basis of new therapeutic strategies for acute and chronic inflammatory pain. ? 2012 Elsevier Inc. All rights reserved.
机译:近年来,证据表明,初级传入伤害者的敏化是与慢性疼痛相关的重要事件已经积累。本研究旨在评估前列腺素和交感神经组分在小鼠中急性炎症诱导的伤膨胀致敏中的参与。角叉菜系的颅内施用鹿茸(100'Og)在30天后,增强了对小剂量PGE2(9ng /爪)或多巴胺(3→G /爪)的伤害反应。这种持久的致敏性依赖于多巴胺能和前列腺体系,因为用氯丙嗪(3→G /爪子)或吲哚美辛(100 ?? G / PAW)预处理,但不是局部(6 ?? G / PAW)或通过吗啡处理的系统性(6mg / kg)治疗,防止了其发展。在此思想的同意中,先前的颅内颅内颅内血吸剂施用型PGE 2或多巴胺也诱导了持久的敏化,其分别用EP4和D1拮抗剂进行预处理完全防止。总之,通过急性炎症刺激和依赖于多巴胺能和前列腺素系统,对小鼠进行长期持久致敏的本作者。目前的数据代表了对外围致敏机制的新见解,这可能有助于建立急性和慢性炎症疼痛的新治疗策略的基础。还2012年elsevier Inc.保留所有权利。

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