کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8351803 | 1541873 | 2013 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Genetic inactivation of pleiotrophin but not midkine potentiates clonidine-induced alpha-2 adrenergic-mediated analgesia
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Genetic deletion of the heparin-binding cytokines pleiotrophin (PTN) or midkine (MK) potentiates morphine-induced antinociceptive effects in animal models. Despite the known interactions between the opioid and noradrenergic systems in the control of pain, the possible roles of PTN and/or MK in analgesia induced by agonists of α2-adrenergic receptors remained to be studied. We have now tested the antinociceptive effects of the α2-adrenergic receptor agonist clonidine in female PTN genetically deficient (PTN â/â), MK genetically deficient (MK â/â) and wild type (WT +/+) mice. We did not find differences among genotypes in the hot-plate test, an assay in which supraspinal and spinal mechanisms contribute to nociceptive responses, suggesting that endogenous expression of PTN and MK is not key in the analgesia induced by clonidine in this test. In contrast, we found that clonidine-induced analgesia was significantly enhanced in PTN â/â mice compared to MK â/â and WT +/+ mice in the tail-immersion test. Interestingly, the α2-adrenergic antagonist yohimbine prevented clonidine-induced analgesia in the tail immersion test in all the 3 genotypes. The data suggest that the spinal antinociceptive effects caused by stimulation of α2-adrenoceptors are differentially regulated by endogenous expression of PTN.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacology Biochemistry and Behavior - Volume 110, September 2013, Pages 185-191
Journal: Pharmacology Biochemistry and Behavior - Volume 110, September 2013, Pages 185-191
نویسندگان
Marta Vicente-RodrÃguez, Carmen Pérez-GarcÃa, Esther Gramage, Gonzalo Herradón,