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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Effects of noradrenergic denervation on L-DOPA-induced dyskinesia and its treatment by α- And β-adrenergic receptor antagonists in hemiparkinsonian rats
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Effects of noradrenergic denervation on L-DOPA-induced dyskinesia and its treatment by α- And β-adrenergic receptor antagonists in hemiparkinsonian rats

机译：去甲肾上腺素能神经支配对L-DOPA引起的运动障碍的影响以及α-和β-肾上腺素能受体拮抗剂对半帕金森病大鼠的治疗

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While L-3,4-dihydroxyphenylalanine (L-DOPA) remains the standard treatment for Parkinson's disease (PD), long-term efficacy is often compromised by L-DOPA-induced dyskinesia (LID). Recent research suggests that targeting the noradrenergic (NE) system may provide relief from both PD and LID, however, most PD patients exhibit NE loss which may modify response to such strategies. Therefore this investigation aimed to characterize the development and expression of LID and the anti-dyskinetic potential of the α2- and β-adrenergic receptor antagonists idazoxan and propranolol, respectively, in rats receiving 6-OHDA lesions with (DA lesion) or without desipramaine protection (DA + NE lesion). Male Sprague-Dawley rats (N = 110) received unilateral 6-hydroxydopamine lesions. Fifty-three rats received desipramine to protect NE neurons (DA lesion) and 57 received no desipramine reducing striatal and hippocampal NE content 64% and 86% respectively. In experiment 1, the development and expression of L-DOPA-induced abnormal involuntary movements (AIMs) and rotations were examined. L-DOPA efficacy using the forepaw adjusting steps (FAS) test was also assessed in DA- and DA + NE-lesioned rats. In experiment 2, DA- and DA + NE-lesioned rats received pre-treatments of idazoxan or propranolol followed by L-DOPA after which the effects of these adrenergic compounds were observed. Results demonstrated that moderate NE loss reduced the development and expression of AIMs and rotations but not L-DOPA efficacy while anti-dyskinetic efficacy of α2- and β-adrenergic receptor blockade was maintained. These findings suggest that the NE system modulates LID and support the continued investigation of adrenergic compounds for the improved treatment of PD.
机译：虽然L-3,4-二羟基苯丙氨酸（L-DOPA）仍然是帕金森氏病（PD）的标准治疗方法，但长期疗效通常会因L-DOPA诱发的运动障碍（LID）而受损。最近的研究表明，靶向去甲肾上腺素（NE）系统可以减轻PD和LID的负担，但是，大多数PD患者表现出NE丢失，可能会改变对此类策略的反应。因此，本研究旨在表征接受（DA病灶）或无地昔拉美保护的6-OHDA损伤大鼠的LID的发育和表达以及α2-和β-肾上腺素能受体拮抗剂idazoxan和普萘洛尔的抗运动障碍潜力。 （DA + NE病变）。雄性Sprague-Dawley大鼠（N = 110）受到单侧6-羟基多巴胺损伤。有53只大鼠接受了地昔帕明保护NE神经元（DA病变），而57只大鼠没有地昔帕明降低纹状体和海马NE含量，分别为64％和86％。在实验1中，研究了L-DOPA诱导的异常非自愿运动（AIM）和旋转的发生和表达。还使用DAA和DA + NE病变的大鼠评估了使用前爪调节步骤（FAS）测试的L-DOPA功效。在实验2中，DA和DA + NE损伤的大鼠接受了唑烷和普萘洛尔的预处理，然后进行L-DOPA，之后观察到这些肾上腺素化合物的作用。结果表明，适度的NE丢失减少了AIM的形成和表达以及旋转，但没有降低L-DOPA的功效，同时维持了α2-和β-肾上腺素受体阻滞剂的抗运动障碍功效。这些发现表明，NE系统调节LID并支持继续研究肾上腺素化合物以改善PD的治疗。

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