Boracı H, Kirazlı Ö, Gülhan R, Yıldız Sercan D, Şehirli Ü S
Department of Anatomy, School of Medicine, Marmara University, Başıbüyük Yolu No: 9/2 Başıbüyük, Maltepe, Istanbul, Turkey.
Department of Medical Pharmacology, School of Medicine, Marmara University, Istanbul, Turkey.
Anat Sci Int. 2020 Sep;95(4):429-439. doi: 10.1007/s12565-020-00538-y. Epub 2020 Mar 21.
In Parkinson's disease (PD), physical therapy is one of the mainstays of supportive treatment modalities. This study focused on the neuroprotective effect of regular exercise on striatal calretinin positive interneurons in a rat model of PD. 6-hydroxydopamine (6-OHDA) was injected unilaterally into the medial forebrain bundle of Wistar rats. 6-OHDA lesioned (Parkinsonian) and unlesioned (control) rats were divided into sedentary and exercise groups. Exercise groups had daily swimming sessions for 30 min for 6 weeks. After 6-OHDA injections, an apomorphine-induced rotation test was performed (0.05 mg/kg, subcutaneous) at the 3rd and 6th weeks. At the end of the 6th week, brains were removed following transcardiac perfusion. The brain sections were stained immunohistochemically for tyrosine hydroxylase and calretinin reactivity. The number of rotations was significantly lower in Parkinsonian exercise group compared to Parkinsonian sedentary group at the 6th week (p = 0.024) and there was significant difference between Parkisonian sedentary groups at the 3rd and 6th weeks (p < 0.002). The calretinin positive interneurons significantly increased in the Parkinsonian exercise group compared to Parkinsonian sedentary group (p = 0.0003) and control exercise group (p < 0.0001). To conclude, the swimming exercise led to a striking increment of calretinin positive interneurons in the striatum of Parkinsonian rat. These findings indicated that the neuroprotective mechanism of exercise increased the number of striatal calretinin positive interneurons that might generate new approaches for the mechanism of neuroprotection. We concluded that striatal calretinin positive interneurons have an important role in the neuroprotective mechanisms of exercise in PD.
在帕金森病（PD）中，物理治疗是支持性治疗方式的主要手段之一。本研究聚焦于规律运动对PD大鼠模型纹状体钙视网膜蛋白阳性中间神经元的神经保护作用。将6-羟基多巴胺（6-OHDA）单侧注射到Wistar大鼠的内侧前脑束。6-OHDA损伤（帕金森病样）和未损伤（对照）大鼠被分为久坐组和运动组。运动组每天进行30分钟的游泳训练，持续6周。注射6-OHDA后，在第3周和第6周进行阿扑吗啡诱导的旋转试验（0.05mg/kg，皮下注射）。在第6周结束时，经心脏灌注后取出大脑。脑切片进行酪氨酸羟化酶和钙视网膜蛋白反应性的免疫组织化学染色。在第6周时，帕金森病运动组的旋转次数显著低于帕金森病久坐组（p = 0.024），且帕金森病久坐组在第3周和第6周之间存在显著差异（p < 0.002）。与帕金森病久坐组相比，帕金森病运动组中钙视网膜蛋白阳性中间神经元显著增加（p = 0.0003），与对照运动组相比也有显著增加（p < 0.0001）。总之，游泳运动导致帕金森病大鼠纹状体中钙视网膜蛋白阳性中间神经元显著增加。这些发现表明，运动的神经保护机制增加了纹状体钙视网膜蛋白阳性中间神经元的数量，这可能为神经保护机制带来新的研究途径。我们得出结论，纹状体钙视网膜蛋白阳性中间神经元在PD运动的神经保护机制中具有重要作用。
