نوع مقاله : مقاله پژوهشی

نویسندگان

1 دانشجوی دکترا شهید بهشتی

2 دانشیار دانشگاه شهید بهشتی

3 دانشیار مرکز تحقیقات علوم اعصاب دانشکاه علوم پزشکی شهید بهشتی

4 دانشیار دانشگاه خوارزمی

چکیده

پیوندگاه عصب ـ عضله(NMJ) طی سالمندی تغییرات عمده‌ای از جمله کاهش فعالیت نیتریک اکساید سنتاز نورونی (nNOS) می‌یابد که در نهایت سبب تضعیف عملکرد جسمانی و بروز سارکوپنیا می‌گردد. هدف از انجام این پژوهش تعیین تأثیر هشت هفته تمرین استقامتی همراه با مهار nNOS بر میزان پروتئین گیرنده‌های نیکوتینی استیل کولین (nAchR) بود. تولید نیتریک اکساید (NO) بوسیله دو دوز mg-1.kg-1.day -1 25 و 100 N G نیترو- L – آرژنین متیل استر ( L-NAME ) (مهارکننده nNOS)، مهار شد. 48 سر موش نر نژاد ویستار مسن (20ماهه) به صورت تصادفی به شش گروه کنترل، LNAME25,100، گروه‌های تمرین همراه با LNAME (Training+LNAME25,100) و گروه تمرین استقامتی (Training) تقسیم شدند. سه روز قبل از اجرای پروتکل مصرف LNAME شروع و تا زمان تشریح حیوانات این کار ادامه داشت. گروه‌های تمرینی به مدت 8 هفته، هر هفته 5 روز و روزی 60 دقیقه با سرعت 28 متر بر دقیقه روی نوارگردان می‌دویدند. 48 ساعت بعد از آخرین جلسه تمرین، پس از بی‌هوش کردن حیوانات، عضله نعلی و عضله دراز انگشتان (EDL) برداشته شد. ب در عضله نعلی و EDL، مصرف LNAME (100 mg-1.kg-1.day -1) سبب کاهش معنادار پروتئین nAchR شد (P<0.05)، نتایج این پژوهش نشان داد که تمرین می‌تواند سبب افزایش nAchR حتی در موش-های صحرایی که LNAME مصرف کردند شود (P<0.05). با توجه به یافته‌های پژوهش حاضر کاهش فعالیت nNOS سبب کاهش میزان پروتئین nAchR می‌گردد و تمرین استقامتی نه تنها سبب افزایش میزان nAchR می‌شود، بلکه می‌تواند محرکی برای افزایش میزان nAchR ناشی از کاهش یا نبود nNOS باشد.

کلیدواژه‌ها

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