مسیرهای پیام رسانی ملکولی دخیل در صرع گیجگاهی

نوع مقاله: مقاله مروری

نویسندگان

1 مرکز تحقیقات علوم اعصاب شفا، بیمارستان خاتم الانبیاء، تهران، ایران.

2 گروه بیوشیمی بالینی، دانشگاه علوم پزشکی شهید بهشتی، تهران، ایران.

3 گروه آناتومی، دانشگاه علوم پزشکی تهران، تهران، ایران.

4 دپارتمان علوم اعصاب، دانشکده پزشکی، دانشگاه علوم پزشکی مشهد

چکیده

 صرع یک اختلال نورولوژیک مزمن است که در نتیجه عدم تعادل بین پتانسیل­های تحریکی و مهاری در مغز ایجاد می­شود و تحت عنوان اختلالی شناخته می­شود که محصول عود و تکرار تشنج می­باشد. علیرغم تلاش های فراوان در سال های اخیر، یک سوم بیماران صرعی مقاوم به درمان های رایج پزشکی می باشند. گزارش داده شده است که عواملی ژنتیکی، کانال­های یونی سیناپسی، نوروترانسمیترهای تحریکی و مهاری و همینطور فعال­شدن گیرنده­های وابسته به گلوتامات یونوتروپیک و متابوتروپیک می­توانند در ایجاد بیماری صرع دخیل می باشند. مطالعات بیشتر جهت بررسی مکانیسم های مولکولی و کانال های یونی در پیشرفت بیماری صرع نیاز می باشد. در این مطالعه مروری، ما بررسی اجمالی بر مسیرهای سینگنالینگ مولکولی دخیل در صرع زایی داریم. علاوه بر این، ما به مکانیسم های مولکولی در صرع لوب گیجگاهی خواهیم پرداخت. فهم و درک مکانیسم های مولکولی می­تواند چشم اندازی جدید برای شناسایی اهداف دارویی در جلوگیری از بیماری صرع فراهم آورد.

کلیدواژه‌ها


عنوان مقاله [English]

Molecular Signaling Pathways involved in Temporal Lobe Epilepsy

نویسندگان [English]

  • Parastoo Morteza-zadeh 1
  • Ali Jahanbazi 2
  • Maryam Borhani-Haghighi 3
  • Sajad Sahab Negah 4
1 Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran.
2 Department of Clinical Biochemistry, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3 Department of Anatomy, Tehran University of Medical Sciences, Tehran, Iran.
4 Department of Neuroscience, Mashhad University of Medical Science, Mashhad, Iran
چکیده [English]

Epilepsy is a chronic neurological disorder that defined as a disorder of recurrent seizures and characterized by an imbalance of excitation and inhibition in the brain. Despite many efforts in recent years, one-third of the epileptic patients are refractory to medical treatment.  It has been reported that genetic factors, synaptic ion channels, excitatory and inhibitory neurotransmitters and activation of various receptors such as ionotropic and metabotropic glutamate receptors in the central nervous system can promote epileptogenesis. Further research to investigate the molecular mechanisms and ions involved in the development of epilepsy is needed. In this review, we present an overview of current status into the molecular signaling pathways involved in epileptogenesis. Furthermore, we will focus on temporal lobe epilepsy (TLE) molecular mechanisms. Understanding of molecular mechanisms could provide new fascinating insights into drug target identification in the prevention of epileptogenesis.
 

کلیدواژه‌ها [English]

  • Epilepsy
  • ion channels
  • Glutamate Receptors
  • Neurotransmitters

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