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Physiology and Pharmacology، جلد ۲۰، شماره ۲، صفحات ۹۸-۱۰۷
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عنوان انگلیسی Minocycline did not prevent the neurotoxic effects of amyloid β on intrinsic electrophysiological properties of hippocampal CA1 pyramidal neurons in a rat model of Alzheimer’s disease
چکیده انگلیسی مقاله Introduction: Although aging is the most important risk factor for Alzheimer's disease (AD), there is evidence indicating that neuroinflammation may contribute to the development and progression of the disease. Several studies indicated that minocycline may exert neuroprotective effects in rodent models of neurodegenerative diseases. Nevertheless, there are also other studies implying that minocycline has no positive beneficial effects. Thus, the aim of the present study was to assess the preventive effect of minocycline against Aβ-induced changes in intrinsic electrophysiological properties in a rat model of AD. Methods: The present study extended this line of research by examining whether inhibition of microglial activation may alter the intrinsic electrophysiological properties of CA1 pyramidal neurons in a rat model of Aβ neurotoxicity, using whole cell patch clamp. Results: Findings showed that bilateral injection of the Aβ (1-42) into the prefrontal cortex caused membrane hyperpolarization, action potential (AP) narrowing and after hyperpolarization (AHP) amplitude enhancement. It was also resulted in a faster decay time of AP, higher rheobase current, lower firing frequency and smaller post stimulus AHP amplitude. Administration of minocycline (45mg/kg, i.p) not only failed to prevent Aβ-induced alterations in the intrinsic electrophysiological properties, but also enhanced the effects of Aβ on neuronal firing behavior. Conclusion: It can be concluded that minocycline, as a microglial inhibitor, may enhance the disruption of electrophysiological properties of CA1 pyramidal neurons induced by Aβ neurotoxin, including AP parameters and intrinsic neuronal excitability.
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نویسندگان مقاله شراره دریانی | sharareh daryani
neuroscience research centre and dept. of physiology, school of medicine, shahid beheshti university of medical sciences, evin, tehran, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی شهید بهشتی (Shahid beheshti university of medical sciences)

علیرضا فرزایی | alireza farzaei
dept. of physiology, medical school, shahid beheshti university of medical sciences, tehran, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی شهید بهشتی (Shahid beheshti university of medical sciences)

نرگس حسین مردی | narges hosseinmardi
neuroscience research centre and dept. of physiology, school of medicine, shahid beheshti university of medical sciences, evin, tehran, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی شهید بهشتی (Shahid beheshti university of medical sciences)

فریده بهرامی | farideh bahrami
neuroscience research centre and department of physiology, faculty of medicine, baqiyatallah university of medical sciences, tehran, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی بقیه الله (Baqiyatallah university of medical sciences)

مهیار جان احمدی | mahyar janahmadi
neuroscience research centre and dept. of physiology, school of medicine, shahid beheshti university of medical sciences, evin, tehran, iran

سازمان اصلی تایید شده: دانشگاه علوم پزشکی شهید بهشتی (Shahid beheshti university of medical sciences)

نشانی اینترنتی http://www.phypha.ir/ppj/browse.php?a_code=A-10-914-1&slc_lang=en&sid=en
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کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده Neurodegeneretive diseases
نوع مقاله منتشر شده Original Research
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