Nastaran Zamani, Ahmad Ali Moazedi, Mohamad Reza Afarinesh Khaki, Mehdi Pourmehdi Boroujeni
{"title":"美金刚对完整和阿尔茨海默病大鼠模型海马CA1锥体神经元自发放电频率的影响：一项电生理研究。","authors":"Nastaran Zamani, Ahmad Ali Moazedi, Mohamad Reza Afarinesh Khaki, Mehdi Pourmehdi Boroujeni","doi":"10.32598/bcn.2021.1970.1","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Memantine (MEM) is a noncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonist clinically used for the treatment of Alzheimer disease (AD) in mild to severe conditions. The present study was conducted to investigate the effects of memantine on the spontaneous firing frequency of CA1 pyramidal neurons in rats caused by an electrical lesion of Nucleus Basalis Magnocellularis (NBM). Then, this model of AD rats was compared with the intact adult male rats.</p><p><strong>Methods: </strong>In this study, adult male rats were divided into two groups. Group I (lesion of NBM, n=53) includes the following subgroups: lesion+saline, sham+saline, lesion+MEM 5 mg/kg, lesion+MEM 10 mg/kg, and lesion+MEM 20mg/kg. Group II (intact, n=48) includes the following subgroups: intact+saline, intact+MEM 3mg/kg, intact+MEM 5mg/kg, and intact+MEM 10mg/kg. Extracellular single-unit recording (15 min baseline+105 min after MEM or saline) was performed under urethane-anesthetized rats.</p><p><strong>Results: </strong>The results showed that the mean frequency of CA1 pyramidal neurons after saline in the lesion+saline (P<0.001) group significantly decreases compared with the intact+saline and sham+saline groups. In addition, after saline and memantine, the mean frequency of CA1 pyramidal neurons in the lesion+MEM 10 mg/kg (P<0.01) and lesion+MEM 20 mg/kg (P<0.001) groups significantly increased compared with the lesion+saline group. Also, the mean frequencies of CA1 pyramidal neurons in the intact+MEM 10 mg/kg (P<0.001) group significantly decreased compared with the intact+saline group.</p><p><strong>Conclusion: </strong>Results showed that memantine increases the electrical activity of CA1 pyramidal neurons in a rat model of AD. Furthermore, in the intact adult male rats, the low-dose memantine, contrary to high dose, does not decrease the electrical activity of CA1 pyramidal neurons.</p>","PeriodicalId":8701,"journal":{"name":"Basic and Clinical Neuroscience","volume":"13 5","pages":"661-674"},"PeriodicalIF":1.0000,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b3/d1/BCN-13-661.PMC10258597.pdf","citationCount":"0","resultStr":"{\"title\":\"Effects of Memantine on the Spontaneous Firing Frequency of Hippocampal CA1 Pyramidal Neurons in Intact and Alzheimer Rat Model: An Electrophysiological Study.\",\"authors\":\"Nastaran Zamani, Ahmad Ali Moazedi, Mohamad Reza Afarinesh Khaki, Mehdi Pourmehdi Boroujeni\",\"doi\":\"10.32598/bcn.2021.1970.1\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Memantine (MEM) is a noncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonist clinically used for the treatment of Alzheimer disease (AD) in mild to severe conditions. The present study was conducted to investigate the effects of memantine on the spontaneous firing frequency of CA1 pyramidal neurons in rats caused by an electrical lesion of Nucleus Basalis Magnocellularis (NBM). Then, this model of AD rats was compared with the intact adult male rats.</p><p><strong>Methods: </strong>In this study, adult male rats were divided into two groups. Group I (lesion of NBM, n=53) includes the following subgroups: lesion+saline, sham+saline, lesion+MEM 5 mg/kg, lesion+MEM 10 mg/kg, and lesion+MEM 20mg/kg. Group II (intact, n=48) includes the following subgroups: intact+saline, intact+MEM 3mg/kg, intact+MEM 5mg/kg, and intact+MEM 10mg/kg. Extracellular single-unit recording (15 min baseline+105 min after MEM or saline) was performed under urethane-anesthetized rats.</p><p><strong>Results: </strong>The results showed that the mean frequency of CA1 pyramidal neurons after saline in the lesion+saline (P<0.001) group significantly decreases compared with the intact+saline and sham+saline groups. In addition, after saline and memantine, the mean frequency of CA1 pyramidal neurons in the lesion+MEM 10 mg/kg (P<0.01) and lesion+MEM 20 mg/kg (P<0.001) groups significantly increased compared with the lesion+saline group. Also, the mean frequencies of CA1 pyramidal neurons in the intact+MEM 10 mg/kg (P<0.001) group significantly decreased compared with the intact+saline group.</p><p><strong>Conclusion: </strong>Results showed that memantine increases the electrical activity of CA1 pyramidal neurons in a rat model of AD. 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Effects of Memantine on the Spontaneous Firing Frequency of Hippocampal CA1 Pyramidal Neurons in Intact and Alzheimer Rat Model: An Electrophysiological Study.
Introduction: Memantine (MEM) is a noncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonist clinically used for the treatment of Alzheimer disease (AD) in mild to severe conditions. The present study was conducted to investigate the effects of memantine on the spontaneous firing frequency of CA1 pyramidal neurons in rats caused by an electrical lesion of Nucleus Basalis Magnocellularis (NBM). Then, this model of AD rats was compared with the intact adult male rats.
Methods: In this study, adult male rats were divided into two groups. Group I (lesion of NBM, n=53) includes the following subgroups: lesion+saline, sham+saline, lesion+MEM 5 mg/kg, lesion+MEM 10 mg/kg, and lesion+MEM 20mg/kg. Group II (intact, n=48) includes the following subgroups: intact+saline, intact+MEM 3mg/kg, intact+MEM 5mg/kg, and intact+MEM 10mg/kg. Extracellular single-unit recording (15 min baseline+105 min after MEM or saline) was performed under urethane-anesthetized rats.
Results: The results showed that the mean frequency of CA1 pyramidal neurons after saline in the lesion+saline (P<0.001) group significantly decreases compared with the intact+saline and sham+saline groups. In addition, after saline and memantine, the mean frequency of CA1 pyramidal neurons in the lesion+MEM 10 mg/kg (P<0.01) and lesion+MEM 20 mg/kg (P<0.001) groups significantly increased compared with the lesion+saline group. Also, the mean frequencies of CA1 pyramidal neurons in the intact+MEM 10 mg/kg (P<0.001) group significantly decreased compared with the intact+saline group.
Conclusion: Results showed that memantine increases the electrical activity of CA1 pyramidal neurons in a rat model of AD. Furthermore, in the intact adult male rats, the low-dose memantine, contrary to high dose, does not decrease the electrical activity of CA1 pyramidal neurons.
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BCN is an international multidisciplinary journal that publishes editorials, original full-length research articles, short communications, reviews, methodological papers, commentaries, perspectives and “news and reports” in the broad fields of developmental, molecular, cellular, system, computational, behavioral, cognitive, and clinical neuroscience. No area in the neural related sciences is excluded from consideration, although priority is given to studies that provide applied insights into the functioning of the nervous system. BCN aims to advance our understanding of organization and function of the nervous system in health and disease, thereby improving the diagnosis and treatment of neural-related disorders. Manuscripts submitted to BCN should describe novel results generated by experiments that were guided by clearly defined aims or hypotheses. BCN aims to provide serious ties in interdisciplinary communication, accessibility to a broad readership inside Iran and the region and also in all other international academic sites, effective peer review process, and independence from all possible non-scientific interests. BCN also tries to empower national, regional and international collaborative networks in the field of neuroscience in Iran, Middle East, Central Asia and North Africa and to be the voice of the Iranian and regional neuroscience community in the world of neuroscientists. In this way, the journal encourages submission of editorials, review papers, commentaries, methodological notes and perspectives that address this scope.
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