scholarly journals Brain-Derived Neurotrophic Factor Is Required for the Neuroprotective Effect of Mifepristone on Immature Purkinje Cells in Cerebellar Slice Culture

2019 ◽  
Vol 20 (2) ◽  
pp. 285 ◽  
Author(s):  
Jennifer Rakotomamonjy ◽  
Abdel Ghoumari
Keyword(s):  
Gabaa Receptors ◽  
Neurotrophic Factor ◽  
Neuroprotective Effect ◽  
Brain Derived Neurotrophic Factor ◽  
Aminobutyric Acid ◽  
Purkinje Neurons ◽  
Slice Culture ◽  
Dependent Activity ◽  
Purkinje Cell Death ◽  
Cerebellar Cultures

Endogenous γ-aminobutyric acid (GABA)-dependent activity induces death of developing Purkinje neurons in mouse organotypic cerebellar cultures and the synthetic steroid mifepristone blocks this effect. Here, using brain-derived neurotrophic factor (BDNF) heterozygous mice, we show that BDNF plays no role in immature Purkinje cell death. However, interestingly, BDNF haploinsufficiency impairs neuronal survival induced by mifepristone and GABAA-receptors antagonist (bicuculline) treatments, indicating that the underlying neuroprotective mechanism requires the neurotrophin full expression.

Possible involvement of induction of brain-derived neurotrophic factor in the neuroprotective effect of a 5-phenylpyrimidine derivative

2003 ◽  
Vol 66 (6) ◽  
pp. 1019-1023 ◽  
Author(s):  
Kayo Matsumoto ◽  
Kyoko Yamamoto ◽  
Yasuko Karasawa ◽  
Noriko Hino ◽  
Atsushi Nakamura ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Neuroprotective Effect ◽  
Brain Derived Neurotrophic Factor

scholarly journals Activated Human T Cells, B Cells, and Monocytes Produce Brain-derived Neurotrophic Factor In Vitro and in Inflammatory Brain Lesions: A Neuroprotective Role of Inflammation?

1999 ◽  
Vol 189 (5) ◽  
pp. 865-870 ◽  
Author(s):  
Martin Kerschensteiner ◽  
Eike Gallmeier ◽  
Lüder Behrens ◽  
Vivian Vargas Leal ◽  
Thomas Misgeld ◽  
...  
Keyword(s):  
T Cells ◽  
Nervous System ◽  
B Cells ◽  
Neurotrophic Factor ◽  
Neuronal Survival ◽  
Neuroprotective Effect ◽  
Brain Derived Neurotrophic Factor ◽  
Human T Cells ◽  
Inflammatory Infiltrates

Brain-derived neurotrophic factor (BDNF) has potent effects on neuronal survival and plasticity during development and after injury. In the nervous system, neurons are considered the major cellular source of BDNF. We demonstrate here that in addition, activated human T cells, B cells, and monocytes secrete bioactive BDNF in vitro. Notably, in T helper (Th)1- and Th2-type CD4+ T cell lines specific for myelin autoantigens such as myelin basic protein or myelin oligodendrocyte glycoprotein, BDNF production is increased upon antigen stimulation. The BDNF secreted by immune cells is bioactive, as it supports neuronal survival in vitro. Using anti-BDNF monoclonal antibody and polyclonal antiserum, BDNF immunoreactivity is demonstrable in inflammatory infiltrates in the brain of patients with acute disseminated encephalitis and multiple sclerosis. The results raise the possibility that in the nervous system, inflammatory infiltrates have a neuroprotective effect, which may limit the success of nonselective immunotherapies.

Modulatory effect of simvastatin on redox status, caspase-3 expression, p-protein kinase B (p-Akt) and brain derived neurotrophic factor (BDNF) in ethanol-induced neurodegeneration

2020 ◽  
Author(s):  
nahla anas nasef ◽  
Walaa Arafa Keshk ◽  
salwa elmelegy ◽  
ahmed abdallah ◽  
wafaa ibrahim
Keyword(s):  
Protein Kinase ◽  
Neurotrophic Factor ◽  
Caspase 3 ◽  
Protein Kinase B ◽  
Neuroprotective Effect ◽  
Brain Derived Neurotrophic Factor ◽  
Ethanol Solution ◽  
Biochemical Changes ◽  
Lipid Lowering ◽  
P Protein

Neurodegenerative diseases are a common cause of morbidity and mortality worldwide with oxidative stress, inflammation and protein aggregation represent the main underlying mechanisms that ultimately lead to cell death. Ethanol has shown strong neurodegenerative consequences in experimental animal brains. Statins are a class of lipid-lowering drugs with many pleotropic effects. Therefore, the aim of the present study was to explore the modulatory effect of simvastatin (10 mg/kg/day) before and after the development of neurodegeneration (for 55 and 25 days, respectively) on redox state, caspase-3 expression, p-protein kinase B (p-Akt) and brain derived neurotrophic factor (BDNF) in ethanol (15% ethanol solution for 55 day) induced neurodegeneration. Seventy female Albino Swiss mice were included and randomly divided into 5 groups: control (c) group; ethanol (E) group; (ES) group treated with simvastatin from the first day of ethanol intake; (E+S) group treated with simvastatin after neurodegeneration development; and simvastatin (S) group. Administration of simvastatin from the first day improved the biochemical changes, suppressed apoptosis, induced autophagy and neurogenesis. However, its administration after the development of neurodegeneration resulted in partial improvement. The histopathological findings confirmed the biochemical changes. In conclusion; simvastatin has a neuroprotective effect against the development of ethanol-induced neurodegeneration and its progression.

scholarly journals The Neuroprotective Mechanism of Low-Frequency rTMS on Nigral Dopaminergic Neurons of Parkinson’s Disease Model Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Qiaoyun Dong ◽  
Yanyong Wang ◽  
Ping Gu ◽  
Rusheng Shao ◽  
Li Zhao ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Line ◽  
Glial Cell ◽  
Neurotrophic Factor ◽  
Dopaminergic Neuron ◽  
Neuroprotective Effect ◽  
Low Frequency ◽  
Brain Derived Neurotrophic Factor ◽  
Low Frequency Rtms

Background. Parkinson’s disease is a neurodegenerative disease in elder people, pathophysiologic basis of which is the severe deficiency of dopamine in the striatum. The purpose of the present study was to evaluate the neuroprotective effect of low-frequency rTMS on Parkinson’s disease in model mice.Methods. The effects of low-frequency rTMS on the motor function, cortex excitability, neurochemistry, and neurohistopathology of MPTP-induced Parkinson’s disease mice were investigated through behavioral detection, electrophysiologic technique, high performance liquid chromatography-electrochemical detection, immunohistochemical staining, and western blot.Results. Low-frequency rTMS could improve the motor coordination impairment of Parkinson’s disease mice: the resting motor threshold significantly decreased in the Parkinson’s disease mice; the degeneration of nigral dopaminergic neuron and the expression of tyrosine hydroxylase were significantly improved by low-frequency rTMS; moreover, the expressions of brain derived neurotrophic factor and glial cell line derived neurotrophic factor were also improved by low-frequency rTMS.Conclusions. Low-frequency rTMS had a neuroprotective effect on the nigral dopaminergic neuron which might be due to the improved expressions of brain derived neurotrophic factor and glial cell line-derived neurotrophic factor. The present study provided a theoretical basis for the application of low-frequency rTMS in the clinical treatment and recovery of Parkinson’s disease.

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