共查询到20条相似文献,搜索用时 15 毫秒
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Changiz Geula Sara R. Dunlop Ivan Ayala Allegra S. Kawles Margaret E. Flanagan Tamar Gefen Marek-Marsel Mesulam 《Journal of neurochemistry》2021,158(6):1394-1411
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Takahiro Fujii Yuta Tanaka Hideyuki Oki Sho Sato Sachio Shibata Takamitsu Maru Yuta Tanaka Maiko Tanaka Tomohiro Onishi 《Journal of neurochemistry》2021,159(3):543-553
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Yixin Yang Jinsong Zhao Yunze Li Xiangyao Li Xiaowei Chen Zhiying Feng 《Journal of neurochemistry》2021,159(3):512-524
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R. J. Scott Lacombe Mackenzie E. Smith Kelly Perlman Gustavo Turecki Naguib Mechawar Richard P. Bazinet 《Journal of neurochemistry》2023,164(1):44-56
Our knowledge surrounding the overall fatty acid profile of the adult human brain has been largely limited to extrapolations from brain regions in which the distribution of fatty acids varies. This is especially problematic when modeling brain fatty acid metabolism, therefore, an updated estimate of whole-brain fatty acid concentration is necessitated. Here, we sought to conduct a comprehensive quantitative analysis of fatty acids from entire well-characterized human brain hemispheres (n = 6) provided by the Douglas-Bell Canada Brain Bank. Additionally, exploratory natural abundance carbon isotope ratio (CIR; δ13C, 13C/12C) analysis was performed to assess the origin of brain fatty acids. Brain fatty acid methyl esters (FAMEs) were quantified by gas chromatography (GC)-flame ionization detection and minor n-6 and n-3 polyunsaturated fatty acid pentafluorobenzyl esters by GC-mass spectrometry. Carbon isotope ratio values of identifiable FAMEs were measured by GC-combustion-isotope ratio mass spectrometry. Overall, the most abundant fatty acid in the human brain was oleic acid, followed by stearic acid (STA), palmitic acid (PAM), docosahexaenoic acid (DHA), and arachidonic acid (ARA). Interestingly, cholesterol as well as saturates including PAM and STA were most enriched in 13C, while PUFAs including DHA and ARA were most depleted in 13C. These findings suggest a contribution of endogenous synthesis utilizing dietary sugar substrates rich in 13C, and a combination of marine, animal, and terrestrial PUFA sources more depleted in 13C, respectively. These results provide novel insights on cerebral fatty acid origin and concentration, the latter serving as a valuable resource for future modeling of fatty acid metabolism in the human brain.
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Georgios Kogias Fang Zheng Liubov S. Kalinichenko Johannes Kornhuber Christian Alzheimer Dirk Mielenz Christian P. Müller 《Journal of neurochemistry》2020,154(4):424-440
Psychostimulants are widely abused drugs that may cause addiction in vulnerable individuals. While the reward circuitry of the brain is involved in addiction establishment, various pathways in the brain may provide protection at the molecular level that limits the acute and chronic effects of drugs. These targets may be used for strategies designed to prevent and treat addiction. Swiprosin-1/EF hand domain 2 (EFhd2) is a Ca2+-binding cytoskeletal adaptor protein involved in sensation-seeking behaviour, anxiety and alcohol addiction. Here, we tested how EFhd2 contributes to the physiological and behavioural effects of the psychostimulant drugs methamphetamine (METH) and cocaine. An in vivo microdialysis study in EFhd2 knockout mice revealed that EFhd2 controls METH- and cocaine-induced changes in extracellular dopamine, serotonin and noradrenaline levels through different mechanisms in the nucleus accumbens and prefrontal cortex. Electrophysiological recordings in a slice preparation showed that a lack of EFhd2 increases dopaminergic neuronal activity in the ventral tegmental area and increases the sensitivity of neurons to stimulation. We report a role of EFhd2 in METH-induced locomotor activation and in the conditioned locomotor effects. No role, however, was observed in the establishment of METH- or cocaine-induced conditioned place preference. These findings may suggest that EFhd2 modulates the activity of the dopaminergic system and the neurochemical effects of METH and cocaine, which translate into a modulation of the behavioural effects of these drugs at the level of the acute and conditioned locomotor activity.
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Robert P. Yasuda 《Journal of neurochemistry》2020,152(3):270-272
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Ruth E. Rosenstein 《Journal of neurochemistry》2020,153(6):671-673
The aim of the present report was to analyze the involvement of glutamate neurotoxicity in retinal ganglion cell loss and optic nerve damage induced by experimental optic neuritis. For this purpose, the authors used an optic neuritis model induced by immunisation with myelin oligodendrocyte glycoprotein (AON). The authors describe a correlation in the timing of retinal ganglion cell (RGC) loss with alterations in the optic nerve actin cytoskeleton dynamic, and visual dysfunction. In addition, they show that an intravitreal injection of glutamate mimics, and an NMDA receptor antagonist avoids the effect of pre-clinical AON on visual functions and RGC number, as well as on optic nerve actin cytoskeleton. Taken together, their results support that avoiding glutamate neurotoxicity could become a new therapeutic approach for optic neuritis treatment.
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Mariana Angoa‐Pérez Michael J. Kane Denise I. Briggs Nieves Herrera‐Mundo David C. Viano Donald M. Kuhn 《Journal of neurochemistry》2014,129(6):916-931
Sports‐related head impact and injury has become a very highly contentious public health and medico‐legal issue. Near‐daily news accounts describe the travails of concussed athletes as they struggle with depression, sleep disorders, mood swings, and cognitive problems. Some of these individuals have developed chronic traumatic encephalopathy, a progressive and debilitating neurodegenerative disorder. Animal models have always been an integral part of the study of traumatic brain injury in humans but, historically, they have concentrated on acute, severe brain injuries. This review will describe a small number of new and emerging animal models of sports‐related head injury that have the potential to increase our understanding of how multiple mild head impacts, starting in adolescence, can have serious psychiatric, cognitive and histopathological outcomes much later in life.
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Validated multi‐step approach for in vivo recording and analysis of optogenetically evoked glutamate in the mouse globus pallidus 下载免费PDF全文
Thomas Viereckel Åsa Konradsson‐Geuken Åsa Wallén‐Mackenzie 《Journal of neurochemistry》2018,145(2):125-138
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The role of S‐nitrosylation of kainate‐type of ionotropic glutamate receptor 2 in epilepsy induced by kainic acid 下载免费PDF全文
Linxiao Wang Yanyan Liu Rulan Lu Guoying Dong Xia Chen Wenwei Yun Xianju Zhou 《Journal of neurochemistry》2018,144(3):255-270
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Junpei Matsubayashi Yuki Kawaguchi Yutaka Kawakami Kohtaro Takei 《Journal of neurochemistry》2023,164(1):29-43
Neurons in the central nervous system (CNS) have limited capacity for axonal regeneration after trauma and neurological disorders due to an endogenous nonpermissive environment for axon regrowth in the CNS. Lateral olfactory tract usher substance (LOTUS) contributes to axonal tract formation in the developing brain and axonal regeneration in the adult brain as an endogenous Nogo receptor-1 (NgR1) antagonist. However, how LOTUS expression is regulated remains unclarified. This study examined molecular mechanism of regulation in LOTUS expression and found that brain-derived neurotrophic factor (BDNF) increased LOTUS expression in cultured hippocampal neurons. Exogenous application of BDNF increased LOTUS expression at both mRNA and protein levels in a dose-dependent manner. We also found that pharmacological inhibition with K252a and gene knockdown by siRNA of tropomyosin-related kinase B (TrkB), BDNF receptor suppressed BDNF-induced increase in LOTUS expression. Further pharmacological analysis of the TrkB signaling pathway revealed that BDNF increased LOTUS expression through mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) cascades, but not phospholipase C-γ (PLCγ) cascade. Additionally, treatment with c-AMP response element binding protein (CREB) inhibitor partially suppressed BDNF-induced LOTUS expression. Finally, neurite outgrowth assay in cultured hippocampal neurons revealed that BDNF treatment-induced antagonism for NgR1 by up-regulating LOTUS expression. These findings suggest that BDNF may acts as a positive regulator of LOTUS expression through the TrkB signaling, thereby inducing an antagonistic action for NgR1 function by up-regulating LOTUS expression. Also, BDNF may synergistically affect axon regrowth through the upregulation of LOTUS expression.
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Microglia modulation through external vagus nerve stimulation in a murine model of Alzheimer's disease 下载免费PDF全文
Robert Kaczmarczyk Dario Tejera Bruce J. Simon Michael T. Heneka 《Journal of neurochemistry》2018,146(1):76-85
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Ruiqian Wan Letitia A. Weigand Ryan Bateman Kathleen Griffioen David Mendelowitz Mark P. Mattson 《Journal of neurochemistry》2014,129(4):573-580
Autonomic control of heart rate is mediated by cardioinhibitory parasympathetic cholinergic neurons located in the brainstem and stimulatory sympathetic noradrenergic neurons. During embryonic development the survival and cholinergic phenotype of brainstem autonomic neurons is promoted by brain‐derived neurotrophic factor (BDNF). We now provide evidence that BDNF regulates heart rate by a mechanism involving increased brainstem cardioinhibitory parasympathetic activity. Mice with a BDNF haploinsufficiency exhibit elevated resting heart rate, and infusion of BDNF intracerebroventricularly reduces heart rate in both wild‐type and BDNF+/? mice. The atropine‐induced elevation of heart rate is diminished in BDNF+/? mice and is restored by BDNF infusion, whereas the atenolol‐induced decrease in heart rate is unaffected by BDNF levels, suggesting that BDNF signaling enhances parasympathetic tone which is diminished with BDNF haploinsufficiency. Whole‐cell recordings from pre‐motor cholinergic cardioinhibitory vagal neurons in the nucleus ambiguus indicate that BDNF haploinsufficiency reduces cardioinhibitory vagal neuron activity by increased inhibitory GABAergic and diminished excitatory glutamatergic neurotransmission to these neurons. Our findings reveal a previously unknown role for BDNF in the control of heart rate by a mechanism involving increased activation of brainstem cholinergic parasympathetic neurons
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This editorial highlights a study by Rodriguez, Sanchez‐Moran et al. (2019) in the current issue of the Journal of Neurochemistry, in which the authors describe a microcephalic boy carrying the novel heterozygous de novo missense mutation c.560A> G; p.Asp187Gly in Cdh1/Fzr1 encoding the APC/C E3‐ubiquitin ligase cofactor CDH1. A functional characterization of mutant APC/CCDH1 confirms an aberrant division of neural progenitor cells, a condition known to determine the mouse brain cortex size. These data suggest that APC/CCDH1 may contribute to the regulation of the human brain size.
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Sulfatide isoform pattern in cerebrospinal fluid discriminates progressive MS from relapsing‐remitting MS 下载免费PDF全文
Lenka Novakova Avadhesh Kumar Singh Markus Axelsson Marcus Ståhlman Martin Adiels Clas Malmeström Henrik Zetterberg Jan Borén Jan Lycke Susanna L. Cardell Maria Blomqvist 《Journal of neurochemistry》2018,146(3):322-332
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Hexokinase 2‐dependent hyperglycolysis driving microglial activation contributes to ischemic brain injury 下载免费PDF全文
Yuan Li Bingzheng Lu Longxiang Sheng Zhu Zhu Hongjiaqi Sun Yuwei Zhou Yang Yang Dongdong Xue Wenli Chen Xuyan Tian Yun Du Min Yan Wenbo Zhu Fan Xing Kai Li Suizhen Lin Pengxin Qiu Xingwen Su Yijun Huang Guangmei Yan Wei Yin 《Journal of neurochemistry》2018,144(2):186-200
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