共查询到20条相似文献,搜索用时 15 毫秒
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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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Robert P. Yasuda 《Journal of neurochemistry》2020,152(3):270-272
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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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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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S‐allyl cysteine activates the Nrf2‐dependent antioxidant response and protects neurons against ischemic injury in vitro and in vivo 下载免费PDF全文
Huanying Shi Xu Jing Xinbing Wei Ruth G. Perez Manru Ren Xiumei Zhang Haiyan Lou 《Journal of neurochemistry》2015,133(2):298-308
Stroke is a devastating clinical condition for which an effective neuroprotective treatment is currently unavailable. S‐allyl cysteine (SAC), the most abundant organosulfur compound in aged garlic extract, has been reported to possess neuroprotective effects against stroke. However, the mechanisms underlying its beneficial effects remain poorly defined. The present study tests the hypothesis that SAC attenuates ischemic neuronal injury by activating the nuclear factor erythroid‐2‐related factor 2 (Nrf2)‐dependent antioxidant response in both in vitro and in vivo models. Our findings demonstrate that SAC treatment resulted in an increase in Nrf2 protein levels and subsequent activation of antioxidant response element pathway genes in primary cultured neurons and mice. Exposure of primary neurons to SAC provided protection against oxygen and glucose deprivation‐induced oxidative insults. In wild‐type (Nrf2+/+) mice, systemic administration of SAC attenuated middle cerebral artery occlusion‐induced ischemic damage, a protective effect not observed in Nrf2 knockout (Nrf2?/?) mice. Taken together, these findings provide the first evidence that activation of the Nrf2 antioxidant response by SAC is strongly associated with its neuroprotective effects against experimental stroke and suggest that targeting the Nrf2 pathway may provide therapeutic benefit for the treatment of stroke.
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Lack of TNF‐alpha receptor type 2 protects motor neurons in a cellular model of amyotrophic lateral sclerosis and in mutant SOD1 mice but does not affect disease progression 下载免费PDF全文
Massimo Tortarolo Antonio Vallarola Dario Lidonnici Elisa Battaglia Gabriella Spaltro Fabio Fiordaliso Alessandro Corbelli Stefano Garetto Elisa Martini Laura Pasetto Marinos Kallikourdis Valentina Bonetto Caterina Bendotti 《Journal of neurochemistry》2015,135(1):109-124
Changes in the homeostasis of tumor necrosis factor α (TNFα) have been demonstrated in patients and experimental models of amyotrophic lateral sclerosis (ALS). However, the contribution of TNFα to the development of ALS is still debated. TNFα is expressed by glia and neurons and acts through the membrane receptors TNFR1 and TNFR2, which may have opposite effects in neurodegeneration. We investigated the role of TNFα and its receptors in the selective motor neuron death in ALS in vitro and in vivo. TNFR2 expressed by astrocytes and neurons, but not TNFR1, was implicated in motor neuron loss in primary SOD1‐G93A co‐cultures. Deleting TNFR2 from SOD1‐G93A mice, there was partial but significant protection of spinal motor neurons, sciatic nerves, and tibialis muscles. However, no improvement of motor impairment or survival was observed. Since the sciatic nerves of SOD1‐G93A/TNFR2?/? mice showed high phospho‐TAR DNA‐binding protein 43 (TDP‐43) accumulation and low levels of acetyl‐tubulin, two indices of axonal dysfunction, the lack of symptom improvement in these mice might be due to impaired function of rescued motor neurons. These results indicate the interaction between TNFR2 and membrane‐bound TNFα as an innovative pathway involved in motor neuron death. Nevertheless, its inhibition is not sufficient to stop disease progression in ALS mice, underlining the complexity of this pathology.
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Alterations in mGlu5 receptor expression and function in the striatum in a rat depression model 下载免费PDF全文
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Liraglutide ameliorated peripheral neuropathy in diabetic rats: Involvement of oxidative stress,inflammation and extracellular matrix remodeling 下载免费PDF全文
Passant E. Moustafa Noha F. Abdelkader Sally A. El Awdan Osama A. El‐Shabrawy Hala F. Zaki 《Journal of neurochemistry》2018,146(2):173-185
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Fisetin provides antidepressant effects by activating the tropomyosin receptor kinase B signal pathway in mice 下载免费PDF全文
Yamin Wang Bin Wang Jiaqi Lu Haixia Shi Siyi Gong Yufan Wang Ronald C. Hamdy Balvin H. L. Chua Lingli Yang Xingshun Xu 《Journal of neurochemistry》2017,143(5):561-568
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M. Stazi A. Megighian G. D'Este S. Negro A. Ivanušec D. Lonati M. Pirazzini I. Križaj C. Montecucco 《Journal of neurochemistry》2024,168(4):428-440
People bitten by Alpine vipers are usually treated with antivenom antisera to prevent the noxious consequences caused by the injected venom. However, this treatment suffers from a number of drawbacks and additional therapies are necessary. The venoms of Vipera ammodytes and of Vipera aspis are neurotoxic and cause muscle paralysis by inducing neurodegeneration of motor axon terminals because they contain a presynaptic acting sPLA2 neurotoxin. We have recently found that any type of damage to motor axons is followed by the expression and activation of the intercellular signaling axis consisting of the CXCR4 receptor present on the membrane of the axon stump and of its ligand, the chemokine CXCL12 released by activated terminal Schwann cells. We show here that also V. ammodytes and V. aspis venoms cause the expression of the CXCL12-CXCR4 axis. We also show that a small molecule agonist of CXCR4, dubbed NUCC-390, induces a rapid regeneration of the motor axon terminal with functional recovery of the neuromuscular junction. These findings qualify NUCC-390 as a promising novel therapeutics capable of improving the recovery from the paralysis caused by the snakebite of the two neurotoxic Alpine vipers.
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Identification and quantification of blood–brain barrier transporters in isolated rat brain microvessels 下载免费PDF全文
Hajar Al Feteisi Zubida M. Al‐Majdoub Brahim Achour Narciso Couto Amin Rostami‐Hodjegan Jill Barber 《Journal of neurochemistry》2018,146(6):670-685
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Clenbuterol reduces GABAergic transmission in prefrontal cortex layer 5/6 pyramidal neurons of juvenile rat via reducing action potentials firing frequency of GABAergic interneurons 下载免费PDF全文
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Reduced blood‐brain barrier expression of fatty acid‐binding protein 5 is associated with increased vulnerability of APP/PS1 mice to cognitive deficits from low omega‐3 fatty acid diets 下载免费PDF全文
Yijun Pan Kwok H. C. Choy Philip J. Marriott Siew Y. Chai Martin J. Scanlon Christopher J. H. Porter Jennifer L. Short Joseph A. Nicolazzo 《Journal of neurochemistry》2018,144(1):81-92
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Astrocytes with previous chronic exposure to amyloid β‐peptide fragment 1–40 suppress excitatory synaptic transmission 下载免费PDF全文
Hiroyuki Kawano Kohei Oyabu Hideaki Yamamoto Kei Eto Yuna Adaniya Kaori Kubota Takuya Watanabe Ayumi Hirano‐Iwata Junichi Nabekura Shutaro Katsurabayashi Katsunori Iwasaki 《Journal of neurochemistry》2017,143(6):624-634
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Dao‐Zhong Jin Ming‐Lei Guo Bing Xue Li‐Min Mao John Q. Wang 《Journal of neurochemistry》2013,127(5):620-631
Two glutamate receptors, metabotropic glutamate receptor 5 (mGluR5), and ionotropic NMDA receptors (NMDAR), functionally interact with each other to regulate excitatory synaptic transmission in the mammalian brain. In exploring molecular mechanisms underlying their interactions, we found that Ca2+/calmodulin‐dependent protein kinase IIα (CaMKIIα) may play a central role. The synapse‐enriched CaMKIIα directly binds to the proximal region of intracellular C terminal tails of mGluR5 in vitro. This binding is state‐dependent: inactive CaMKIIα binds to mGluR5 at a high level whereas the active form of the kinase (following Ca2+/calmodulin binding and activation) loses its affinity for the receptor. Ca2+ also promotes calmodulin to bind to mGluR5 at a region overlapping with the CaMKIIα‐binding site, resulting in a competitive inhibition of CaMKIIα binding to mGluR5. In rat striatal neurons, inactive CaMKIIα constitutively binds to mGluR5. Activation of mGluR5 Ca2+‐dependently dissociates CaMKIIα from the receptor and simultaneously promotes CaMKIIα to bind to the adjacent NMDAR GluN2B subunit, which enables CaMKIIα to phosphorylate GluN2B at a CaMKIIα‐sensitive site. Together, the long intracellular C‐terminal tail of mGluR5 seems to serve as a scaffolding domain to recruit and store CaMKIIα within synapses. The mGluR5‐dependent Ca2+ transients differentially regulate CaMKIIα interactions with mGluR5 and GluN2B in striatal neurons, which may contribute to cross‐talk between the two receptors.
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Marta Vicente‐Rodríguez Carmen Pérez‐García Marcel Ferrer‐Alcón María Uribarri María G. Sánchez‐Alonso María P. Ramos Gonzalo Herradón 《Journal of neurochemistry》2014,131(5):688-695
Pleiotrophin (PTN) is a cytokine with important roles in dopaminergic neurons. We found that an acute ethanol (2.0 g/kg, i.p.) administration causes a significant up‐regulation of PTN mRNA and protein levels in the mouse prefrontal cortex, suggesting that endogenous PTN could modulate behavioural responses to ethanol. To test this hypothesis, we studied the behavioural effects of ethanol in PTN knockout (PTN?/?) mice and in mice with cortex‐ and hippocampus‐specific transgenic PTN over‐expression (PTN‐Tg). Ethanol (1.0 and 2.0 g/kg) induced an enhanced conditioned place preference in PTN?/? compared to wild type mice, suggesting that PTN prevents ethanol rewarding effects. Accordingly, the conditioning effects of ethanol were completely abolished in PTN‐Tg mice. The ataxic effects induced by ethanol (2.0 g/kg) were not affected by the genotype. However, the sedative effects of ethanol (3.6 g/kg) tested in a loss of righting reflex paradigm were significantly reduced in PTN‐Tg mice, suggesting that up‐regulation of PTN levels prevents the sedative effects of ethanol. These results indicate that PTN may be a novel genetic factor of importance in alcohol use disorders, and that potentiation of the PTN signalling pathway may be a promising therapeutic strategy in the treatment of these disorders.