共查询到20条相似文献,搜索用时 15 毫秒
1.
Barbara Trattner Sarah Berner Benedikt Grothe Lars Kunz 《Journal of neurochemistry》2013,127(1):78-90
The neuronal endocannabinoid system is known to depress synaptic inputs retrogradely in an activity‐dependent manner. This mechanism has been generally described for excitatory glutamatergic and inhibitory GABAergic synapses. Here, we report that neurones in the auditory brainstem of the Mongolian gerbil (Meriones unguiculatus) retrogradely regulate the strength of their inputs via the endocannabinoid system. By means of whole‐cell patch‐clamp recordings, we found that retrograde endocannabinoid signalling attenuates both glycinergic and glutamatergic post‐synaptic currents in the same types of neurones. Accordingly, we detected the cannabinoid receptor 1 in excitatory and inhibitory pre‐synapses as well as the endocannabinoid‐synthesising enzymes (diacylglycerol lipase α/β, DAGLα/β) post‐synaptically through immunohistochemical stainings. Our study was performed with animals aged 10–15 days, that is, in the time window around the onset of hearing. Therefore, we suggest that retrograde endocannabinoid signalling has a role in adapting inputs during the functionally important switch from spontaneously generated to sound‐related signals.
2.
Epigenetic control of early neurodegenerative events in diabetic retinopathy by the histone deacetylase SIRT6 下载免费PDF全文
Ada Yeste Francisco J. Quintana Debra Toiber Raul Mostoslavsky Dafne M. Silberman 《Journal of neurochemistry》2018,144(2):128-138
3.
Dorit Trudler Orly Weinreb Silvia A. Mandel Moussa B. H. Youdim Dan Frenkel 《Journal of neurochemistry》2014,129(3):434-447
DJ‐1 is an oxidative stress sensor that localizes to the mitochondria when the cell is exposed to oxidative stress. DJ‐1 mutations that result in gene deficiency are linked to increased risk of Parkinson's disease (PD). Activation of microglial stress conditions that are linked to PD may result in neuronal death. We postulated that DJ‐1 deficiency may increase microglial neurotoxicity. We found that down‐regulation of DJ‐1 in microglia using an shRNA approach increased cell sensitivity to dopamine as measured by secreted pro‐inflammatory cytokines such as IL‐1β and IL‐6. Furthermore, we discovered that DJ‐1‐deficient microglia had increased monoamine oxidase activity that resulted in elevation of intracellular reactive oxygen species and nitric oxide leading to increased dopaminergic neurotoxicity. Rasagaline, a monoamine oxidase inhibitor approved for treatment of PD, reduced the microglial pro‐inflammatory phenotype and significantly reduced neurotoxicity. Moreover, we discovered that DJ‐1‐deficient microglia have reduced expression of triggering receptor expressed on myeloid cells 2 (TREM2), previously suggested as a risk factor for pro‐inflammation in neurodegenerative diseases. Further studies of DJ‐1‐mediated cellular pathways in microglia may contribute useful insights into the development of PD providing future avenues for therapeutic intervention.
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Yuval Nash Eran Schmukler Dorit Trudler Ronit Pinkas‐Kramarski Dan Frenkel 《Journal of neurochemistry》2017,143(5):584-594
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p75 neurotrophin receptor interacts with and promotes BACE1 localization in endosomes aggravating amyloidogenesis 下载免费PDF全文
Khalil Saadipour Noralyn B. Mañucat‐Tan Yoon Lim Damien J. Keating Kevin S. Smith Jin‐hua Zhong Hong Liao Larisa Bobrovskaya Yan‐Jiang Wang Moses V. Chao Xin‐Fu Zhou 《Journal of neurochemistry》2018,144(3):302-317
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Adropin preserves the blood‐brain barrier through a Notch1/Hes1 pathway after intracerebral hemorrhage in mice 下载免费PDF全文
Lingyan Yu Zhengyang Lu Sherrefa Burchell Derek Nowrangi Anatol Manaenko Xue Li Yang Xu Ningbo Xu Jiping Tang Haibin Dai John H. Zhang 《Journal of neurochemistry》2017,143(6):750-760
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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
9.
Different effects of bisphenol‐A on memory behavior and synaptic modification in intact and estrogen‐deprived female mice 下载免费PDF全文
Bisphenol‐A (BPA) has the capability of interfering with the effects of estrogens on modulating brain function. The purpose of this study was to investigate the effects of BPA on memory and synaptic modification in the hippocampus of female mice under different levels of cycling estrogen. BPA exposure (40, 400 μg/kg/day) for 8 weeks did not affect spatial memory and passive avoidance task of gonadally intact mice but improved ovariectomy (Ovx)‐induced memory impairment, whereas co‐exposure of BPA with estradiol benzoate (EB) diminished the rescue effect of EB on memory behavior of Ovx mice. The results of morphometric measurement showed that BPA positively modified the synaptic interface structure and increased the synaptic density of CA1 pyramidal cell in the hippocampus of Ovx females, but inhibited the enhancement of EB on synaptic modification and synaptogenesis of Ovx mice. Furthermore, BPA up‐regulated synaptic proteins synapsin I and PSD‐95 and NMDA receptor NR2B but inhibited EB‐induced increase in PSD‐95 and NR2B in the hippocampus of Ovx mice. These results suggest that BPA interfered with normal hormonal regulation in synaptic plasticity and memory of female mice as a potent estrogen mimetic and as a disruptor of estrogen under various concentrations of cycling estrogen.
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Protein components of post‐synaptic density lattice,a backbone structure for type I excitatory synapses 下载免费PDF全文
Tatsuo Suzuki Kiyokazu Kametani Weiheng Guo Weidong Li 《Journal of neurochemistry》2018,144(4):390-407
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Alaa Elkordy Eikan Mishima Kuniyasu Niizuma Yasutoshi Akiyama Miki Fujimura Teiji Tominaga Takaaki Abe 《Journal of neurochemistry》2018,146(5):560-569
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Protein misfolding cyclic amplification induces the conversion of recombinant prion protein to PrP oligomers causing neuronal apoptosis 下载免费PDF全文
Zhen Yuan Lifeng Yang Baian Chen Ting Zhu Mohammad Farooque Hassan Xiaomin Yin Xiangmei Zhou Deming Zhao 《Journal of neurochemistry》2015,133(5):722-729
The formation of neurotoxic prion protein (PrP) oligomers is thought to be a key step in the development of prion diseases. Recently, it was determined that the sonication and shaking of recombinant PrP can convert PrP monomers into β‐state oligomers. Herein, we demonstrate that β‐state oligomeric PrP can be generated through protein misfolding cyclic amplification from recombinant full‐length hamster, human, rabbit, and mutated rabbit PrP, and that these oligomers can be used for subsequent research into the mechanisms of PrP‐induced neurotoxicity. We have characterized protein misfolding cyclic amplification‐induced monomer‐to‐oligomer conversion of PrP from three species using western blotting, circular dichroism, size‐exclusion chromatography, and resistance to proteinase K (PK) digestion. We have further shown that all of the resulting β‐oligomers are toxic to primary mouse cortical neurons independent of the presence of PrPC in the neurons, whereas the corresponding monomeric PrP were not toxic. In addition, we found that this toxicity is the result of oligomer‐induced apoptosis via regulation of Bcl‐2, Bax, and caspase‐3 in both wild‐type and PrP?/? cortical neurons. It is our hope that these results may contribute to our understanding of prion transformation within the brain.
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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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Calmodulin‐like skin protein protects against spatial learning impairment in a mouse model of Alzheimer disease 下载免费PDF全文
Shinya Kusakari Mikiro Nawa Katsuko Sudo Masaaki Matsuoka 《Journal of neurochemistry》2018,144(2):218-233
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Kinning Poon Hui T. Ho Jessica R. Barson Sarah F. Leibowitz 《Journal of neurochemistry》2014,131(4):509-520
Neuroinflammation is a feedback mechanism against infection, with recent studies suggesting a neuromodulatory role. The chemokine, (C‐C motif) ligand 2 (CCL2), and its receptor, (C‐C motif) receptor type 2 (CCR2), affect neuromodulation and migration in response to damage. Although CCL2 co‐localizes with neuropeptides in the hypothalamus that control voluntary behavior, the function of CCL2/CCR2 is unknown. This led us to consider the possibility that CCL2 acting through CCR2, under natural conditions, may affect the migration and peptide levels of hypothalamic neurons that control voluntary behavior. This study used primary embryonic hypothalamic neurons to examine the effect of CCL2 on migratory behavior and on levels of the peptides, enkephalin (ENK) and galanin. Treatment with CCL2 led to a significant, dose‐dependent increase in the number of migrated neurons and an increase in the velocity and distance traveled. CCL2 also significantly increased the number of ENK‐expressing and CCR2/ENK co‐expressing neurons and the percentage of neurons that contain higher levels of ENK. Lastly, CCL2 produced a dose‐dependent increase in expression of ENK and galanin. These results provide evidence for a stimulatory effect of CCL2 on embryonic hypothalamic neurons involving changes in migratory behavior, expression, and synthesis of neuropeptides that function in controlling behavior.
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Hannah Scheiblich Anna Schlütter Douglas T. Golenbock Eicke Latz Pilar Martinez‐Martinez Michael T. Heneka 《Journal of neurochemistry》2017,143(5):534-550
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Liping Xu Chandrashekhar Voshavar Yevgeniya Shurubor Flint Beal Aloke K. Dutta 《Journal of neurochemistry》2014,131(1):74-85
In this study, in vitro and in vivo experiments were carried out with the high‐affinity multifunctional D2/D3 agonist D‐512 to explore its potential neuroprotective effects in models of Parkinson's disease and the potential mechanism(s) underlying such properties. Pre‐treatment with D‐512 in vitro was found to rescue rat adrenal Pheochromocytoma PC12 cells from toxicity induced by 6‐hydroxydopamine administration in a dose‐dependent manner. Neuroprotection was found to coincide with reductions in intracellular reactive oxygen species, lipid peroxidation, and DNA damage. In vivo, pre‐treatment with 0.5 mg/kg D‐512 was protective against neurodegenerative phenotypes associated with systemic administration of MPTP, including losses in striatal dopamine, reductions in numbers of DAergic neurons in the substantia nigra (SN), and locomotor dysfunction. These observations strongly suggest that the multifunctional drug D‐512 may constitute a novel viable therapy for Parkinson's disease.
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Oriol Busquets uria Eritja Blanca M. Lpez Miren Ettcheto Patricia R. Manzine Rubn D. Castro‐Torres Ester Verdaguer Jordi Olloquequi Manuel Vzquez‐Carrera Carme Auladell Jaume Folch Antoni Camins 《Journal of neurochemistry》2019,149(2):255-268
Insulin resistance has negative consequences on the physiological functioning of the nervous system. The appearance of type 3 diabetes in the brain leads to the development of the sporadic form of Alzheimer's disease. The c‐Jun N‐terminal kinases (JNK), a subfamily of the Mitogen Activated Protein Kinases, are enzymes composed by three different isoforms with differential modulatory activity against the insulin receptor (IR) and its substrate. This research focused on understanding the regulatory role of JNK2 on the IR, as well as study the effect of a high‐fat diet (HFD) in the brain. Our observations determined how JNK2 ablation did not induce compensatory responses in the expression of the other isoforms but led to an increase in JNKs total activity. HFD‐fed animals also showed an increased activity profile of the JNKs. These animals also displayed endoplasmic reticulum stress and up‐regulation of the protein tyrosine phosphatase 1B (PTP1B) and the suppressor of cytokine signalling 3 protein. Consequently, a reduction in insulin sensitivity was detected and it is correlated with a decrease on the signalling of the IR. Moreover, cognitive impairment was observed in all groups but only wild‐type genotype animals fed with HFD showed neuroinflammatory responses. In conclusion, HFD and JNK2 absence cause alterations in normal cognitive activity by altering the signalling of the IR. These affectations are related to the appearance of endoplasmic reticulum stress and an increase in the levels of inhibitory proteins like PTP1B and suppressor of cytokine signalling 3 protein.
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Veronica Murta Priscila Schilrreff Gerardo Rosciszewski Maria Jose Morilla Alberto Javier Ramos 《Journal of neurochemistry》2018,144(6):748-760