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https://www.readbyqxmd.com/read/29351171/spinal-pkc-erk-signal-pathway-mediates-hyperalgesia-priming
#1
Wei-Hsin Chen, Ya-Ting Chang, Yong-Cyuan Chen, Sin-Jhong Cheng, Chien-Chang Chen
Chronic pain can be initiated by one or more acute stimulations to sensitize neurons into the primed state. In the primed state, the basal nociceptive thresholds of the animal are normal, but in response to another hyperalgesic stimulus, the animal develops enhanced and prolonged hyperalgesia. The exact mechanism of how primed state is formed is not completely understood. Here we showed that spinal PKC/ERK signal pathway is required for neuronal plasticity change, hyperalgesic priming formation and the development of chronic hyperalgesia using acid-induced muscle pain (AIMP) model in mice...
January 18, 2018: Pain
https://www.readbyqxmd.com/read/29344647/autophagy-regulates-the-degeneration-of-the-auditory-cortex-through-the-ampk-mtor-ulk1-signaling-pathway
#2
Jie Yuan, Xueyan Zhao, Yujuan Hu, Haiying Sun, Guoqing Gong, Xiang Huang, Xubo Chen, Mingyu Xia, Chen Sun, Qilin Huang, Yu Sun, Wen Kong, Weijia Kong
Presbycusis is the most common sensory impairment associated with aging; however, the underlying molecular mechanism remains unclear. Autophagy has been demonstrated to serve a key role in diverse diseases; however, no studies have examined its function in central presbycusis. The aim of the present study was to investigate the changes of autophagy in the physiological processes of the auditory cortex and its role in the degeneration of the auditory cortex, as well as the related mechanisms using naturally aging rats and a D‑galactose (D‑gal)‑induced mimetic rat model of aging...
January 17, 2018: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29339018/nicotine-alleviates-chronic-stress-induced-anxiety-and-depressive-like-behavior-and-hippocampal-neuropathology-via-regulating-autophagy-signaling
#3
Xi Xiao, Xueliang Shang, Baohui Zhai, Hui Zhang, Tao Zhang
Recently, we reported that chronic nicotine significantly improved chronic stress-induced impairments of cognition and the hippocampal synaptic plasticity in mice, however, the underlying mechanism still needs to be explored. In the present study, 32 male C57BL/6 mice were divided into four groups: control (CON), stress (CUS), stress with chronic nicotine administration (CUS + Nic) and chronic nicotine administration (Nic). The anxiety-like behavior and neuropathological alteration of DG neurons were examined...
January 12, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29334873/nobiletin-prevents-cadmium-induced-neuronal-apoptosis-by-inhibiting-reactive-oxygen-species-and-modulating-jnk-erk1-2-and-akt-mtor-networks-in-rats
#4
Youyang Qu, Yu Liu, Li Chen, Yanmei Zhu, Xingjun Xiao, Di Wang, Yulan Zhu
Objectives Cadmium (Cd), an extremely noxious environmental pollutant is known to induce oxidative stress leading to neurodegenerative diseases. Nobiletin, a citrus flavonoid is reported to possess various pharmacological properties. This study investigates the effects of nobiletin over Cd-induced neuronal apoptosis in rodent experimental model. Methods To separate group of male Sprague Dawley rats, Cd (2 mL/kg/day) was subcutaneously injected for one month which results in a dose level of 1 mg/kg Cd. Couple of days prior to Cd injection, the treatment group rats regularly received nobiletin (50, 100, or 200 mg/kg b...
January 16, 2018: Neurological Research
https://www.readbyqxmd.com/read/29329236/gender-associated-impact-of-early-leucine-supplementation-on-adult-predisposition-to-obesity-in-rats
#5
Nora López, Juana Sánchez, Andreu Palou, Francisca Serra
Early nutrition plays an important role in development and may constitute a relevant contributor to the onset of obesity in adulthood. The aim of this study was to evaluate the long-term impact of maternal leucine (Leu) supplementation during lactation on progeny in rats. A chow diet, supplemented with 2% Leu, was supplied during lactation (21 days) and, from weaning onwards, was replaced by a standard chow diet. Then, at adulthood (6 months of age), this was replaced with hypercaloric diets (either with high-fat (HF) or high-carbohydrate (HC) content), for two months, to induce obesity...
January 12, 2018: Nutrients
https://www.readbyqxmd.com/read/29328494/pterostilbene-inhibits-reactive-oxygen-species-production-and-apoptosis-in-primary-spinal-cord-neurons-by-activating-autophagy-via-the-mechanistic-target-of-rapamycin-signaling-pathway
#6
Jing-Lan He, Xiao-Hui Dong, Zong-Hu Li, Xiao-Ying Wang, Zhi-An Fu, Na Shen
Autophagy is an important self-adaptive mechanism that is involved in inhibiting reactive oxygen species (ROS) in spinal cord neurons. Pterostilbene, a natural plant extract, has been demonstrated to possess antioxidant effects; however, it has not yet been investigated whether pterostilbene could activate autophagy and protect spinal cord neurons from oxidative stress. In the present study, primary spinal cord neurons of Sprague Dawley rats were cultured. Cell counting kit‑8 analysis was used to detect cytotoxicity of pterostilbene...
January 9, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29324300/hippocampal-insulin-resistance-links-maternal-obesity-with-impaired-neuronal-plasticity-in-adult-offspring
#7
Lisa Schmitz, Rebecca Kuglin, Inga Bae-Gartz, Ruth Janoschek, Sarah Appel, Andrea Mesaros, Igor Jakovcevski, Christina Vohlen, Marion Handwerk, Regina Ensenauer, Jörg Dötsch, Eva Hucklenbruch-Rother
OBJECTIVE: Maternal obesity and a disturbed metabolic environment during pregnancy and lactation have been shown to result in many long-term health consequences for the offspring. Among them, impairments in neurocognitive development and performance belong to the most dreaded ones. So far, very few mechanistic approaches have aimed to determine the responsible molecular events. METHODS: In a mouse model of maternal diet-induced obesity and perinatal hyperinsulinemia, we assessed adult offspring's hippocampal insulin signaling as well as concurrent effects on markers of hippocampal neurogenesis, synaptic plasticity and function using western blotting and immunohistochemistry...
December 28, 2017: Psychoneuroendocrinology
https://www.readbyqxmd.com/read/29315934/effect-of-euk-134-on-akt-mtor-signaling-in-the-rat-soleus-during-7-days-of-mechanical-unloading
#8
J Matthew Kuczmarski, Jeff M Hord, Yang Lee, Vinicius Guzzoni, Dinah Rodriguez, Matthew S Lawler, Erika L Garcia-Villatoro, Dylan Holly, Patrick Ryan, Kristian Falcon, Marcela Garcia, Mariana Janini Gomes, James D Fluckey, John M Lawler
Mechanical unloading stimulates rapid changes in skeletal muscle morphology, characterized by atrophy of muscle fiber cross-sectional area (CSA) and a partial fiber-type shift from slow to fast-twitch. Recent studies revealed that oxidative stress contributes to activation of FoxO3a, proteolytic signaling and unloading-induced muscle atrophy via translocation of the mu-splice variant of neuronal nitric oxide synthase (nNOSμ) and activation of FoxO3a. Yet, there is limited understanding of the role of reactive oxygen species (ROS) on the Akt-mTOR pathway signaling during unloading...
January 8, 2018: Experimental Physiology
https://www.readbyqxmd.com/read/29311141/a-unique-homeostatic-signaling-pathway-links-synaptic-inactivity-to-postsynaptic-mtorc1
#9
Fredrick E Henry, Xiao Wang, David Serrano, Amanda S Perez, Cynthia J L Carruthers, Edward L Stuenkel, Michael A Sutton
mTORC1-dependent translational control plays a key role in several enduring forms of synaptic plasticity such as long term potentiation (LTP) and mGluR-dependent long term depression. Recent evidence demonstrates an additional role in regulating synaptic homeostasis in response to inactivity, where dendritic mTORC1 serves to modulate presynaptic function via retrograde signaling. Presently, it is unclear if LTP and homeostatic plasticity utilize a common route to mTORC1-dependent signaling or if each engage mTORC1 through distinct pathways...
January 8, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29305122/liraglutide-ameliorates-cognitive-decline-by-promoting-autophagy-via-the-amp-activated-protein-kinase-mammalian-target-of-rapamycin-pathway-in-a-streptozotocin-induced-mouse-model-of-diabetes
#10
Fei-Juan Kong, Jia-Hua Wu, Shui-Ya Sun, Lei-Lei Ma, Jia-Qiang Zhou
Diabetic cognitive dysfunction has gained widespread attention for its deleterious impact on individuals with diabetes. However, few clinical interventions are available to prevent the disorder. The glucagon-like peptide-1 analog liraglutide exerts neuroprotective effects in several models of neurodegenerative diseases. We investigated the effect of liraglutide pretreatment on diabetes-induced cognitive decline and explored the underlying mechanisms in vivo and in vitro. Liraglutide pretreatment prevented diabetes-induced cognitive impairment as assessed by the Morris Water Maze test, and alleviated neuronal injuries and ultrastructural damage to synapses in the hippocampal CA1 region...
January 2, 2018: Neuropharmacology
https://www.readbyqxmd.com/read/29281825/somatic-mutations-activating-the-mtor-pathway-in-dorsal-telencephalic-progenitors-cause-a-continuum-of-cortical-dysplasias
#11
Alissa M D'Gama, Mollie B Woodworth, Amer A Hossain, Sara Bizzotto, Nicole E Hatem, Christopher M LaCoursiere, Imad Najm, Zhong Ying, Edward Yang, A James Barkovich, David J Kwiatkowski, Harry V Vinters, Joseph R Madsen, Gary W Mathern, Ingmar Blümcke, Annapurna Poduri, Christopher A Walsh
Focal cortical dysplasia (FCD) and hemimegalencephaly (HME) are epileptogenic neurodevelopmental malformations caused by mutations in mTOR pathway genes. Deep sequencing of these genes in FCD/HME brain tissue identified an etiology in 27 of 66 cases (41%). Radiographically indistinguishable lesions are caused by somatic activating mutations in AKT3, MTOR, and PIK3CA and germline loss-of-function mutations in DEPDC5, NPRL2, and TSC1/2, including TSC2 mutations in isolated HME demonstrating a "two-hit" model...
December 26, 2017: Cell Reports
https://www.readbyqxmd.com/read/29274432/a-mouse-model-of-depdc5-related-epilepsy-neuronal-loss-of-depdc5-causes-dysplastic-and-ectopic-neurons-increased-mtor-signaling-and-seizure-susceptibility
#12
Christopher J Yuskaitis, Brandon M Jones, Rachel L Wolfson, Chloe E Super, Sameer C Dhamne, Alexander Rotenberg, David M Sabatini, Mustafa Sahin, Annapurna Poduri
DEPDC5 is a newly identified epilepsy-related gene implicated in focal epilepsy, brain malformations, and Sudden Unexplained Death in Epilepsy (SUDEP). In vitro, DEPDC5 negatively regulates amino acid sensing by the mTOR complex 1 (mTORC1) pathway, but the role of DEPDC5 in neurodevelopment and epilepsy has not been described. No animal model of DEPDC5-related epilepsy has recapitulated the neurological phenotypes seen in patients, and germline knockout rodent models are embryonic lethal. Here, we establish a neuron-specific Depdc5 conditional knockout mouse by cre-recombination under the Synapsin1 promotor...
December 20, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29260451/amyloid-%C3%AE-derived-diffusible-ligands-addls-induce-abnormal-autophagy-associated-with-a%C3%AE-aggregation-degree
#13
Jie Wen, Fang Fang, Shu-Han Guo, Ying Zhang, Xiang-Lei Peng, Wei-Min Sun, Xiao-Ran Wei, Jin-Sheng He, Tao Hung
Autophagy is disturbed in Alzheimer's disease (AD) and maintaining normal autophagy homeostasis is a new therapeutic strategy for AD treatment. Amyloid β-derived diffusible ligands (ADDLs), the most toxic species of which are oligomeric forms of amyloid β peptide (Aβ) that originate from amyloid β precursor protein (APP) via autophagy; however, whether ADDLs are involved in autophagy-related AD pathogenesis remains unclear. In this study, we primarily defined the specific subsets of ADDLs, A-0, A-12, A-24, and A-48, which were generated from ADDL aggregation mixtures at different time courses of assembly...
December 19, 2017: Journal of Molecular Neuroscience: MN
https://www.readbyqxmd.com/read/29242531/long-noncoding-rna-expression-profile-reveals-lncrnas-signature-associated-with-extracellular-matrix-degradation-in-kashin-beck-disease
#14
Cuiyan Wu, Huan Liu, Feng'e Zhang, Wanzhen Shao, Lei Yang, Yujie Ning, Sen Wang, Guanghui Zhao, Byeong Jae Lee, Mikko Lammi, Xiong Guo
Kashin-Beck disease (KBD) is a deformative, endemic osteochondropathy involving degeneration and necrosis of growth plates and articular cartilage. The pathogenesis of KBD is related to gene expression and regulation mechanisms, but long noncoding RNAs (lncRNAs) in KBD have not been investigated. In this study, we identified 316 up-regulated and 631 down-regulated lncRNAs (≥ 2-fold change) in KBD chondrocytes using microarray analysis, of which more than three-quarters were intergenic lncRNAs and antisense lncRNAs...
December 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29239329/activation-of-the-akt-mtor-signaling-pathway-a-potential-response-to-long-term-neuronal-loss-in-the-hippocampus-after-sepsis
#15
Jia-Nan Guo, Lin-Yu Tian, Wen-Yu Liu, Jie Mu, Dong Zhou
Survivors of sepsis may suffer chronic cognitive impairment as a long-term sequela. However, the precise mechanisms of cognitive dysfunction after sepsis are not well understood. We employed the cecal ligation-and-puncture-induced septic mouse model. We observed elevated phosphorylation of Akt, mammalian target of rapamycin (mTOR) and p70S6K on days 14 and 60, progressive neuronal loss in the cornu ammonis 1 region, and abnormal neuronal morphology in the hippocampus in the sepsis mouse model. These findings indicate that changes in neuronal morphology and number in the hippocampus after sepsis were associated with strong activation of the Akt/mTOR signaling pathway, and may reflect a "self-rescuing" feedback response to neuronal loss after sepsis...
November 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/29233655/recombinant-human-erythropoietin-protects-against-brain-injury-through-blunting-the-mtorc1-pathway-in-the-developing-brains-of-rats-with-seizures
#16
Qinrui Li, Ying Han, Junbao Du, Hongfang Jin, Jing Zhang, Manman Niu, Jiong Qin
AIMS: Recurrent seizures can result in neuronal death, cognitive deficits and intellectual disability, which causes devastating damage in children. Recombinant human erythropoietin (rhEPO) is considered a neuroprotective factor in many nervous system diseases. However, the precise mechanisms through which rhEPO exerts its neuroprotective effects on epilepsy remain unknown. Thus, in this study, we determined whether rhEPO protects against brain injury by inducing cortical neuronal autophagy through blunting the mammalian target of rapamycin complex 1 (mTORC1) pathway in the developing brains of rats with seizures...
December 9, 2017: Life Sciences
https://www.readbyqxmd.com/read/29232822/microglia-m2a-polarization-as-potential-link-between-food-allergy-and-autism-spectrum-disorders
#17
REVIEW
Hans O Kalkman, Dominik Feuerbach
Atopic diseases are frequently co-morbid with autism spectrum disorders (ASD). Allergic responses are associated with an activation of mast cells, innate lymphoid cells, and Th2 cells. These cells produce type-2 cytokines (IL4 and IL13), which stimulate microglia and macrophages to adopt a phenotype referred to as 'alternative activation' or 'M2A'. M2A-polarized macrophages and microglia play a physiological role in tissue repair by secreting growth factors such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1...
December 9, 2017: Pharmaceuticals
https://www.readbyqxmd.com/read/29222553/ghrelin-attenuates-retinal-neuronal-autophagy-and-apoptosis-in-an-experimental-rat-glaucoma-model
#18
Ke Zhu, Meng-Lu Zhang, Shu-Ting Liu, Xue-Yan Li, Shu-Min Zhong, Fang Li, Ge-Zhi Xu, Zhongfeng Wang, Yanying Miao
Purpose: Ghrelin, a natural ligand for the growth hormone secretagogue receptor type 1a (GHSR-1a), may protect retinal neurons against glaucomatous injury. We therefore characterized the underlying mechanism of the ghrelin/GHSR-1a-mediated neuroprotection with a rat chronic intraocular hypertension (COH) model. Methods: The rat COH model was produced by blocking episcleral veins. A combination of immunohistochemistry, Western blot, TUNEL assay, and retrograde labeling of retinal ganglion cells (RGCs) was used...
December 1, 2017: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/29218081/tetramethylpyrazine-phosphate-and-borneol-combination-therapy-synergistically-attenuated-ischemia-reperfusion-injury-of-the-hypothalamus-and-striatum-via-regulation-of-apoptosis-and-autophagy-in-a-rat-model
#19
Bin Yu, Ming Ruan, Tao Liang, Shi-Wen Huang, Sheng-Jin Liu, Hai-Bo Cheng, Xiang-Chun Shen
The combination of tetramethylpyrazine (TMP) and borneol (BO) has shown promise for treatment of cerebral ischemia in clinical and experimental studies. However, the mechanism for the synergistic effect of these compounds is unclear. In this study, global cerebral ischemia-reperfusion (GCIR) was induced in rats that were subsequently treated with tetramethylpyrazine phosphate (TMPP) (13.3 mg/kg), BO (0.16 g/kg), or the combination TMPP + BO. Neuronal ultrastructure and intracellular calcium [Ca2+]i levels were evaluated in hypothalamus and striatum...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/29209172/the-role-of-netrin-1-in-improving-functional-recovery-through-autophagy-stimulation-following-spinal-cord-injury-in-rats
#20
Liangjie Bai, Xifan Mei, Yanfeng Wang, Yajiang Yuan, Yunlong Bi, Gang Li, Hongyu Wang, Peng Yan, Gang Lv
Our previous findings indicated that treatment with Netrin-1 could improve functional recovery through the stimulation of autophagy, by activating the AMP-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) signaling pathway in rats following spinal cord injury (SCI). However, the underlying mechanisms were not elucidated. The purpose of this study was to investigate the underlying mechanisms by which Netrin-1 promotes autophagy and improves functional recovery after SCI. Following controlled SCI in Sprague-Dawley rats, we observed that the autophagic flux in neurons was impaired, as reflected by the accumulation of light chain 3-II (LC3-II)-positive and LC3-positive autophagosomes (APs), accompanied by the accumulation of the autophagic substrate, Sequestosome 1 (SQSTM1; also known as p62)...
2017: Frontiers in Cellular Neuroscience
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