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Neurochemical Research

Seojin Hwang, Seong-Eun Lee, Sang-Gun Ahn, Gum Hwa Lee
Upon synaptic stimulation and glutamate release, glutamate receptors are activated to regulate several downstream effectors and signaling pathways resulting in synaptic modification. One downstream intracellular effect, in particular, is the expression of immediate-early genes (IEGs), which have been proposed to be important in synaptic plasticity because of their rapid expression following synaptic activation and key role in memory formation. In this study, we screened a natural compound library in order to find a compound that could induce the expression of IEGs in primary cortical neurons and discovered that psoralidin, a natural compound isolated from the seeds of Psoralea corylifolia, stimulated synaptic modulation...
November 13, 2018: Neurochemical Research
Patrick Dutar, Brigitte Potier
Aging, as the major risk factor of Alzheimer's disease (AD), may increase susceptibility to neurodegenerative diseases through many gradual molecular and biochemical changes. Extracellular glutamate homeostasis and extrasynaptic glutamate N-methyl-D-aspartate receptors (NMDAR) are among early synaptic targets of oligomeric amyloid β (Aβo), one of the AD related synaptotoxic protein species. In this study, we asked for the effects of Aβo on long-term depression (LTD), a form of synaptic plasticity dependent on extrasynaptic NMDAR activation, and on a tonic current (TC) resulting from the activation of extrasynaptic NMDAR by ambient glutamate in hippocampal slices from young (3-6-month-old) and aged (24-28-month-old) Sprague-Dawley rats...
November 13, 2018: Neurochemical Research
Yuqing Shen, Huanhuan Zhao, Ping Li, Yaqin Peng, Pengfei Cui, Fengqin Miao, Ying Zhang, Aifeng Zhang, Jianqiong Zhang
Neuronal MHC class I proteins have been previously reported to regulate synaptic plasticity. Several reports indicate MHC class I proteins are expressed early during development of the nervous system, suggesting they may also play a role in neuronal development. Using cultured cortical neurons, we show MHC class I proteins aggregate at specific sites in neuronal cell bodies, which overlap with the actin cytoskeleton. Knockout of MHC class I in cultured neurons increases total dendritic length and the number of branch points...
November 8, 2018: Neurochemical Research
Helen A Rowland, Nigel M Hooper, Katherine A B Kellett
Developing cellular models of sporadic Alzheimer's disease (sAD) is challenging due to the unknown initiator of disease onset and the slow disease progression that takes many years to develop in vivo. The use of human induced pluripotent stem cells (iPSCs) has revolutionised the opportunities to model AD pathology, investigate disease mechanisms and screen potential drugs. The majority of this work has, however, used cells derived from patients with familial AD (fAD) where specific genetic mutations drive disease onset...
November 1, 2018: Neurochemical Research
Adriana Fernanda K Vizuete, Fernanda Hansen, Carollina Da Ré, Miriara B Leal, Fabiana Galland, Marina Concli Leite, Carlos-Alberto Gonçalves
Astrocytes are the major glial cells in brain tissue and are involved, among many functions, ionic and metabolic homeostasis maintenance of synapses. These cells express receptors and transporters for neurotransmitters, including GABA. GABA signaling is reportedly able to affect astroglial response to injury, as evaluated by specific astrocyte markers such as glial fibrillary acid protein and the calcium-binding protein, S100B. Herein, we investigated the modulatory effects of the GABAA receptor on astrocyte S100B secretion in acute hippocampal slices and astrocyte cultures, using the agonist, muscimol, and the antagonists pentylenetetrazol (PTZ) and bicuculline...
November 1, 2018: Neurochemical Research
Pingping Sun, Xiaoke Nie, Xiaoxu Chen, Lifeng Yin, Jiashan Luo, Lingli Sun, Chunhua Wan, Shengyang Jiang
Perfluorooctanesulfonate (PFOS) may cause neurotoxicity through the initiation of oxidative stress. In the current study, we investigated the role of anti-oxidant nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in PFOS-induced neurotoxicity. We found that human neuroblastoma SH-SY5Y cells exhibited significant apoptotic cell death following PFOS exposure, and this process was accompanied with apparent accumulation of reactive oxidative species (ROS). In addition, we revealed that PFOS exposure caused marked activation of Nrf2 pathway and the expression of Nrf2 transcription target heme oxygenase-1...
October 31, 2018: Neurochemical Research
Dazhi Ding, Peipei Zhang, Yuxi Liu, Yi Wang, Weiwei Sun, Zhaohui Yu, Zhen Cheng, Youhua Wang
Runx2, also known as Cbfa1, is a multifunctional transcription factor essential for osteoblast differentiation. It also plays major roles in chondrocyte maturation, mesenchymal stem cell differentiation, cleidocranial dysplasia, and the growth and metastasis of tumors. The present study was performed to investigate the functions of Runx2 in the differentiation and migration of Schwann cells and outgrowth of neurites after peripheral nervous system injury. In a model of sciatic nerve crush (SNC) injury, we found a gradual increase in the expression of Runx2, which reached a peak after 1 week...
October 29, 2018: Neurochemical Research
Thaiany Quevedo Melo, Sjef J C V M Copray, Merari F R Ferrari
Parkinson's disease (PD) is characterized by the presence of insoluble protein clusters containing α-synuclein. Impairment of mitochondria, endoplasmic reticulum, autophagy and intracellular trafficking proper function has been suggested to be caused by α-synuclein toxicity, which is also associated with the higher levels of ROS found in the aged brain and in PD. Oxidative stress leads to protein oligomerization and aggregation that impair autophagy and mitochondrial dynamics leading to a vicious cycle of organelles damage and neurodegeneration...
October 28, 2018: Neurochemical Research
Bing Wang, Guoxin Zhang, Mei Yang, Ning Liu, Yu-Xiang Li, Hanxiang Ma, Lin Ma, Tao Sun, Huanran Tan, Jianqiang Yu
Neuropathic pain is an intractable disease with few definitive therapeutic options. Anethole (AN) has been confirmed to possess potent anti-inflammatory and neuroprotective properties, but its effect on neuropathic pain has not been reported. The present study was designed to investigate the antinociceptive effect of AN on chronic constriction injury (CCI)-induced neuropathic pain in mice. AN (125, 250, and 500 mg/kg) and pregabalin (40 mg/kg) were intragastric administered for 8 consecutive days from the 7th day post-surgery...
October 26, 2018: Neurochemical Research
Phan H Truong, Giuseppe D Ciccotosto, Roberto Cappai
The amyloid precursor protein (APP) is a member of a conserved gene family that includes the amyloid precursor-like proteins 1 (APLP1) and 2 (APLP2). APP and APLP2 share a high degree of similarity, and have overlapping patterns of spatial and temporal expression in the central and peripheral tissues, in particular at the neuromuscular junction. APP-family knockout (KO) studies have helped elucidate aspects of function and functional redundancy amongst the APP-family members. In the present study, we investigated motor performance of APLP2-KO mice and the effect sex differences and age-related changes have on motor performance...
October 25, 2018: Neurochemical Research
Toyanji Joseph Punchaichira, Smita Neelkanth Deshpande, B K Thelma
Dopamine-β-hydroxylase (DBH, EC is an enzyme with implications in various neuropsychiatric and cardiovascular diseases and is a known drug target. There is a dearth of cost effective and fast method for estimation of activity of this enzyme. A sensitive UHPLC based method for the estimation of DBH activity in human sera samples based on separation of substrate tyramine from the product octopamine in 3 min is described here. In this newly developed protocol, a Solid Phase Extraction (SPE) sample purification step prior to LC separation, selectively removes interferences from the reaction cocktail with almost no additional burden on analyte recovery...
October 24, 2018: Neurochemical Research
Sicong Wang, Xin Wang, Wenxuan Lin, Suhao Bao, Benfu Wang, Binbin Wu, Ying Su, Qingquan Lian
Propofol has been proven to be potentially abused by humans and laboratory animals; however, studies that have examined propofol relapse behavior are limited, and its underlying mechanism remains unclear. In this study, we examined whether basolateral amygdala-specific or systematic administration of the dopamine receptor antagonist alters cue-induced propofol-seeking behaviors in a rat model. Male Sprague-Dawley rats first received 14 days of propofol self-administration training, where active nose poke resulted in the delivery of propofol infusion paired with a tone and light cues...
October 24, 2018: Neurochemical Research
Natalia V Gulyaeva
The hippocampus is not a homogeneous brain area, and the complex organization of this structure underlies its relevance and functional pleiotropism. The new data related to the involvement of the ventral hippocampus in the cognitive function, behavior, stress response and its association with brain pathology, in particular, depression, are analyzed with a focus on neuroplasticity, specializations of the intrinsic neuronal network, corticosteroid signaling through mineralocorticoid and glucocorticoid receptors and neuroinflammation in the hippocampus...
October 24, 2018: Neurochemical Research
Sumiko Kiryu-Seo, Kenichi Nagata, Takaomi C Saido, Hiroshi Kiyama
Our understanding of the physiological relevance of unique Damage-induced neuronal endopeptidase (DINE) [also termed Endothelin-converting enzyme-like 1 (ECEL1)] has recently expanded. DINE/ECEL1 is a type II membrane-bound metalloprotease, belonging to a family including the neprilysin (NEP) and endothelin-converting enzyme (ECE). The family members degrade and/or process peptides such as amyloid β and big-endothelins, which are closely associated with pathological conditions. Similar to NEP and ECE, DINE has been expected to play an important role in injured neurons as well as in developing neurons, because of its remarkable transcriptional response to neuronal insults and predominant neuronal expression from the embryonic stage...
October 24, 2018: Neurochemical Research
Federico A Prestia, Pablo Galeano, Pamela V Martino Adami, Sonia Do Carmo, Eduardo M Castaño, A Claudio Cuello, Laura Morelli
Alzheimer's disease (AD) is associated to depressed brain energy supply and impaired cortical and hippocampal synaptic function. It was previously reported in McGill-R-Thy1-APP transgenic (Tg(+/+)) rats that Aβ deposition per se is sufficient to cause abnormalities in glucose metabolism and neuronal connectivity. These data support the utility of this animal model as a platform for the search of novel AD biomarkers based on bioenergetic status. Recently, it has been proposed that energy dysfunction can be dynamically tested in platelets (PLTs) of nonhuman primates...
October 24, 2018: Neurochemical Research
Hong Xie, Haojun Huang, Min Tang, Yan Wu, Rongzhong Huang, Zhao Liu, Mi Zhou, Wei Liao, Jian Zhou
Mounting studies show that hippocampal synaptic transmission and plasticity are abnormal in depression. It has been suggested that impairment of synaptic mitochondrial functions potentially occurs in the hippocampus. Thus, the synaptic mitochondria may be a crucial therapeutic target in the course of depression. Here, we investigated the potential dysregulation of synaptic mitochondrial proteins in the hippocampus of a chronic mild stress (CMS) rat model. Proteomic changes of hippocampal synaptosomes containing synaptic mitochondria were quantitatively examined using the isobaric tag for relative and absolute quantitation labeling combined with tandem mass spectrometry...
October 22, 2018: Neurochemical Research
Wen-Tung Wang, Phil Lee, Dongwei Hui, Elias K Michaelis, In-Young Choi
Ethanol (EtOH) intake leads to modulation of glutamatergic transmission, which may contribute to ethanol intoxication, tolerance and dependence. To study metabolic responses to the hyper glutamatergic status at synapses during ethanol exposure, we used Glud1 transgenic (tg) mice that over-express the enzyme glutamate dehydrogenase in brain neurons and release excess glutamate (Glu) in synapses. We measured neurochemical changes in the hippocampus and striatum of tg and wild-type (wt) mice using proton magnetic resonance spectroscopy before and after the animals were fed with diets within which EtOH constituting up to 6...
October 17, 2018: Neurochemical Research
Min Sung Gee, Sang-Won Kim, Namkwon Kim, Soo Jin Lee, Myung Sook Oh, Hee Kyung Jin, Jae-Sung Bae, Kyung-Soo Inn, Nam-Jung Kim, Jong Kil Lee
Neuroinflammation is an important pathological feature in neurodegenerative diseases. Accumulating evidence has suggested that neuroinflammation is mainly aggravated by activated microglia, which are macrophage like cells in the central nervous system. Therefore, the inhibition of microglial activation may be considered for treating neuroinflammatory diseases. p38 mitogen-activated protein kinase (MAPK) has been identified as a crucial enzyme with inflammatory roles in several immune cells, and its activation also relates to neuroinflammation...
October 16, 2018: Neurochemical Research
Jianjun Xue, Huili Li, Ziqing Xu, Danxu Ma, Ruijuan Guo, Kehu Yang, Yun Wang
The mechanisms underlying the pronociceptive effect of paradoxical sleep deprivation (PSD) are not fully established. The modulation of BDNF signaling-mediated descending facilitation from the rostral ventromedial medulla (RVM) of brain stem has been demonstrated in persistent pain models of inflammatory pain, but not in incisional pain model. Recent study has shown that PSD increases the expression of brain-derived neurotrophic factor (BDNF) in the brainstem structure. Therefore, in the current study, we asked whether the BDNF signaling-mediated descending facilitation was involved in the PSD-induced pronociceptive effect on incisional pain and delay the recovery period of postoperative pain in rats...
October 15, 2018: Neurochemical Research
Chang Liu, Bingquan Leng, Yi Li, Hong Jiang, Weisong Duan, Yansu Guo, Chunyan Li, Kun Hong
Amyotrophic lateral sclerosis (ALS) is a rapidly progressive motor neuron disease for which only limited effective therapeutics are available. Currently, TAR DNA-binding protein 43 (TDP-43) is recognized as a pathological and biochemical marker for ALS. Increases in the levels of aggregated or mislocalized forms of TDP-43 might result in ALS pathology. Therefore, clearance pathways for intracellular protein aggregates have been suggested as potential therapeutic targets for the treatment of ALS. Here we report that treatment of motor neuron-like NSC34 cells overexpressing TDP-43 with diallyl trisulfide (DATS) induced neuronal autophagy and lysosomal clearance of TDP-43 and C-terminal TDP-43 fragments...
October 13, 2018: Neurochemical Research
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