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Journal of Neurochemistry

Qian-Ru Zhao, Jun-Mei Lu, Zhao-Yang Li, Yan-Ai Mei
Neuritin is a neurotrophic factor that is activated by neural activity and neurotrophins. Its major function is to promote neurite growth and branching; however, the underlying mechanisms are not fully understood. To address this issue, the present study investigated the effects of neuritin on neurite and spine growth and intracellular Ca2+ concentration in rat cerebellar granule neurons (CGNs). Incubation of CGNs for 24 h with neuritin increased neurite length and spine density; this effect was mimicked by insulin and abolished by inhibiting insulin receptor (IR) or mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) activity...
June 19, 2018: Journal of Neurochemistry
Saori Kikuchihara, Shouta Sugio, Kenji F Tanaka, Takaki Watanabe, Masanobu Kano, Yoshihiko Yamazaki, Masahiko Watanabe, Kazuhiro Ikenaka
Mlc1 is a causative gene for megalencephalic leukoencephalopathy with subcortical cysts (MLC), and is expressed in astrocytes. Mlc1-overexpressing mice represent an animal model of early-onset leukoencephalopathy, which manifests as astrocytic swelling followed by myelin membrane splitting in the white matter. It has previously reported that Mlc1 is highly expressed in Bergmann glia, while the cerebellar phenotypes of Mlc1-overexpressing mouse have not been characterized. Here, we examined the cerebellum of Mlc1-overexpressing mouse and found that the distribution of BG was normally compacted along the PC layer until postnatal day 10 (P10), while most BG were dispersed throughout the molecular layer by P28...
June 19, 2018: Journal of Neurochemistry
Soo Min Cho, Ayelet Vardi, Nicolas Platt, Anthony H Futerman
Approximately 70 lysosomal storage diseases are currently known, resulting from mutations in genes encoding lysosomal enzymes and membrane proteins. Defects in lysosomal enzymes that hydrolyze sphingolipids have been relatively well studied. Gaucher disease is caused by the loss of activity of glucocerebrosidase, leading to accumulation of glucosylceramide. Gaucher disease exhibits a number of subtypes, with types 2 and 3 showing significant neuropathology. Sandhoff disease results from the defective activity of β-hexosaminidase, leading to accumulation of ganglioside GM2...
June 14, 2018: Journal of Neurochemistry
Shaomei Sui, Jing Tian, Esha Gauba, Qi Wang, Lan Guo, Heng Du
Recent studies have highlighted the role of mitochondria in dendritic protrusion growth and plasticity. However, the detailed mechanisms that mitochondria regulate dendritic filopodia morphogenesis remain elusive. Cyclophilin D (CypD, gene name: Ppif) controls the opening of mitochondrial permeability transition pore (mPTP). Although the pathological relevance of CypD has been intensively investigated, little is known about its physiological function in neurons. Here, we have found that genetic depletion of or pharmaceutical inhibiton of CypD blunts the outgrowth of dendritic filopodia in response to KCl-stimulated neuronal depolarization...
June 14, 2018: Journal of Neurochemistry
Arsalan S Haqqani, George Thom, Matthew Burrell, Christie E Delaney, Eric Brunette, Ewa Baumann, Caroline Sodja, Anna Jezierski, Carl Webster, Danica B Stanimirovic
The blood-brain barrier (BBB) is a formidable obstacle to the delivery of therapeutics to the brain. Antibodies that bind transferrin receptor, which is enriched in brain endothelial cells, have been shown to cross the BBB and are being developed as fusion proteins to deliver therapeutic cargos to brain targets. Various antibodies have been developed for this purpose and their in vivo evaluation demonstrated that either low affinity or mono-valent receptor binding re-directs their transcellular trafficking away from lysosomal degradation and towards improved exocytosis on the abluminal side of the BBB...
June 7, 2018: Journal of Neurochemistry
Maria Burkovetskaya, Megan E Bosch, Nikolay Karpuk, Rachel Fallet, Tammy Kielian
Juvenile Neuronal Ceroid Lipofuscinosis (JNCL) is an autosomal recessive lysosomal storage disease caused by loss-of-function mutations in CLN3. Symptoms appear between 5-10 years of age, beginning with blindness and seizures, followed by progressive cognitive and motor decline, and premature death. Glial activation and impaired neuronal activity are early signs of pathology in the Cln3Δex7/8 mouse model of JNCL, whereas neuron death occurs much later in the disease process. We previously reported that Cln3Δex7/8 microglia are primed towards a pro-inflammatory phenotype typified by exaggerated caspase-1 inflammasome activation and here we extend those findings to demonstrate heightened caspase activity in the Cln3Δex7/8 mouse brain...
June 5, 2018: Journal of Neurochemistry
Jocelyn Widagdo, Victor Anggono
Research over the past decade has provided strong support for the importance of various epigenetic mechanisms, including DNA and histone modifications in regulating activity-dependent gene expression in the mammalian central nervous system. More recently, the emerging field of epitranscriptomics revealed an equally important role of post-transcriptional RNA modifications in shaping the transcriptomic landscape of the brain. This review will focus on the methylation of the adenosine base at the N6 position, termed N6 methyladenosine (m6A), which is the most abundant internal modification that decorates eukaryotic messenger RNAs...
June 5, 2018: Journal of Neurochemistry
Peter Müller, Andreas Draguhn, Alexei V Egorov
Axonal excitability is an important determinant for the accuracy, direction and velocity of neuronal signaling. The mechanisms underlying spike generation in the axonal initial segment and transmitter release from presynaptic terminals have been intensely studied and revealed a role for several specific ionic conductances, including the persistent sodium current (IN aP ). Recent evidence indicates that action potentials can also be generated at remote locations along the axonal fiber, giving rise to ectopic action potentials (eAP) during physiological states (e...
June 4, 2018: Journal of Neurochemistry
Li-Juan Zhu, Huan-Yu Ni, Rong Chen, Lei Chang, Hu-Jiang Shi, Dan Qiu, Zhan Zhang, Dan-Lian Wu, Zhao-Chun Jiang, Hong-Liang Xin, Qi-Gang Zhou, Dong-Ya Zhu
Anxiety disorders are associated with a high social burden worldwide. Recently, increasing evidence suggests that nuclear factor kappa B (NF-κB) has significant implications for psychiatric diseases, including anxiety and depressive disorders. However, the molecular mechanisms underlying the role of NF-κB in stress-induced anxiety behaviors are poorly understood. In this study, we show that chronic mild stress (CMS) and glucocorticoids dramatically increased the expression of NF-κB subunits p50 and p65, phosphorylation and acetylation of p65, and the level of nuclear p65 in vivo and in vitro, implicating activation of NF-κB signaling in chronic stress-induced pathological processes...
June 2, 2018: Journal of Neurochemistry
Julieta Saba, Juan Turati, Delia Ramírez, Lila Carniglia, Daniela Durand, Mercedes Lasaga, Carla Caruso
Astrocytes are glial cells that help maintain brain homeostasis and become reactive in neurodegenerative processes releasing both harmful and beneficial factors. We have demonstrated that brain-derived neurotrophic factor (BDNF) expression is induced by melanocortins in astrocytes but BDNF actions in astrocytes are largely unknown. We hypothesize that BDNF may prevent astrocyte death resulting in neuroprotection. We found that BDNF increased astrocyte viability, preventing apoptosis induced by serum deprivation by decreasing active caspase-3 and p53 expression...
May 31, 2018: Journal of Neurochemistry
Kunihiko Kanatsu, Yukiko Hori, Ihori Ebinuma, Yung Wen Chiu, Taisuke Tomita
The aberrant metabolism of amyloid-β protein (Aβ) in the human brain has been implicated in the etiology of Alzheimer disease (AD). γ-Secretase is the enzyme that generates various forms of Aβ, such as Aβ40 and Aβ42, the latter being an aggregation-prone toxic peptide that is involved in the pathogenesis of AD. Recently, we found that clathrin-mediated endocytosis of γ-secretase affects the production and deposition of Aβ42 in vivo, suggesting that the membrane trafficking of γ-secretase affects its enzymatic activity...
May 31, 2018: Journal of Neurochemistry
Julie Fourneau, Marie-Hélène Canu, Caroline Cieniewski-Bernard, Bruno Bastide, Erwan Dupont
In human, a chronic sensorimotor perturbation (SMP) through prolonged body immobilization alters motor task performance through a combination of peripheral and central factors. Studies performed on a rat model of SMP have shown biomolecular changes and a reorganization of sensorimotor cortex through events such as morphological modifications of dendritic spines (number, length, functionality). However, underlying mechanisms are still unclear. It is well known that phosphorylation regulates a wide field of synaptic activity leading to neuroplasticity...
May 28, 2018: Journal of Neurochemistry
Margaret H Hastings, Alvin Qiu, Congyao Zha, Carole A Farah, Yacine Mahdid, Larissa Ferguson, Wayne S Sossin
The Small Optic Lobes (SOL) calpain is a highly conserved member of the calpain family expressed in the nervous system. A dominant negative form of the SOL calpain inhibited consolidation of one form of synaptic plasticity, non-associative facilitation, in sensory-motor neuronal cultures in Aplysia, presumably by inhibiting cleavage of protein kinase Cs (PKCs) into constitutively active protein kinase Ms (PKMs) (Hu et al, 2017a). SOL calpains have a conserved set of 5-6 N-terminal zinc fingers. Bioinformatic analysis suggests that these zinc fingers could bind to ubiquitin...
May 28, 2018: Journal of Neurochemistry
Corey J Anderson, Anja Kahl, Liping Qian, Anna Stepanova, Anatoly Starkov, Giovanni Manfredi, Costantino Iadecola, Ping Zhou
Prohibitin (PHB) is a ubiquitously expressed and evolutionarily conserved mitochondrial protein with multiple functions. We have recently shown that PHB upregulation offers robust protection against neuronal injury in models of cerebral ischemia in vitro and in vivo, but the mechanism by which PHB affords neuroprotection remains to be elucidated. Here, we manipulated PHB expression in PC12 neural cells to investigate its impact on mitochondrial function and the mechanisms whereby it protects cells exposed to oxidative stress...
May 28, 2018: Journal of Neurochemistry
Sarah C Hopp, Nathan A Bihlmeyer, John P Corradi, Charles Vanderburg, Angela M Cacace, Sudeshna Das, Timothy W Clark, Rebecca A Betensky, Bradley T Hyman, Eloise Hudry
Synaptic dysfunction and loss are core pathological features in Alzheimer disease (AD). In the vicinity of amyloid-β plaques in animal models, synaptic toxicity occurs and is associated with chronic activation of the phosphatase calcineurin (CN). Indeed, pharmacological inhibition of CN blocks amyloid-β synaptotoxicity. We therefore hypothesized that CN-mediated transcriptional changes may contribute to AD neuropathology and tested this by examining the impact of CN overexpression on neuronal gene expression in vivo...
May 28, 2018: Journal of Neurochemistry
Diana Scholz, Yana Chernyshova, Anna-Katharina Ückert, Marcel Leist
The initial step in the amyloidogenic cascade of amyloid precursor protein (APP) processing is catalyzed by beta-site APP-cleaving enzyme (BACE), and this protease has increased activities in affected areas of Alzheimer's disease brains. We hypothesized that altered APP processing, due to augmented BACE activity, would affect the actions of direct and indirect BACE inhibitors. We therefore compared postmitotic human neurons (LUHMES) with their BACE-overexpressing counterparts (BLUHMES). Although β-cleavage of APP was strongly increased in BLUHMES, they produced less full-length and truncated amyloid beta (Aβ) than LUHMES...
May 27, 2018: Journal of Neurochemistry
Matteo Audano, Anja Schneider, Nico Mitro
In the last decades, lysosomes and mitochondria were considered distinct and physically separated organelles involved in different cellular functions. While lysosomes were thought to exclusively be the rubbish dump of the cell involved in the degradation of proteins and other cell compartments, mitochondria were considered solely involved in the oxidation of energy substrate to get ATP, together with other minor duties. Nowadays, our view of these organelles is profoundly changed since studies demonstrated that mitochondria and lysosome are mutually functional, maintaining proper cell homeostasis...
May 27, 2018: Journal of Neurochemistry
Mandana Hunter, Nicholas J Demarais, Richard L M Faull, Angus C Grey, Maurice A Curtis
The human subventricular zone (SVZ) has a defined cytological and neurochemical architecture, with four constituent laminae that act in concert to support its neurogenic activity. Lipidomic specialisation has previously been demonstrated in the neurologically-normal human SVZ, with enrichment of functionally important lipid classes in each lamina. The SVZ is also responsive to neurodegenerative disorders, where thickening of the niche and enhanced proliferation of resident cells were observed in Huntington's disease (HD) brains...
May 27, 2018: Journal of Neurochemistry
Rishi Sharma, Pradeep Sahota, Mahesh M Thakkar
Binge alcohol drinking, a risky pattern of alcohol consumption, has severe consequences toward health and well-being of an individual, his family and society. Although, binge drinking has detrimental effects on sleep, underlying mechanisms are unknown. We used adult male C57BL/6J mice and exposed them to a single, four-hour session of binge alcohol self-administration, in stress-free environment, to examine neuronal mechanisms affecting sleep. We first verified binge pattern of alcohol consumption. When allowed to self-administer alcohol in a non-stressful environment, mice consumed alcohol in a binge pattern...
May 27, 2018: Journal of Neurochemistry
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