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Molecular and Cellular Neurosciences

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https://www.readbyqxmd.com/read/28433463/actin-regulation-by-tropomodulin-and-tropomyosin-in-neuronal-morphogenesis-and-function
#1
REVIEW
Kevin T Gray, Alla S Kostyukova, Thomas Fath
Actin is a profoundly influential protein; it impacts, among other processes, membrane morphology, cellular motility, and vesicle transport. Actin can polymerize into long filaments that push on membranes and provide support for intracellular transport. Actin filaments have polar ends: the fast-growing (barbed) end and the slow-growing (pointed) end. Depolymerization from the pointed end supplies monomers for further polymerization at the barbed end. Tropomodulins (Tmods) cap pointed ends by binding onto actin and tropomyosins (Tpms)...
April 19, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28427888/dopamine-elevates-intracellular-zinc-concentration-in-cultured-rat-embryonic-cortical-neurons-through-the-camp-nitric-oxide-signaling-cascade
#2
Hui-Hsing Hung, Lung-Sen Kao, Pei-Shan Liu, Chien-Chang Huang, De-Ming Yang, Chien-Yuan Pan
Zinc ion (Zn(2+)), the second most abundant transition metal after iron in the body, is essential for neuronal activity and also induces toxicity if the concentration is abnormally high. Our previous results show that exposure of cultured cortical neurons to dopamine elevates intracellular Zn(2+) concentrations ([Zn(2+)]i) and induces autophagosome formation but the mechanism is not clear. In this study, we characterized the signaling pathway responsible for the dopamine-induced elevation of [Zn(2+)]i and the effect of [Zn(2+)]i in modulating the autophagy in cultured rat embryonic cortical neurons...
April 17, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28414095/crosstalk-control-and-limits-of-physiological-c-jun-n-terminal-kinase-activity-for-cell-viability-and-neurite-stability-in-differentiated-pc12-cells
#3
Vicki Waetzig, Milana Belzer, Wiebke Haeusgen, Ruwen Boehm, Ingolf Cascorbi, Thomas Herdegen
The c-Jun N-terminal kinases (JNKs) are important mediators of cell viability and structural integrity in postmitotic neurons, which is required for maintaining synaptic connections and neural plasticity. In the present study, we chose differentiated PC12 cells as a well-characterised neuronal model system to selectively examine the regulation of basal JNK activity by extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt. We detected a complex interaction between the kinases to prevent cell death and neurite loss...
April 14, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28414096/lysine-specific-demethylase-1-lsd1-depletion-disrupts-monogenic-and-monoallelic-odorant-receptor-or-expression-in-an-olfactory-neuronal-cell-line
#4
Rutesh Vyas, Diane Meredith, Robert P Lane
Function of the mammalian olfactory system depends on specialized olfactory sensory neurons (OSNs) that each express only one allele ("monoallelic") of one odorant receptor (OR) gene ("monogenic"). The lysine-specific demethylase-1 (LSD1) protein removes activating H3K4 or silencing H3K9 methylation marks in a variety of developmental contexts, and is thought to be important for proper OR regulation. Most of the focus in the field has been on a potential "activating" function for LSD1; e.g., in the demethylation of H3K9 associated with the expressed OR allele...
April 13, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28404507/paclitaxel-inhibits-the-activity-and-membrane-localization-of-pkc%C3%AE-and-pkc%C3%AE-i-ii-to-elicit-a-decrease-in-stimulated-calcitonin-gene-related-peptide-release-from-cultured-sensory-neurons
#5
Lisa M Darby, Hongdi Meng, Jill C Fehrenbacher
Peripheral neuropathy is a dose-limiting and debilitating side effect of the chemotherapeutic drug, paclitaxel. Consequently, elucidating the mechanisms by which this drug alters sensory neuronal function is essential for the development of successful therapeutics for peripheral neuropathy. We previously demonstrated that chronic treatment with paclitaxel (3-5days) reduces neuropeptide release stimulated by agonists of TRPV1. Because the activity of TRPV1 channels is modulated by conventional and novel PKC isozymes (c/nPKC), we investigated whether c/nPKC mediate the loss of neuropeptide release following chronic treatment with paclitaxel (300nM; 3 and 5days)...
April 9, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28385508/molecular-and-cellular-neuroscience-special-issue
#6
EDITORIAL
Takeshi Sakurai, Alexander Dityatev, Andreas Faissner, Fritz Rathjen, Esther Stoeckli, Gianfranco Gennarini, Andrew Furley, Daniela Puzzo, Peter Burbach
No abstract text is available yet for this article.
April 3, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28363876/neuronal-polarization-from-spatiotemporal-signaling-to-cytoskeletal-dynamics
#7
REVIEW
Max Schelski, Frank Bradke
Neuronal polarization establishes distinct molecular structures to generate a distinct axon and multiple dendrites. Studies over the past years indicate that this efficient separation is brought about by a network of feedback loops. Axonal growth seems to play a major role in fueling those feedback loops and thereby stabilizing neuronal polarity. Indeed, various effectors involved in feedback loops play key roles in axonal growth by ultimately acting on the actin and microtubule cytoskeleton. These effectors have key roles in interconnecting actin and microtubule dynamics - a mechanism crucial to commanding the growth of axons...
March 28, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28359843/it-takes-a-village-to-raise-a-branch-cellular-mechanisms-of-the-initiation-of-axon-collateral-branches
#8
REVIEW
Lorena Armijo-Weingart, Gianluca Gallo
The formation of axon collateral branches from the pre-existing shafts of axons is an important aspect of neurodevelopment and the response of the nervous system to injury. This article provides an overview of the role of the cytoskeleton and signaling mechanisms in the formation of axon collateral branches. Both the actin filament and microtubule components of the cytoskeleton are required for the formation of axon branches. Recent work has begun to shed light on how these two elements of the cytoskeleton are integrated by proteins that functionally or physically link the cytoskeleton...
March 27, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28347630/tubulins-and-brain-development-the-origins-of-functional-specification
#9
REVIEW
Martin W Breuss, Ines Leca, Thomas Gstrein, Andi H Hansen, David A Keays
The development of the vertebrate central nervous system is reliant on a complex cascade of biological processes that include mitotic division, relocation of migrating neurons, and the extension of dendritic and axonal processes. Each of these cellular events requires the diverse functional repertoire of the microtubule cytoskeleton for the generation of forces, assembly of macromolecular complexes and transport of molecules and organelles. The tubulins are a multi-gene family that encode for the constituents of microtubules, and have been implicated in a spectrum of neurological disorders...
March 24, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28318914/systemic-and-network-functions-of-the-microtubule-associated-protein-tau-implications-for-tau-based-therapies
#10
REVIEW
Lidia Bakota, Abdala Ussif, Gunnar Jeserich, Roland Brandt
Tau is a microtubule-associated neuronal protein, whose primary role was long thought to regulate axonal microtubule assembly. Tau is subject to many posttranslational modifications and can aggregate into neurofibrillary tangles, which are considered to be a hallmark of several neurodegenerative diseases collectively called "tauopathies". The most common tauopathy is Alzheimer's disease, where tau pathology correlates with sites of neurodegeneration. Tau belongs to the class of intrinsically disordered proteins, which are known to interact with many partners and are considered to be involved in various signaling, regulation and recognition processes...
March 16, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28300646/developmental-changes-in-trak-mediated-mitochondrial-transport-in-neurons
#11
Omar Loss, F Anne Stephenson
Previous studies established that the kinesin adaptor proteins, TRAK1 and TRAK2, play an important role in mitochondrial transport in neurons. They link mitochondria to kinesin motor proteins via a TRAK acceptor protein in the mitochondrial outer membrane, the Rho GTPase, Miro. TRAKs also associate with enzyme, O-linked N-acetylglucosamine transferase (OGT), to form a quaternary, mitochondrial trafficking complex. A recent report suggested that TRAK1 preferentially controls mitochondrial transport in axons of hippocampal neurons whereas TRAK2 controls mitochondrial transport in dendrites...
March 11, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28286248/cell-migration-in-schizophrenia-patient-derived-cells-do-not-regulate-motility-in-response-to-extracellular-matrix
#12
Jing Yang Tee, Ratneswary Sutharsan, Yongjun Fan, Alan Mackay-Sim
Schizophrenia is a highly heritable psychiatric disorder linked to a large number of risk genes. The function of these genes in disease etiology is not fully understood but pathway analyses of genomic data suggest developmental dysregulation of cellular processes such as neuronal migration and axon guidance. Previous studies of patient-derived olfactory cells show them to be more motile than control-derived cells when grown on a fibronectin substrate, motility that is dependent on focal adhesion kinase signaling...
March 9, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28286294/specific-suppression-of-microgliosis-cannot-circumvent-the-severe-neuropathology-in-peroxisomal-%C3%AE-oxidation-deficient-mice
#13
L Beckers, S Stroobants, S Verheijden, B West, R D'Hooge, M Baes
An important hallmark of various neurodegenerative disorders is the proliferation and activation of microglial cells, the resident immune cells of the central nervous system (CNS). Mice that lack multifunctional protein-2 (MFP2), the key enzyme in peroxisomal β-oxidation, develop excessive microgliosis that positively correlates with behavioral deficits whereas no neuronal loss occurs. However, the precise contribution of neuroinflammation to the fatal neuropathology of MFP2 deficiency remains largely unknown...
March 7, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28286293/a-role-for-astrocytes-in-cerebellar-deficits-in-frataxin-deficiency-protection-by-insulin-like-growth-factor-i
#14
C Franco, L Genis, J A Navarro, P Perez-Domper, A M Fernandez, S Schneuwly, I Torres Alemán
Inherited neurodegenerative diseases such as Friedreich's ataxia (FRDA), produced by deficiency of the mitochondrial chaperone frataxin (Fxn), shows specific neurological deficits involving different subset of neurons even though deficiency of Fxn is ubiquitous. Because astrocytes are involved in neurodegeneration, we analyzed whether they are also affected by frataxin deficiency and contribute to the disease. We also tested whether insulin-like growth factor I (IGF-I), that has proven effective in increasing frataxin levels both in neurons and in astrocytes, also exerts in vivo protective actions...
March 7, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28268126/actin-based-growth-cone-motility-and-guidance
#15
REVIEW
Omotola F Omotade, Stephanie L Pollitt, James Q Zheng
Nerve growth cones, the dilated tip of developing axons, are equipped with exquisite abilities to sense environmental cues and to move rapidly through complex terrains of developing brain, leading the axons to their specific targets for precise neuronal wiring. The actin cytoskeleton is the major component of the growth cone that powers its directional motility. Past research has provided significant insights into the mechanisms by which growth cones translate extracellular signals into directional migration...
March 6, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28238890/time-lapse-imaging-of-p65-and-i%C3%AE%C2%BAb%C3%AE-translocation-kinetics-following-ca-2-induced-neuronal-injury-reveals-biphasic-translocation-kinetics-in-surviving-neurons
#16
Robert Schwamborn, Heiko Düssmann, Hans-Georg König, Jochen H M Prehn
The transcription factor nuclear factor-κB (NF-κB) regulates neuronal differentiation, plasticity and survival. It is well established that excitatory neurotransmitters such as glutamate control NF-κB activity. Glutamate receptor overactivation is also involved in ischemic- and seizure-induced neuronal injury and neurodegeneration. However, little is known at the single cell-level how NF-κB signaling relates to neuronal survival during excitotoxic injury. We found that silencing of p65/NF-κB delayed N-methyl-d-aspartate (NMDA)-induced excitotoxic injury in hippocampal neurons, suggesting a functional role of p65 in excitotoxicity...
February 24, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28254618/parkin-promotes-proteasomal-degradation-of-synaptotagmin-iv-by-accelerating-polyubiquitination
#17
Hiroyuki Kabayama, Naoko Tokushige, Makoto Takeuchi, Miyuki Kabayama, Mitsunori Fukuda, Katsuhiko Mikoshiba
Parkin is an E3 ubiquitin ligase whose mutations cause autosomal recessive juvenile Parkinson's disease (PD). Unlike the human phenotype, parkin knockout (KO) mice show no apparent dopamine neuron degeneration, although they demonstrate reduced expression and activity of striatal mitochondrial proteins believed to be necessary for neuronal survival. Instead, parkin-KO mice show reduced striatal evoked dopamine release, abnormal synaptic plasticity, and non-motor symptoms, all of which appear to mimic the preclinical features of Parkinson's disease...
February 22, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28188885/trpm5-expression-in-the-olfactory-epithelium
#18
Martina Pyrski, Eugenia Eckstein, Andreas Schmid, Bernd Bufe, Jan Weiss, Vladimir Chubanov, Ulrich Boehm, Frank Zufall
The Ca(2+)-activated monovalent cation channel Trpm5 is a key element in chemotransduction of taste receptor cells of the tongue, but the extent to which Trpm5 channels are expressed in olfactory sensory neurons (OSNs) of the main olfactory epithelium (MOE) of adult mice as part of a specific pheromonal detection system is debated. Here, we used a novel Trpm5-IRES-Cre knockin strain to drive Cre recombinase expression, employed previously validated Trpm5 antibodies, performed in situ hybridization experiments to localize Trpm5 RNA, and searched extensively for Trpm5 splice variants in genetically-labeled, Trpm5-expressing MOE cells...
February 8, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28185854/a-dual-role-for-the-rhogef-ephexin5-in-regulation-of-dendritic-spine-outgrowth
#19
A M Hamilton, J T Lambert, L K Parajuli, O Vivas, D K Park, I S Stein, J N Jahncke, M E Greenberg, S S Margolis, K Zito
The outgrowth of new dendritic spines is closely linked to the formation of new synapses, and is thought to be a vital component of the experience-dependent circuit plasticity that supports learning. Here, we examined the role of the RhoGEF Ephexin5 in driving activity-dependent spine outgrowth. We found that reducing Ephexin5 levels increased spine outgrowth, and increasing Ephexin5 levels decreased spine outgrowth in a GEF-dependent manner, suggesting that Ephexin5 acts as an inhibitor of spine outgrowth...
February 7, 2017: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/28163190/rho-gtpase-activating-proteins-regulators-of-rho-gtpase-activity-in-neuronal-development-and-cns-diseases
#20
REVIEW
Guo-Hui Huang, Zhao-Liang Sun, Hong-Jiang Li, Dong-Fu Feng
The Rho family of small GTPases was considered as molecular switches in regulating multiple cellular events, including cytoskeleton reorganization. The Rho GTPase-activating proteins (RhoGAPs) are one of the major families of Rho GTPase regulators. RhoGAPs were initially considered negative mediators of Rho signaling pathways via their GAP domain. Recent studies have demonstrated that RhoGAPs also regulate numerous aspects of neuronal development and are related to various neurodegenerative diseases in GAP-dependent and GAP-independent manners...
February 3, 2017: Molecular and Cellular Neurosciences
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