Journal of Neurochemistry
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In AβPP-over expressing cultured human muscle fibers proteasome inhibition enhances phosphorylation of AβPP751 and GSK3β activation: effects mitigated by lithium and apparently relevant to sporadic inclusion-body
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Muscle fiber degeneration in sporadic inclusion-body myositis (s-IBM) is characterized by accumulation of multiprotein aggregates, including aggregated amyloid-[beta] (A[beta])-precursor protein 751 (A[beta]PP751), A[beta], phosphorylated tau, and other 'Alzheimer-characteristic' proteins. Proteasome inhibition is an important component of the s-IBM pathogenesis. In brains of Alzheimer's disease (AD) patients and AD transgenic-mouse models, phosphorylation of neuronal A[beta]PP695 (p-A[beta]PP) on Thr668 (equivalent to T724 of A[beta]PP751) is considered detrimental because it increases generation of cytotoxic A[beta] and ...
Source: Journal of Neurochemistry - November 18, 2009 Category: Neurology Authors: Chiara Terracciano, Anna Nogalska, W. King Engel, Valerie Askanas Source Type: journals
ACh receptors link two signaling pathways to neuroprotection against glutamate-induced excitotoxicity in isolated RGCsEmail this article to a colleague.
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Previous studies have reported that activation of nicotinic acetylcholine (ACh) receptors (nAChRs) on cultured pig retinal ganglion cells (RGCs) has a neuroprotective effect against glutamate-induced excitotoxicity. However, the mechanism linking nAChRs to neuroprotection is unknown. Here, we tested the hypothesis that signaling cascades involving p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) [rarr] Akt are involved in linking activation of nAChRs to neuroprotection in isolated pig RGCs. In ELISA studies, regulation of phosphorylated p38 MAPK and Akt were analyzed after inducing excit...
Source: Journal of Neurochemistry - November 12, 2009 Category: Neurology Authors: Chinwe O. Asomugha, David M. Linn, Cindy L. Linn Source Type: journals
The loop between β-strands β2 and β3 and its interaction with the N-terminal α-helix is essential for biogenesis of α7 nicotinic receptorsEmail this article to a colleague.
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Recently, we have shown that the [alpha]-helix present at the N-termini of [alpha]7 nicotinic acetylcholine receptors plays a crucial role in their biogenesis. Structural data suggest that this helix interacts with the loop linking [beta]-strands [beta]2 and [beta]3 (loop 3). We studied the role of this loop as well as its interaction with the helix in membrane receptor expression. Residues from Asp62 to Val75 in loop 3 were mutated. Mutations of conserved amino acids, such as Asp62, Leu65 and Trp67 abolished membrane receptor expression in Xenopus oocytes. Others mutations, at residues Asn68, Ala69, Ser70, Tyr72, Gly74, a...
Source: Journal of Neurochemistry - November 7, 2009 Category: Neurology Authors: Manuel Criado, José Mulet, Mar Castillo, Susana Gerber, Salvador Sala, Francisco Sala Source Type: journals
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(Source: Journal of Neurochemistry)
Source: Journal of Neurochemistry - November 6, 2009 Category: Neurology Source Type: journals
Granulocyte-macrophage colony-stimulating factor antibody suppresses microglial activity: implications for anti-inflammatory effects in Alzheimer's Disease and multiple sclerosisEmail this article to a colleague.
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The objective of our study was to determine granulocyte-macrophage colony-stimulating factor (GM-CSF) activity in the brain following GM-CSF induction. We injected recombinant mouse GM-CSF into the brains of 8-month-old C57BL6 mice via intracerebroventricular injections and studied the activities of microglia, astrocytes, and neurons. We also sought to determine whether an anti-GM-CSF antibody could suppress endogenous microglial activity in the C57BL6 mice and could also suppress microglial activity induced by the recombinant mouse GM-CSF in another group of C57BL6 mice. Using quantitative real-time RT-PCR, we assessed mi...
Source: Journal of Neurochemistry - November 4, 2009 Category: Neurology Authors: P. Hemachandra Reddy, Maria Manczak, Wei Zhao, Kazuhiro Nakamura, Christopher Bebbington, Geoffrey Yarranton, Peizhong Mao Source Type: journals
Cholesterol metabolism and transport in the pathogenesis of Alzheimer's diseaseEmail this article to a colleague.
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Alzheimer's disease (AD) is the most common neurodegenerative disorder, affecting millions of people worldwide. Apart from age, the major risk factor identified so far for the sporadic form of AD is possession of the ɛ4 allele of apolipoprotein E (APOE), which is also a risk factor for coronary artery disease (CAD). Other apolipoproteins known to play an important role in CAD such as apolipoprotein B are now gaining attention for their role in AD as well. AD and CAD share other risk factors, such as altered cholesterol levels, particularly high levels of low density lipoproteins together with low levels of high dens...
Source: Journal of Neurochemistry - November 3, 2009 Category: Neurology Authors: Ian J. Martins, Tamar Berger, Matthew J. Sharman, Giuseppe Verdile, Stephanie J. Fuller, Ralph N. Martins Source Type: journals
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(Source: Journal of Neurochemistry)
Source: Journal of Neurochemistry - October 30, 2009 Category: Neurology Source Type: journals
The microtubule interacting drug candidate NAP protects against kainic acid toxicity in a rat model of epilepsyEmail this article to a colleague.
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NAP (NAPVSIPQ, generic name, davunetide), a neuroprotective peptide in clinical development for neuroprotection against Alzheimer's disease and other neurodegenerative indications, has been recently shown to provide protection against kainic acid excitotoxicity in hippocampal neuronal cultures. In vivo, kainic acid toxicity models status epilepticus that is associated with hippocampal cell death. Kainic acid toxicity has been previously suggested to involve the microtubule cytoskeleton and NAP is a microtubule-interacting drug candidate. In the current study, kainic acid-treated rats showed epileptic seizures and neuronal ...
Source: Journal of Neurochemistry - October 29, 2009 Category: Neurology Authors: Ilona Zemlyak, Nathan Manley, Inna Vulih-Shultzman, Andrew B. Cutler, Kevin Graber, Robert M. Sapolsky, Illana Gozes Source Type: journals
AP-1 inhibitory peptides are neuroprotective following acute glutamate excitotoxicity in primary cortical neuronal culturesEmail this article to a colleague.
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In this study, we tested 19 recently isolated AP-1 inhibitory peptides, fused to the cell penetrating peptide TAT, for their efficacy in preventing cell death in cortical neuronal cultures following glutamate excitotoxicity. Five peptides (PYC19D-TAT, PYC35D-TAT, PYC36D-TAT, PYC38D-TAT, PYC41D-TAT) displayed neuroprotective activity in concentration responses in both l- and retro-inverso d-isoforms with increasing levels of neuroprotection peaking at 83%. Interestingly, the D-TAT peptide displayed a neuroprotective effect increasing neuronal survival to 25%. Using an AP-1 luciferase reporter assay, we confirmed that the AP...
Source: Journal of Neurochemistry - October 28, 2009 Category: Neurology Authors: Amanda J. Meade, Bruno P. Meloni, Jane Cross, Anthony J. Bakker, Mark W. Fear, Frank L. Mastaglia, Paul M. Watt, Neville W. Knuckey Source Type: journals
A point mutation in the ectodomain-transmembrane 2 interface eliminates the inhibitory effects of ethanol in P2X4 receptorsEmail this article to a colleague.
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ATP-gated P2X4 receptors (P2X4R) are abundantly expressed in the CNS. However, little is known about the molecular targets for ethanol action in P2X4Rs. The current investigation tested the hypothesis that the ectodomain-transmembrane (TM) interface contains residues that are important for the action of ethanol in P2X4Rs. Wild type (WT) and mutant P2X4R were expressed in Xenopus oocytes. ATP concentration[ndash]response curves and ethanol (10[ndash]200 mM)-induced changes in ATP EC10-gated currents were determined using two-electrode voltage clamp ([minus]70 mV). Alanine substitution at the ectodomain-TM1 interface (positi...
Source: Journal of Neurochemistry - October 28, 2009 Category: Neurology Authors: Maya Popova, Liana Asatryan, Olga Ostrovskaya, Letisha R. Wyatt, Kaixun Li, Ronald L. Alkana, Daryl L. Davies Source Type: journals
Relative positioning of diazepam in the benzodiazepine-binding-pocket of GABAA receptorsEmail this article to a colleague.
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We describe here such proximity-accelerated chemical coupling reactions of [alpha]1S205C and [alpha]1T206C with a diazepam derivative modified at the C-3 position with a reactive isothiocyanate group ([ndash]NCS). We also provide new data that identify [alpha]1H101C and [alpha]1N102C as exclusive sites of the reaction of a diazepam derivative where the [ndash]Cl atom is replaced by a [ndash]NCS group. Based on these observations we propose a relative positioning of diazepam within the benzodiazepine-binding site of [alpha]1[beta]2[gamma]2 receptors. (Source: Journal of Neurochemistry)
Source: Journal of Neurochemistry - October 28, 2009 Category: Neurology Authors: Kelly R. Tan, Roland Baur, Sébastien Charon, Maurice Goeldner, Erwin Sigel Source Type: journals
Structural and functional characterization of a novel FE65 protein product up-regulated in cognitively impaired FE65 knockout miceEmail this article to a colleague.
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FE65 is a multi-modular adaptor protein that binds the cytoplasmic tail of the [beta]-amyloid precursor protein (APP). Genetic evidence suggests that APP is intimately involved in the pathogenesis of dementias of the Alzheimer type, neurodegenerative disorders that affect multiple cognitive domains, including learning and memory. Evidence from p97FE65-specific knockout mice (lacking the 97 kDa full-length FE65 protein, p97FE65) suggests an important role for FE65 in learning and memory. Interpretation of the learning and memory phenotype, however, is complicated by the up-regulation (compared with wild-type mice) of a nove...
Source: Journal of Neurochemistry - October 27, 2009 Category: Neurology Authors: Bethany H. Cool, Galynn Zitnik, George M. Martin, Qubai Hu Source Type: journals
Elevated sulfatide levels in neurons cause lethal audiogenic seizures in miceEmail this article to a colleague.
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Galactosylceramide (GalCer) and 3-O-sulfo-GalCer (sulfatide) are abundant sphingolipids in myelinating glial cells. However, low levels of GalCer and sulfatide have also been found in neurons, though their physiological role in these cells is unknown. Transgenic mice over-expressing UDP-galactose : ceramide galactosyltransferase (CGT) under control of the Thy1.2 promoter synthesize C18 : 0 fatty acid containing GalCer and sulfatide in neurons. Depending on the genetic background, these transgenic mice have a significantly reduced life span. Transgenic mice were extremely sensitive to sound stimuli and displayed lethal audi...
Source: Journal of Neurochemistry - October 27, 2009 Category: Neurology Authors: Rebekka van Zyl, Volkmar Gieselmann, Matthias Eckhardt Source Type: journals
Combinatorial interaction between two human serotonin transporter gene variable number tandem repeats and their regulation by CTCFEmail this article to a colleague.
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Two distinct variable number tandem repeats (VNTRs) within the human serotonin transporter gene (SLC6A4) have been implicated as predisposing factors for CNS disorders. The linked polymorphic region in the 5'-promoter exists as short (s) and long (l) alleles of a 22 or 23 bp elements. The second within intron 2 (Stin2) exists as three variants containing 9, 10 or 12 copies of a 16 or 17 bp element. These VNTRs, individually or in combination, supported differential reporter gene expression in rat neonate prefrontal cortical cultures. The level of reporter gene activity from the dual VNTR constructs indicated combinatorial ...
Source: Journal of Neurochemistry - October 26, 2009 Category: Neurology Authors: Fahad R. Ali, Sylvia A. Vasiliou, Kate Haddley, Ursula M. Paredes, Julian C. Roberts, Fabio Miyajima, Elena Klenova, Vivien J. Bubb, John P. Quinn Source Type: journals
Photoperiodic regulation of retinoic acid signaling in the hypothalamusEmail this article to a colleague.
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Both retinoic acid (RA) and thyroid hormone (TH) regulate transcription via specific nuclear receptors. TH regulates hypothalamic homeostasis and active T3 is generated by deiodinase enzymes in tanycytes surrounding the third ventricle. However, RA has not been previously considered in such a role. Data presented here highlights novel parallels between the TH and RA synthetic pathways in the hypothalamus implying that RA also acts to regulate hypothalamic gene expression and function. Key elements of the RA cellular signaling pathway were shown to be regulated in the rodent hypothalamus. Retinoid synthetic enzymes and the ...
Source: Journal of Neurochemistry - October 26, 2009 Category: Neurology Authors: Kirsty D. Shearer, Timothy H. Goodman, Alexander W. Ross, Laura Reilly, Peter J. Morgan, Peter J. McCaffery Source Type: journals
Nature and consequences of mammalian brain and CSF efflux transporters: four decades of progressEmail this article to a colleague.
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In the last 40 years, especially with the application of new neurochemical and molecular biological techniques, there has been explosive progress in understanding how certain ligands and drugs are transported across the blood-brain barrier and choroid plexus out of brain and CSF. In the CNS, there are several separate efflux transporters with very broad specificity that are responsible for much of the efflux transport. This review focuses on three such transporters: organic acid transporter-3, peptide transporter-2 and P-glycoprotein for which there is substantial new information including 'knockout' models in mice and, in...
Source: Journal of Neurochemistry - October 26, 2009 Category: Neurology Authors: Reynold Spector Source Type: journals
A novel role for calcium/calmodulin kinase II within the brainstem pedunculopontine tegmentum for the regulation of wakefulness and rapid eye movement sleepEmail this article to a colleague.
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Considerable evidence suggests that the brainstem pedunculopontine tegmentum (PPT) neurons are critically involved in the regulation of rapid eye movement (REM) sleep and wakefulness (W); however, the molecular mechanisms operating within the PPT to regulate these two behavioral states remain relatively unknown. Here we demonstrate that the levels of calcium/calmodulin kinase II (CaMKII) and phosphorylated CaMKII expression in the PPT decreased and increased with 'low W with high REM sleep' and 'high W/low REM sleep' periods, respectively. These state-specific expression changes were not observed in the cortex, or in the i...
Source: Journal of Neurochemistry - October 26, 2009 Category: Neurology Authors: Edward C. Stack, Frank Desarnaud, Donald F. Siwek, Subimal Datta Source Type: journals
Changes in cholesterol biosynthetic and transport pathways after excitotoxicityEmail this article to a colleague.
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The present study was carried out to elucidate changes in the gene expression and activity of cholesterol biosynthetic enzymes and transporters in the rat hippocampus after kainate excitotoxicity. Significantly increased cholesterol level was detected in the degenerating hippocampus, reaching double normal levels at 1 week after kainate injury. RT-PCR analyses of hippocampal homogenates showed significantly decreased mRNA expression of the transcription factor controlling cholesterol biosynthesis SREBP-2, and the rate-controlling enzyme HMG-CoA (3-hydroxy-3-methyl-glutaryl-CoA) reductase at all time points after kainate in...
Source: Journal of Neurochemistry - October 24, 2009 Category: Neurology Authors: Ji-Hyun Kim, Jinatta Jittiwat, Wei-Yi Ong, Akhlaq A. Farooqui, Andrew M. Jenner Source Type: journals
Disease-toxicant screen reveals a neuroprotective interaction between Huntington's disease and manganese exposureEmail this article to a colleague.
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We report that striatal cells expressing mutant Huntingtin exhibit elevated sensitivity to cadmium toxicity and resistance to manganese toxicity. This neuroprotective gene[ndash]environment interaction with manganese is highly specific, as it does not occur with iron, copper, zinc, cobalt, cadmium, lead, or nickel ions. Analysis of the Akt cell stress signaling pathway showed diminished activation with manganese exposure and elevated activation after cadmium exposure in the mutant cells. Direct examination of intracellular manganese levels found that mutant cells have a significant impairment in manganese accumulation. Fur...
Source: Journal of Neurochemistry - October 21, 2009 Category: Neurology Authors: B. Blairanne Williams, Daphne Li, Michal Wegrzynowicz, Bhavin K. Vadodaria, Joel G. Anderson, Gunnar F. Kwakye, Michael Aschner, Keith M. Erikson, Aaron B. Bowman Source Type: journals
The TRPC6 channel activator hyperforin induces the release of zinc and calcium from mitochondriaEmail this article to a colleague.
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This study was undertaken to further characterize the cellular neuronal responses induced by hyperforin. Experiments conducted on cortical neurons in primary culture and loaded with fluorescent probes for Ca2+ (Fluo-4) and Zn2+ (FluoZin-3) showed that it not only controls the activity of plasma membrane channels but it also mobilizes these two cations from internal pools. Experiments conducted on isolated brain mitochondria indicated that hyperforin, like the inhibitor of oxidative phosphorylation, carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP), collapses the mitochondrial membrane potential. Furthermore, it p...
Source: Journal of Neurochemistry - October 21, 2009 Category: Neurology Authors: Peng Tu, Julien Gibon, Alexandre Bouron Source Type: journals
Delayed activin A administration attenuates tissue death after transient focal cerebral ischemia and is associated with decreased stress-responsive kinase activationEmail this article to a colleague.
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In this study, the ability of exogenous activin A to attenuate injury from transient middle cerebral artery occlusion was tested in adult mice. Intracerebroventricular administration of activin A prior to middle cerebral artery occlusion reduced infarct volume apparent 1 day after experimental stroke. A single activin A administration at 6 h following ischemia/reperfusion reduced lesion volumes at 1 and 3 days and led to improved neurobehavior. Moreover, activin A treatment spared neurons within the ischemic hemisphere and led to a concomitant reduction in microglial activation. Activation of the stress-responsive kinases ...
Source: Journal of Neurochemistry - October 20, 2009 Category: Neurology Authors: Shibani S. Mukerji, Riley N. Rainey, Jamie L. Rhodes, Alison K. Hall Source Type: journals
Inactivation of cytochrome c oxidase by mutant SOD1s in mouse motoneuronal NSC-34 cells is independent from copper availability but is because of nitric oxideEmail this article to a colleague.
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The copper-enzyme cytochrome c oxidase (Cytox) has been indicated as a primary molecular target of mutant copper, zinc superoxide dismutase (SOD1) in familial amyotrophic lateral sclerosis (fALS); however, the mechanism underlying its inactivation is still unclear. As the toxicity of mutant SOD1s could arise from their selective recruitment to mitochondria, it is conceivable that they might compete with Cytox for the mitochondrial copper pool causing Cytox inactivation. To investigate this issue, we used mouse motoneuronal neuroblastoma × spinal cord cell line-34, stably transfected for the inducible expression of low amo...
Source: Journal of Neurochemistry - October 20, 2009 Category: Neurology Authors: Mario Arciello, Concetta Rosa Capo, Mauro Cozzolino, Alberto Ferri, Monica Nencini, Maria Teresa Carrì, Luisa Rossi Source Type: journals
Blood levels of kynurenines, interleukin-23 and soluble human leucocyte antigen-G at different stages of Huntington's diseaseEmail this article to a colleague.
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There is substantial evidence that abnormal concentrations of oxidised tryptophan metabolites, produced via the kynurenine pathway, contribute to progressive neurodegeneration in Huntington's disease. We have now examined the blood levels of these metabolites in patients at different stages of Huntington's disease, assessed both in terms of clinical disease severity and numbers of CAG repeats. Close relatives of the patients were included in the study as well as unrelated healthy controls. Levels of lipid peroxidation products, the pro-inflammatory cytokine interleukin (IL)-23 and the soluble human leucocyte antigen-G (sHL...
Source: Journal of Neurochemistry - October 20, 2009 Category: Neurology Authors: Caroline M. Forrest, Gillian M. Mackay, Nicholas Stoy, Sarah L. Spiden, Rohan Taylor, Trevor W. Stone, L. Gail Darlington Source Type: journals
Hypoxia-inducible factor 1: a new hope to counteract neurodegeneration?Email this article to a colleague.
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Neurodegenerative diseases, generally characterized by a progressive deterioration in the structure and function of the brain, represent one of the world's major unsolved health problems. Therefore, it is urgent to discover therapeutic targets for the design of effective strategies for the treatment of these diseases. Recent findings demonstrated that the induction of the hypoxia signaling pathway with the concomitant stabilization and transcriptional activation of the transcription factor hypoxia-inducible factor 1 (HIF-1) could mediate neuroprotective events. It has been shown that HIF-1 triggers the expression of genes ...
Source: Journal of Neurochemistry - October 20, 2009 Category: Neurology Authors: Sónia C. Correia, Paula I. Moreira Source Type: journals
Murine cathepsin D deficiency is associated with dysmyelination/myelin disruption and accumulation of cholesteryl esters in the brainEmail this article to a colleague.
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Cathepsin D (CTSD) deficiencies are fatal neurological diseases that in human infants and in sheep are characterized by extreme loss of neurons and myelin. To date, similar morphological evidence for myelin disruption in CTSD knockout mice has not been reported. Here, we show that CTSD deficiency leads to pronounced myelin changes in the murine brain: myelin-related proteolipid protein and myelin basic protein were both markedly reduced at postnatal day 24, and the amount of lipids characteristically high in myelin (e.g. plasmalogen-derived alkenyl chains and glycosphingolipid-derived 20- and 24-carbon acyl chains) were si...
Source: Journal of Neurochemistry - October 20, 2009 Category: Neurology Authors: Aino-Liisa Mutka, Aleksi Haapanen, Reijo Käkelä, Maria Lindfors, Ann K. Wright, Teija Inkinen, Martin Hermansson, Anne Rokka, Garry Corthals, Matti Jauhiainen, Thomas H. Gillingwater, Elina Ikonen, Jaana Tyynelä Source Type: journals
Immunoreactivity of the phosphorylated axonal neurofilament H subunit (pNF-H) in blood of ALS model rodents and ALS patients: evaluation of blood pNF-H as a potential ALS biomarkerEmail this article to a colleague.
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Levels of neurofilament subunits, potential biomarkers of motor axon breakdown, are increased in amyotrophic lateral sclerosis (ALS) patient's CSF but data on blood are not available. We measured blood levels of the phosphorylated axonal form of neurofilament H (pNF-H) by ELISA in transgenic rodent models of superoxide dismutase 1 (SOD1) ALS, and in 20 ALS patients and 20 similar aged controls monthly for 4 months. All symptomatic rodent ALS models showed robust levels of blood pNF-H, while control rodents or mice transgenic for unmutated SOD1 showed no detectable blood pNF-H. Average pNF-H levels in the G93A SOD1 mouse pr...
Source: Journal of Neurochemistry - October 18, 2009 Category: Neurology Authors: Kevin Boylan, Cui Yang, Julia Crook, Karen Overstreet, Michael Heckman, Yong Wang, David Borchelt, Gerry Shaw Source Type: journals
Vesicular monoamine transporter 2 and dopamine transporter are molecular targets of Pitx3 in the ventral midbrain dopamine neuronsEmail this article to a colleague.
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Midbrain dopamine (mDA) neurons play critical roles in the regulation of voluntary movement and their dysfunction is associated with Parkinson's disease. Pitx3 has been implicated in the proper development of mDA neurons in the substantia nigra pars compacta, which are selectively lost in Parkinson's disease. However, the basic mechanisms underlying its role in mDA neuron development and/or survival are poorly understood. Toward this goal, we sought to identify downstream target genes of Pitx3 by comparing gene expression profiles in mDA neurons of wild-type and Pitx3-deficient aphakia mice. This global gene expression ana...
Source: Journal of Neurochemistry - October 16, 2009 Category: Neurology Authors: Dong-Youn Hwang, Sunghoi Hong, Joo-Won Jeong, Sangdun Choi, Hansoo Kim, Jangwoo Kim, Kwang-Soo Kim Source Type: journals
Nemo-like kinase is involved in NGF-induced neurite outgrowth via phosphorylating MAP1B and paxillinEmail this article to a colleague.
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Nerve growth factor (NGF) promotes neurite outgrowth through regulating cytoskeletal organization and cell adhesion. These activities are modulated by protein phosphorylation. Nemo-like kinase (NLK) is an evolutionarily conserved MAP kinase-like kinase that phosphorylates several transcription factors. Although NLK is known to be expressed at relatively high levels in the nervous system, its function is not well understood. We found that NGF promotes the translocation of NLK to PC12 cells' leading edges, and triggers NLK kinase activity in them. Activated NLK directly phosphorylates microtubule-associated protein-1B (MAP1B...
Source: Journal of Neurochemistry - October 15, 2009 Category: Neurology Authors: Tohru Ishitani, Shizuka Ishitani, Kunihiro Matsumoto, Motoyuki Itoh Source Type: journals
Increased intranuclear matrix metalloproteinase activity in neurons interferes with oxidative DNA repair in focal cerebral ischemiaEmail this article to a colleague.
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Increased matrix metalloproteinase (MMP) activity is implicated in proteolysis of extracellular matrix in ischemic stroke. We recently observed intranuclear MMP activity in ischemic brain neurons at early reperfusion, suggesting a possible role in nuclear matrix proteolysis. Nuclear proteins, poly-ADP-ribose polymerase-1 (PARP-1) and X-ray cross-complementary factor 1 (XRCC1), as well as DNA repair enzymes, are important in DNA fragmentation and cell apoptosis. We hypothesized that intranuclear MMP activity facilitates oxidative injury in neurons during early ischemic insult by cleaving PARP-1 and XRCC1, interfering with D...
Source: Journal of Neurochemistry - October 15, 2009 Category: Neurology Authors: Yi Yang, Eduardo Candelario-Jalil, Jeffrey F. Thompson, Eloy Cuadrado, Eduardo Y. Estrada, Anna Rosell, Joan Montaner, Gary A. Rosenberg Source Type: journals
Early undernutrition increases glycogen content and reduces the activated forms of GSK3, AMPK, p38 MAPK, and JNK in the cerebral cortex of suckling ratsEmail this article to a colleague.
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In this study, we examined the effects of early undernutriton on molecular targets of insulin actions such as glucose transporters, glycogen, glycogen synthase kinase-3 (GSK3) and mitogen-activated protein kinases, as well as proteins involved in apoptosis in the cortex from 10-day-old rats. We show that undernutrition results in an enhanced glycogen content which is confined to astrocytes, according to our histochemical approaches. Cortical phospho-GSK3 is also increased. In addition to glycogen synthesis, GSK3 regulates crucial cellular processes. Therefore, its elevated degree of phosphorylation may have an impact on th...
Source: Journal of Neurochemistry - October 15, 2009 Category: Neurology Authors: Esther Lizárraga-Mollinedo, Elisa Fernández-Millán, Laura de Miguel-Santos, Carlos José Martínez-Honduvilla, Carmen Alvarez, Fernando Escrivá Source Type: journals
CaMKII associates with CaV1.2 L-type calcium channels via selected β subunits to enhance regulatory phosphorylationEmail this article to a colleague.
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Calcium/calmodulin-dependent kinase II (CaMKII) facilitates L-type calcium channel (LTCC) activity physiologically, but may exacerbate LTCC-dependent pathophysiology. We previously showed that CaMKII forms stable complexes with voltage-gated calcium channel (VGCC) [beta]1b or [beta]2a subunits, but not with the [beta]3 or [beta]4 subunits (Grueter et al. 2008). CaMKII-dependent facilitation of CaV1.2 LTCCs requires Thr498 phosphorylation in the [beta]2a subunit (Grueter et al. 2006), but the relationship of this modulation to CaMKII interactions with LTCC subunits is unknown. Here we show that CaMKII co-immunoprecipitates ...
Source: Journal of Neurochemistry - October 15, 2009 Category: Neurology Authors: Sunday A. Abiria, Roger J. Colbran Source Type: journals
Regulation of increased glutamatergic input to spinal dorsal horn neurons by mGluR5 in diabetic neuropathic painEmail this article to a colleague.
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Diabetic neuropathic pain is associated with increased glutamatergic input in the spinal dorsal horn. Group I metabotropic glutamate receptors (mGluRs) are involved in the control of neuronal excitability, but their role in the regulation of synaptic transmission in diabetic neuropathy remains poorly understood. Here we studied the role of spinal mGluR5 and mGluR1 in controlling glutamatergic input in a rat model of painful diabetic neuropathy induced by streptozotocin. Whole-cell patch-clamp recordings of lamina II neurons were performed in spinal cord slices. The amplitude of excitatory post-synaptic currents (EPSCs) evo...
Source: Journal of Neurochemistry - October 15, 2009 Category: Neurology Authors: Ji-Qing Li, Shao-Rui Chen, Hong Chen, You-Qing Cai, Hui-Lin Pan Source Type: journals
Protein aggregation in neurons following OGD: a role for Na+ and Ca2+ ionic dysregulationEmail this article to a colleague.
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In this study, we investigated whether disruption of Na+ and Ca2+ homeostasis via activation of Na+-K+-Cl[minus] cotransporter isoform 1 (NKCC1) and reversal of Na+/Ca2+ exchange (NCXrev) affects protein aggregation and degradation following oxygen[ndash]glucose deprivation (OGD). Cultured cortical neurons were subjected to 2 h OGD and 1[ndash]24 h reoxygenation (REOX). Redistribution of ubiquitin and formation of ubiquitin-conjugated protein aggregates occurred in neurons as early as 2 h REOX. The protein aggregation progressed further by 8 h REOX. There was no significant recovery at 24 h REOX. Moreover, the proteasome a...
Source: Journal of Neurochemistry - October 15, 2009 Category: Neurology Authors: Xinzhi Chen, Douglas B. Kintner, Akemichi Baba, Toshio Matsuda, Gary E. Shull, Dandan Sun Source Type: journals
Multifunctional roles of enolase in Alzheimer's disease brain: beyond altered glucose metabolismEmail this article to a colleague.
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Enolase enzymes are abundantly expressed, cytosolic carbon-oxygen lyases known for their role in glucose metabolism. Recently, enolase has been shown to possess a variety of different regulatory functions, beyond glycolysis and gluconeogenesis, associated with hypoxia, ischemia, and Alzheimer's disease (AD). AD is an age-associated neurodegenerative disorder characterized pathologically by elevated oxidative stress and subsequent damage to proteins, lipids, and nucleic acids, appearance of neurofibrillary tangles and senile plaques, and loss of synapse and neuronal cells. It is unclear if development of a hypometabolic env...
Source: Journal of Neurochemistry - October 13, 2009 Category: Neurology Authors: D. Allan Butterfield, Miranda L. Bader Lange Source Type: journals
Hippocampal seizures alter the expression of the pannexin and connexin transcriptomeEmail this article to a colleague.
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Some forms of seizure activity can be stopped by gap junctional (GJ) blockade. Here, we found that GJ blockers attenuate hippocampal seizure activity induced by a novel seizuregenic protocol using Co2+. We hypothesized that this activity may occur because of the altered expression of connexin (Cx) and/or pannexin (Panx) mRNAs and protein. We found a 1.5-, 1.4-, and 2-fold increase in Panx1, Panx2, and Cx43 mRNAs, respectively. Significant post-translational modifications of the proteins Cx43 and Panx1 were also observed after the Co2+ treatment. No changes were observed in the presence of tetrodotoxin, indicating that seiz...
Source: Journal of Neurochemistry - October 13, 2009 Category: Neurology Authors: Shanthini Mylvaganam, Liang Zhang, Chiping Wu, Zhang Jane Zhang, Marina Samoilova, James Eubanks, Peter L. Carlen, Michael O. Poulter Source Type: journals
Role of M2, M3, and M4 muscarinic receptor subtypes in the spinal cholinergic control of nociception revealed using siRNA in ratsEmail this article to a colleague.
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Muscarinic acetylcholine receptors (mAChRs) are involved in the control of nociception in the spinal cord. The M2, M3, and M4 mAChR subtypes are present in the spinal dorsal horn. However, the role of the individual subtypes in the anti-nociceptive effect produced by mAChR agonists is uncertain. Here, we determined the contribution of M2, M3, and M4 subtypes to spinal muscarinic analgesia by using small-interference RNA (siRNA) targeting specific mAChR subtypes in rats. The neuronal uptake and distribution of a chitosan-siRNA conjugated fluorescent dye in the spinal cord and dorsal root ganglion were confirmed after intrat...
Source: Journal of Neurochemistry - October 12, 2009 Category: Neurology Authors: You-Qing Cai, Shao-Rui Chen, Hee-Dong Han, Anil K. Sood, Gabriel Lopez-Berestein, Hui-Lin Pan Source Type: journals
Alzheimer's β-amyloid peptide blocks vascular endothelial growth factor mediated signaling via direct interaction with VEGFR-2Email this article to a colleague.
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In this study, we examined the effects of A[beta]1[ndash]42 on vascular endothelial growth factor receptor 2 (VEGFR-2) signaling, which plays a key role in angiogenesis. A[beta] inhibited VEGF-induced migration of endothelial cells, as well as VEGF-induced permeability of an in vitro model of the blood brain barrier. Consistently, exogenous VEGF dose-dependently antagonized the anti-angiogenic activity of A[beta] in a capillary network assay. A[beta]1[ndash]42 also blocked VEGF-induced tyrosine phosphorylation of VEGFR-2 in two types of primary endothelial cells, suggesting an antagonistic action of A[beta] toward VEGFR-2 ...
Source: Journal of Neurochemistry - October 10, 2009 Category: Neurology Authors: Nikunj S. Patel, Venkatarajan S. Mathura, Corbin Bachmeier, David Beaulieu-Abdelahad, Vincent Laporte, Ophelia Weeks, Michael Mullan, Daniel Paris Source Type: journals
Bilirubin selectively inhibits cytochrome c oxidase activity and induces apoptosis in immature cortical neurons: assessment of the protective effects of glycoursodeoxycholic acidEmail this article to a colleague.
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High levels of unconjugated bilirubin (UCB) may initiate encephalopathy in neonatal life, mainly in pre-mature infants. The molecular mechanisms of this bilirubin-induced neurologic dysfunction (BIND) are not yet clarified and no neuroprotective strategy is currently worldwide accepted. Here, we show that UCB, at conditions mimicking those of hyperbilirubinemic newborns (50 [mu]M UCB in the presence of 100 [mu]M human serum albumin), rapidly (within 1 h) inhibited cytochrome c oxidase activity and ascorbate-driven oxygen consumption in 3 days in vitro rat cortical neurons. This was accompanied by a bioenergetic and oxidati...
Source: Journal of Neurochemistry - October 10, 2009 Category: Neurology Authors: Ana Rita Vaz, Maria Delgado-Esteban, Maria Alexandra Brito, Juan P. Bolaños, Dora Brites, Angeles Almeida Source Type: journals
In vivo neurochemical profiling of rat brain by 1H-[13C] NMR spectroscopy: cerebral energetics and glutamatergic/GABAergic neurotransmissionEmail this article to a colleague.
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The quantification of excitatory and inhibitory neurotransmission and the associated energy metabolism is crucial for a proper understanding of brain function. Although the detection of glutamatergic neurotransmission in vivo by 13C NMR spectroscopy is now relatively routine, the detection of GABAergic neurotransmission in vivo has remained elusive because of the low GABA concentration and spectral overlap. Using 1H-[13C] NMR spectroscopy at high magnetic field in combination with robust spectral modeling and the use of different substrates, [U-13C6]-glucose and [2-13C]-acetate, it is shown that GABAergic, as well as gluta...
Source: Journal of Neurochemistry - October 10, 2009 Category: Neurology Authors: Pieter van Eijsden, Kevin L. Behar, Graeme F. Mason, Kees P. J. Braun, Robin A. de Graaf Source Type: journals
Membrane-initiated estradiol signaling increases tyrosine hydroxylase promoter activity with ERα in PC12 cellsEmail this article to a colleague.
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Tyrosine hydroxylase (TH) promoter activity is induced by 17[beta]-estradiol (E2) in PC12 cells expressing estradiol receptor-alpha (ER[alpha]) requiring a cAMP/calcium response element (CRE/CaRE) at [minus]45. To examine whether membrane-initiated estradiol signaling is underlying this induction, cells co-transfected with TH reporter construct and ER[alpha] expression vector were exposed to membrane-impermeant estradiol conjugate ([beta]-estradiol-6-(O-carboxy-methyl) oxime-bovine serum albumin, E2BSA). TH promoter activity was elevated by E2BSA in dose- and time-dependent manner. E2BSA also elicited rapid phosphorylation...
Source: Journal of Neurochemistry - October 10, 2009 Category: Neurology Authors: Shreekrishna Maharjan, Lidia I. Serova, Esther L. Sabban Source Type: journals
Mechanisms involved in the neurotoxic effects of environmental toxicants such as polychlorinated biphenyls and brominated flame retardantsEmail this article to a colleague.
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Many toxic substances have been distributed to the environment, some of which have properties that promote accumulation and biomagnification in living organisms. Approximately 1.2 million metric tons of polychlorinated biphenyls (PCBs) have been produced and about 30% have been discharged to the environment. Approximately 200 000 metric tons of brominated flame retardants (BFRs) are produced annually, of which considerable amounts have been spread globally, even to the Polar Regions. Behavioral testing of animals has shown that these compounds may affect learning, memory and fine motor functions. Animals are most sensitive...
Source: Journal of Neurochemistry - October 10, 2009 Category: Neurology Authors: Frode Fonnum, Espen Mariussen Source Type: journals
Cyclo(His-Pro) up-regulates heme oxygenase 1 via activation of Nrf2-ARE signallingEmail this article to a colleague.
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Paraquat (1,1'-dimethyl-4,4'-bipyridinium), a widely used non-selective herbicide, is a redox cycling agent with adverse effects on dopamine systems. Epidemiological data have shown that exposure to paraquat is one of the several risk factors for Parkinson's disease. We have already shown that cyclo(His-Pro), an endogenous cyclic dipeptide produced by the cleavage of the thyrotropin releasing hormone, has a cytoprotective effect through a mechanism involving Nrf2 activation that decreases production of reactive oxygen species and increases glutathione synthesis. Using primary neuronal cultures and PC12 cells as targets of ...
Source: Journal of Neurochemistry - October 8, 2009 Category: Neurology Authors: Alba Minelli, Carmela Conte, Silvia Grottelli, Ilaria Bellezza, Carla Emiliani, Juan P. Bolaños Source Type: journals
Inactivation of neuronal forebrain A2A receptors protects dopaminergic neurons in a mouse model of Parkinson's diseaseEmail this article to a colleague.
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Adenosine A2A receptors antagonists produce neuroprotective effects in animal models of Parkinson's disease (PD). As neuroinflammation is involved in PD pathogenesis, both neuronal and glial A2A receptors might participate to neuroprotection. We employed complementary pharmacologic and genetic approaches to A2A receptor inactivation, in a multiple MPTP mouse model of PD, to investigate the cellular basis of neuroprotection by A2A antagonism. MPTP·HCl (20 mg/kg daily for 4 days) was administered in mice treated with the A2A antagonist SCH58261, or in conditional knockout mice lacking A2A receptors on forebrain neurons (fbn...
Source: Journal of Neurochemistry - October 8, 2009 Category: Neurology Authors: Anna R. Carta, Anil Kachroo, Nicoletta Schintu, Kui Xu, Michael A. Schwarzschild, Jadwiga Wardas, Micaela Morelli Source Type: journals
The molecular physiology of activity-dependent bulk endocytosis of synaptic vesiclesEmail this article to a colleague.
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Central nerve terminals release neurotransmitter in response to a wide variety of stimuli. Because maintenance of neurotransmitter release is dependent on the continual supply of synaptic vesicles (SVs), nerve terminals possess an array of endocytosis modes to retrieve and recycle SV membrane and proteins. During mild stimulation conditions, single SV retrieval modes such as clathrin-mediated endocytosis predominate. However, during increased neuronal activity, additional SV retrieval capacity is required, which is provided by activity-dependent bulk endocytosis (ADBE). ADBE is the dominant SV retrieval mechanism during el...
Source: Journal of Neurochemistry - October 7, 2009 Category: Neurology Authors: Emma L. Clayton, Michael A. Cousin Source Type: journals
Central amylin expression and its induction in rat damsEmail this article to a colleague.
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In this study, regulations of postpartum mRNA expressions were investigated in the preoptic area of the hypothalamus. mRNA levels of lactating dams and mothers whose pups were removed immediately after delivery were compared in microarray experiments. There were 20 genes identified with significantly increased and 14 with decreased expression 9 days postpartum. Amylin mRNA level demonstrated the largest change, a 25.7 times increase. Quantitative RT-PCR measurements validated the increase in the mRNA level of amylin in the preoptic area of lactating dams while the expression level of other members of the calcitonin gene-re...
Source: Journal of Neurochemistry - October 7, 2009 Category: Neurology Authors: Arpád Dobolyi Source Type: journals
Functional effects of somatostatin receptor 1 activation on synaptic transmission in the mouse hippocampusEmail this article to a colleague.
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Somatostatin-14 (SRIF) co-localizes with GABA in the hippocampus and regulates neuronal excitability. A role of SRIF in the control of hippocampal activity has been proposed, although the exact contribution of each SRIF receptor (sst1[ndash]sst5) in mediating SRIF action requires some clarification. We used hippocampal slices of wild-type and sst1 knockout (KO) mice and selective pharmacological tools to provide conclusive evidence for a role of sst1 in mediating SRIF inhibition of synaptic transmission. With single- and double-label immunohistochemistry, we determined the distribution of sst1 in hippocampal slices and we ...
Source: Journal of Neurochemistry - October 7, 2009 Category: Neurology Authors: Maurizio Cammalleri, Davide Martini, Anna Maria Timperio, Paola Bagnoli Source Type: journals
Amyloid precursor protein 695 associates with assembled NR2A- and NR2B-containing NMDA receptors to result in the enhancement of their cell surface deliveryEmail this article to a colleague.
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This is a study of the interaction between the two NMDA neurotransmitter receptor subtypes, NR1/NR2A and NR1/NR2B, and amyloid precursor protein (APP) 695, the major APP variant expressed in neurones. APP695 co-immunoprecipitated with assembled NR1-1a/NR2A and NR1-1a/NR2B NMDA receptors following expression in mammalian cells. Single NR1-1a, NR1-2a, NR1-4bc-Myc, or NR2 subunit transfections revealed that co-association of APP695 with assembled NMDA receptors was mediated via the NR1 subunit; it was independent of the NR1 C1, C2, and C2' cassettes and, the use of an NR1-2ac-Myc-trafficking mutant suggested that interaction ...
Source: Journal of Neurochemistry - October 7, 2009 Category: Neurology Authors: Sarah L. Cousins, Sarah E. A. Hoey, F. Anne Stephenson, Michael S. Perkinton Source Type: journals
Nitric oxide and cyclic nucleotide signal transduction modulates synaptic vesicle turnover in human model neuronsEmail this article to a colleague.
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The human Ntera2 (NT2) teratocarcinoma cell line can be induced to differentiate into post-mitotic neurons. Here, we report that the human NT2 neurons generated by a spherical aggregate cell culture method express increasing levels of typical pre-synaptic proteins (synapsin and synaptotagmin I) along the neurite depending on the length of in vitro culture. By employing an antibody directed against the luminal domain of synaptotagmin I and the fluorescent dye N-(3-triethylammoniumpropyl)-4-(4-(dibutylamino)styryl)pyridinium dibromide, we show that depolarized NT2 neurons display calcium-dependent exo-endocytotic synaptic ve...
Source: Journal of Neurochemistry - October 6, 2009 Category: Neurology Authors: Million Adane Tegenge, Michael Stern, Gerd Bicker Source Type: journals
Cannabinoids prevent the opposite regulation of astroglial connexin43 hemichannels and gap junction channels induced by pro-inflammatory treatmentsEmail this article to a colleague.
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Brain injuries as well as neurodegenerative diseases, are associated with neuro-inflammation characterized by astroglial and microglial activation and/or proliferation. Recently, we reported that lipopolysaccharide (LPS)-activation of microglia inhibits junctional channels and promotes hemichannels, two connexin43 functions in astrocytes. This opposite regulation is mediated by two pro-inflammatory cytokines, interleukin-1 beta and tumor necrosis factor-alpha, released from activated microglia. Because cannabinoids (CBs) have anti-inflammatory properties and their receptors are expressed by glial cells, we investigated on ...
Source: Journal of Neurochemistry - October 5, 2009 Category: Neurology Authors: Nicolas Froger, Juan A. Orellana, Martine Cohen-Salmon, Pascal Ezan, Edwige Amigou, Juan C. Sáez, Christian Giaume Source Type: journals
Amyloid β serves as an NGF-like neurotrophic factor or acts as a NGF antagonist depending on its concentrationEmail this article to a colleague.
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In the nervous system, both the shape and connectivity of neurons are strongly influenced by soluble, extracellular factors. Indeed, we recently demonstrated that after binding to p75NTR, the common neurotrophin receptor, nerve growth factor (NGF) controls the morphology and connectivity of cultured mouse hippocampal neurons by encouraging the production of fewer yet longer dendrites, and by augmenting GABAergic connectivity. These effects of NGF are mediated by the differential expression of Enhancer-of-split 1/5 homologs and neurogenin 3. Amyloid [beta] (A[beta]), a pathogenic agent in Alzheimer's disease (AD) is known t...
Source: Journal of Neurochemistry - October 5, 2009 Category: Neurology Authors: Maria-Ángeles Arevalo, Pedro M. Roldan, Pedro J. Chacón, Alfredo Rodríguez-Tebar Source Type: journals
