Journal of Neurochemistry (J NEUROCHEM)
The Journal of Neurochemistry is the leading source for current research worldwide on the molecular chemical and cellular biology of the nervous system. Each issue contains dozens of full-length presentations of significant original findings written by investigators at leading medical and research institutions around the world. The Journal of Neurochemistry is devoted to the prompt publication of high-quality original findings in areas relevant to molecular chemical and cell biological aspects of the nervous system. Papers that are wholly pharmalogical histochemical or immunological and methods papers or the cloning of confirmatory sequences that do not advance knowledge in neurochemistry are not normally considered. The Journal particularly encourages submissions in the areas of molecular and cellular biology. A highlight of each issue is the Journal's critically acclaimed Rapid Communications section presenting new ideas and data of particular importance and timeliness. The Journal's Mini-Reviews present concise self-contained summaries of current research in particularly important areas.
- Impact factor4.06Show impact factor historyHide impact factor history
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Other titlesJournal of neurochemistry, JNC
Material typePeriodical, Internet resource
Document typeJournal / Magazine / Newspaper, Internet Resource
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Publications in this journal
Journal of Neurochemistry 04/2013;
Article: Near complete adaptation of the PRiMA knockout to the lack of central acetylcholinesterase.Farar V, Mohr F, Legrand M, Lamotte d'Incamps B, Cendelin J, Leroy J, Abitbol M, Bernard V, Baud F, Fournet V, Houze P, Klein J, Plaud B, Tuma J, Zimmermann M, Ascher P, Hrabovska A, Myslivecek J, Krejci E.J Neurochem. 2012 Jul 2. doi: 10.1111/j.1471-4159.2012.07856.x. [Epub ahead of print][show abstract] [hide abstract]
ABSTRACT: Acetylcholinesterase (AChE) rapidly hydrolyzes acetylcholine. At the neuromuscular junction, AChE is mainly anchored in the extracellular matrix by the collagen Q (ColQ), whereas in the brain, AChE is tethered by the proline-rich membrane anchor (PRiMA). The AChE-deficient mice in which AChE has been deleted from all tissues, have severe handicaps. Surprisingly, PRiMA KO mice in which AChE is mostly eliminated from the brain show very few deficits. We now report that most of the changes observed in the brain of AChE-deficient mice, and in particular the high levels of ambient extracellular acetylcholine and the massive decrease of muscarinic receptors, are also observed in the brain of PRiMA KO. However, the two groups of mutants differ in their responses to AChE inhibitors. Since PRiMA KO mice and AChE-deficient mice have similar low AChE concentrations in the brain but differ in the AChE content of the peripheral nervous system, these results suggest that peripheral nervous system AChE, is a major target of AChE inhibitors, and that its absence in AChE- deficient mice is the main cause of the slow development and vulnerability of these mice. At the level of the brain, the adaptation to the absence of AChE is nearly complete. © 2012 The Authors Journal of Neurochemistry © 2012 International Society for Neurochemistry.Journal of Neurochemistry 07/2012; doi: 10.1111/j.1471-4159.2012.07856.x. [Epub ahead of print](doi: 10.1111/j.1471-4159.2012.07856.x. [Epub ahead of print]).
Article: 98. George Stoica, Gina Lungu, Nicole L. Bjorklund, Giulio Taglialatela, Zhang Xing, Veronica Chiu, Herbert H. Hill, James O. Schenk and Ian Murray. (2012) Potential role of alpha-synuclein in neurodegeneration: studies in a rat animal model. Journal of Neurochemistry. J. Neurochem. (2012) 10.1111/j.1471-4159.2012.07805.xJournal of Neurochemistry 06/2012;
Article: Elevated expression of brain-derived neurotrophic factor facilitates visual imprinting in chicks.Journal of Neurochemistry 01/2012;
Article: NEUROPROTECTION AFFORDED BY ADENOSINE A2A RECEPTOR BLOCKADE IS MODULATED BY CORTICOTROPHIN-RELEASING FACTOR (CRF) IN GLUTAMATE INJURED CORTICAL NEURONSJournal of Neurochemistry 01/2012;
Article: Role of the extracellular transmembrane domain interface in gating and pharmacology of a heteromeric neuronal nicotinic receptor. Aldea M, Castillo M, Mulet J, Sala S, Criado M, Sala F.Journal of Neurochemistry 05/2010;
Article: Reduced cerebral blood flow and oxygen consumption in cirrhosis patients with acute hepatic encephalopathyJournal of Neurochemistry 05/2009; 109:269-270.
Article: Melatonin and salicylic acid protect against striatal generation of 6-OHDA in mice treated with L-DOPA and MPTPJournal of Neurochemistry 07/2008; Vol 106 (Suppl-1)(9-28):56-57.
Article: Inhibitory effects of aripiprazole on interferon-gamma-induced microglial activation via intracellular Ca2+ regulation in vitro[show abstract] [hide abstract]
ABSTRACT: The activation of the inflammatory/immunological response system is suggested to be related to the pathophysiology of schizophrenia. Aripiprazole is a novel atypical antipsychotic, which is a high-affinity dopamine D(2) receptor partial agonist. Atypical antipsychotics, all of which have dopamine D(2) receptor antagonism, have recently reported to have significantly inhibitory effects on interferon (IFN)-gamma-induced microglial activation in vitro. In the present study, we investigated whether or not aripiprazole also has anti-inflammatory effect on IFN-gamma-induced microglial activation. Not quinpirole, dopamine D(2) full agonist, but aripiprazole significantly inhibited the generation of nitric oxide (NO) and tumor necrosis factor (TNF)-alpha from IFN-gamma-activated microglia and suppressed the IFN-gamma-induced elevation of intracellular Ca(2+) concentrations ([Ca(2+)](i)) in murine microglial cells. Increased [Ca(2+)](i) has been reported to be required, but by itself not sufficient, for the release of NO and certain cytokines. As a result, we can speculate that aripiprazole may inhibit IFN-gamma-induced microglial activation through the suppression of IFN-gamma-induced elevation of [Ca(2+)](i) in microglia. Our results demonstrated that not only antipsychotics which have dopamine D(2) receptor antagonism but also aripiprazole have anti-inflammatory effects via the inhibition of microglial activation. Antipsychotics may therefore have a potentially useful therapeutic effect on patients with schizophrenia by reducing the microglial inflammatory reactions.Journal of Neurochemistry 01/2008; 106(2):815-25.
Article: Adult astroglia is competent for Na+/Ca2+ exchanger-operated exocytotic glutamate release triggered by mild depolarization.[show abstract] [hide abstract]
ABSTRACT: Glutamate release induced by mild depolarization was studied in astroglial preparations from the adult rat cerebral cortex, that is acutely isolated glial sub-cellular particles (gliosomes), cultured adult or neonatal astrocytes, and neuron-conditioned astrocytes. K+ (15, 35 mmol/L), 4-aminopyridine (0.1, 1 mmol/L) or veratrine (1, 10 micromol/L) increased endogenous glutamate or [3H]D-aspartate release from gliosomes. Neurotransmitter release was partly dependent on external Ca2+, suggesting the involvement of exocytotic-like processes, and partly because of the reversal of glutamate transporters. K+ increased gliosomal membrane potential, cytosolic Ca2+ concentration [Ca2+]i, and vesicle fusion rate. Ca2+ entry into gliosomes and glutamate release were independent from voltage-sensitive Ca2+ channel opening; they were instead abolished by 2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiurea (KB-R7943), suggesting a role for the Na+/Ca2+ exchanger working in reverse mode. K+ (15, 35 mmol/L) elicited increase of [Ca2+]i and Ca2+-dependent endogenous glutamate release in adult, not in neonatal, astrocytes in culture. Glutamate release was even more marked in in vitro neuron-conditioned adult astrocytes. As seen for gliosomes, K+-induced Ca2+ influx and glutamate release were abolished by KB-R7943 also in cultured adult astrocytes. To conclude, depolarization triggers in vitro glutamate exocytosis from in situ matured adult astrocytes; an aptitude grounding on Ca2+ influx driven by the Na+/Ca2+ exchanger working in the reverse mode.Journal of Neurochemistry 12/2007; 103(3):1196-207.
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ABSTRACT: Seizures are a major complication of viral encephalitis. However, the mechanisms of seizure-associated neuronal dysfunction remain poorly understood. We report that intranasal inoculation with West Nile virus (WNV) (Sarafend) causes limbic seizures in C57BL/6 mice, but not in interferon (IFN)-gamma-deficient (IFN-gamma-/-) mice. Both strains showed similar levels of virus in the brain, as well as similar concentrations of the cytokines, tumor necrosis factor and interleukin-6, both of which can alter neuronal excitability. Experiments in chimeric IFN-gamma-/- mice reconstituted with IFN-gamma-producing leukocytes showed that IFN-gamma is not required during central nervous system infection for limbic seizure development, suggesting a role for IFN-gamma in the developing brain. This was supported responses to pentylenetetrazole, kainic acid (KA), and N-methyl-d-aspartate (NMDA). Both strains of mice exhibited similar behavior after pentylenetetrazole challenge. However, while NMDA and KA treatment resulted in characteristic seizures in C57BL/6 mice, these responses were diminished (NMDA treatment) or absent (KA treatment) in IFN-gamma-/- mice. Furthermore, NMDA-receptor blockade with MK-801 in WNV-infected C57BL/6 mice abrogated seizures and prolonged survival. Our data show that IFN-gamma plays an important role in the development of the excitatory seizure pathways in the brain and that these cascades become pathogenic in encephalitic WNV infection.Journal of Neurochemistry 12/2007; 103(3):1019-30.
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ABSTRACT: Incorporation of the epsilon subunit into the GABAA receptor has been suggested to confer unusual, but variable, biophysical and pharmacological characteristics to both recombinant and native receptors. Due to their structural similarity with the gamma subunits, epsilon subunits have been assumed to substitute at the single position of the gamma subunit in assembled receptors. However, prior work suggests that functional variability in epsilon-containing receptors may reflect alternative sites of incorporation and of not just one, but possibly multiple epsilon subunits in the pentameric receptor complex. Here we present data indicating that increased expression of epsilon, in conjunction with alpha2 and beta3 subunits, results in expression of GABAA receptors with correspondingly altered rectification, deactivation and levels of spontaneous openings, but not increased total current density. We also provide data that the epsilon subunit, like the beta3 subunit, can self-export and data from chimeric receptors suggesting that similarities between the assembly domains of the beta3 and the epsilon subunits may allow the epsilon subunit to replace the beta, as well as the gamma, subunit. The substitution of an epsilon for a beta, as well as the gamma subunit and formation of receptors with alternative patterns of assembly with respect to epsilon incorporation may underlie the observed variability in both biophysical and pharmacological properties noted not only in recombinant, but also in native receptors.Journal of Neurochemistry 12/2007; 103(3):1258-71.
Article: Modulation of amyloid-beta-induced and age-associated changes in rat hippocampus by eicosapentaenoic acid.[show abstract] [hide abstract]
ABSTRACT: The age-related deficit in long-term potentiation (LTP) in the dentate gyrus is positively correlated with hippocampal concentration of the pro-inflammatory cytokine, interleukin-1beta (IL-1beta). Previous evidence also indicates that the inhibition of LTP induced by intracerebroventricular injection of amyloid-beta(1-40) (Abeta) is accompanied by increased hippocampal IL-1beta concentration and IL-1beta-stimulated signalling, specifically activation of the stress-activated protein kinase, c-jun N-terminal kinase (JNK). We considered that the underlying age-related neuroinflammation may render older rats more susceptible to Abeta administration and, to investigate this, young, middle-aged and aged rats were injected intracerebroventricularly with Abeta or vehicle. Hippocampal IL-1beta concentration, JNK phosphorylation, expression of the putative Abeta receptor, Receptor for advanced glycation end products (RAGE) and the microglial cell surface marker, CD40 were assessed. We report that Abeta inhibited LTP in a concentration-dependent manner in young rats and that this was accompanied by concentration-dependent increases in hippocampal IL-1beta and expression of phosphorylated JNK, RAGE and CD40. While 20 micromol/L Abeta exerted no significant effect on LTP in young rats, it inhibited LTP in middle-aged and aged rats and the increased vulnerability of aged rats was associated with increased IL-1beta concentration. Treatment of rats with eicosapentaenoic acid attenuated the inhibitory effect of 60 micromol/L Abeta on LTP in young rats and the effect of 20 micromol/L Abeta in middle-aged and aged rats. We present evidence which indicates that the effect of eicosapentaenoic acid may be linked with its ability to stimulate activation of peroxisome proliferator-activated receptor gamma.Journal of Neurochemistry 12/2007; 103(3):914-26.
Article: bFGF promotes photoreceptor cell survival in vitro by PKA-mediated inactivation of glycogen synthase kinase 3beta and CREB-dependent Bcl-2 up-regulation.[show abstract] [hide abstract]
ABSTRACT: Although there is substantial evidence supporting the neuroprotective efficacy of basic fibroblast growth factor (bFGF) in the rodent retina there is no consensus to date as to the protective mechanism involved. We hypothesise that bFGF can assert its neuroprotective effects directly on mouse photoreceptors transduced via the activation of specific intracellular signalling pathways. In mouse photoreceptor-derived 661W cells, bFGF promoted a rapid inactivation of glycogen synthase kinase 3beta (GSK3beta) by phosphorylation at Ser9. The effects of bFGF on GSK3beta were dependent on protein kinase A (PKA) activation, as inhibition of this pathway blocked inactivation. Furthermore, bFGF protection against oxidative stress was dependent on PKA inactivation of GSK3beta as PKA inhibition attenuated bFGF-induced protection. Furthermore, transfection of cells with mutant dominant negative GSK3betaS9A that cannot be phosphorylated on Ser9 also abrogated neuroprotection. Activation of the transcription factor cAMP-response element binding protein (CREB) and subsequent up-regulation of Bcl-2 in response to bFGF was also dependent on PKA as inhibition with H-89 attenuated increased pCREB levels and Bcl-2 expression. These results indicate that the protective efficacy of bFGF in mouse photoreceptors involves PKA-dependent inactivation of GSK3beta and subsequent up-regulation of Bcl-2 via CREB activation.Journal of Neurochemistry 12/2007; 103(3):860-70.
Article: Early release of arachidonic acid prevents an otherwise immediate formation of toxic levels of peroxynitrite in astrocytes stimulated with lipopolysaccharide/interferon-gamma.[show abstract] [hide abstract]
ABSTRACT: Addition of bacterial lipopolysaccharides (LPS) and interferon-gamma (IFN-gamma) to rat astrocytes in primary culture promotes an early release of arachidonic acid (ARA) associated with an immediate inhibition of neuronal nitric oxide synthase (nNOS). Preventing the release of constitutive nitric oxide (NO) is indeed critical for activation of the nuclear factor kappa B, and for the expression of inducible nitric oxide synthase responsible for the formation of large amounts of NO. LPS/IFN-gamma also promotes an early release of superoxide, via activation of NADPH oxidase, but the generation of peroxynitrite (ONOO-) is prevented by the different timing of superoxide (minutes) and NO (hours) formation. Upstream inhibition of the ARA-dependent nNOS inhibitory signaling, however, caused the parallel release of superoxide and constitutive NO, thereby leading to formation of ONOO- levels triggering loss of ATP and mitochondrial membrane potential followed by the mitochondrial release of cytochrome c, activation of caspase 3 and morphological evidence of apoptosis. Nanomolar levels of exogenous ARA prevented all these events via inhibition of early ONOO- formation. Thus, the ARA-dependent nNOS inhibition observed in astrocytes exposed to pro-inflammatory stimuli, as LPS/IFN-gamma, is critical for both the expression of nuclear factor kappa B-dependent genes and for survival.Journal of Neurochemistry 12/2007; 103(3):904-13.
Article: Strain differences in basal and post-citalopram extracellular 5-HT in the mouse medial prefrontal cortex and dorsal hippocampus: relation with tryptophan hydroxylase-2 activity.[show abstract] [hide abstract]
ABSTRACT: We used the microdialysis technique to compare basal extracellular serotonin (5-HT) and the response to citalopram in different strains of mice with functionally different allelic forms of tryptophan hydroxylase-2 (TPH-2), the rate-limiting enzyme in brain 5-HT synthesis. DBA/2J, DBA/2N and BALB/c mice carrying the 1473G allele of TPH-2 had less dialysate 5-HT in the medial prefrontal cortex and dorsal hippocampus (DH) (20-40% reduction) than C57BL/6J and C57BL/6N mice carrying the 1473C allele. Extracellular 5-HT estimated by the zero-net flux method confirmed the result of conventional microdialysis. Citalopram, 1.25, 5 and 20 mg/kg, dose-dependently raised extracellular 5-HT in the medial prefrontal cortex of C57BL/6J mice, with maximum effect at 5 mg/kg, but had significantly less effect in DBA/2J and BALB/c mice and in the DH of DBA/2J mice. A tryptophan (TRP) load enhanced basal extracellular 5-HT in the medial prefrontal cortex of DBA/2J mice but did not affect citalopram's ability to raise cortical and hippocampal extracellular 5-HT. The impairment of 5-HT synthesis quite likely accounts for the reduction of basal 5-HT and the citalopram-induced rise in mice carrying the mutated enzyme. These findings might explain why DBA/2 and BALB/c mice do not respond to citalopram in the forced swimming test. Although TRP could be a useful strategy to improve the antidepressant effect of citalopram (Cervo et al. 2005), particularly in subjects with low 5-HT synthesis, the contribution of serotonergic and non-serotonergic mechanisms to TRP's effect remains to be elucidated.Journal of Neurochemistry 12/2007; 103(3):1111-20.
Article: Ethanol alters lipid profiles and phosphorylation status of AMP-activated protein kinase in the neonatal mouse brain.[show abstract] [hide abstract]
ABSTRACT: Previously, we have shown that ethanol-induced apoptosis in cultured neurons is accompanied by changes in cellular lipid profiles. In the present study, the effects of ethanol on brain lipid metabolism were studied using 7-day-old C57BL/6ByJ mice, which display apoptotic neurodegeneration upon exposure to ethanol. The brain lipids were extracted 4-24 h after the ethanol or saline treatment, and analyzed by TLC. We found that the levels of triglyceride, cholesterol ester, ceramide, and N-acylphosphatidylethanolamine increased significantly in the brains of ethanol-treated mice compared to those of saline-treated mice. Concomitantly, ethanol reduced Thr172 phosphorylation of AMP-activated protein kinase (AMPK) alpha subunits. Ethanol also reduced phosphorylation of acetyl-CoA carboxylase, a substrate of AMPK and a lipogenic enzyme known to be activated by dephosphorylation. In contrast, lipid profiles of 19-day-old mouse brains, which scarcely manifested neurodegeneration upon ethanol exposure, were not significantly affected by ethanol. Also, the basal levels of Thr172-phosphorylated AMPK alpha were lower in these brains than in 7-day-old mouse brains, and no detectable changes in the phosphorylation status were observed by ethanol treatment. Our findings indicate that the ethanol-induced apoptotic neurodegeneration observed in mice during restricted developmental periods is accompanied by alterations in both the lipid content and the activity of AMPK in the brain.Journal of Neurochemistry 12/2007; 103(3):1208-18.
Article: Peroxisome proliferator-activated receptor-alpha is required for the neurotrophic effect of oleic acid in neurons.[show abstract] [hide abstract]
ABSTRACT: Oleic acid synthesized by astrocytes behaves as a neurotrophic factor for neurons, up-regulating the molecular markers of axonal and dendritic outgrowth, growth-associated protein 43 and microtubule-associated protein 2. In this work, the nature of the receptor involved in this neurotrophic effect was investigated. As oleic acid has been reported to be a ligand and activator of the peroxisome proliferator-activated receptor (PPAR), we focus on this family of receptors. Our results show that PPARalpha, beta/delta, and gamma are expressed in neurons in culture. However, only the agonists of PPARalpha, Wy14643, GW7647 and oleoylethanolamide, promoted neuronal differentiation, while PPAR beta/delta and gamma agonists did not modify neuronal differentiation. Consequently, we investigated the involvement of PPARalpha (Nr1c1) in oleic acid-induced neuronal differentiation. Our results indicate that oleic acid activates PPARalpha in neurons. In addition, the effect of oleic acid on neuronal morphology, growth-associated protein 43 and microtubule-associated protein 2 expression decreases in neurons after PPARalpha has been silenced by small interfering RNA. Taken together, our results suggest that PPARalpha could be the receptor for oleic acid in neurons, further broadening the range of functions attributed to this family of transcription factors. Although several works have reported that PPARalpha could be involved in neuroprotection, the present work provides the first evidence suggesting a role of PPARalpha in neuronal differentiation.Journal of Neurochemistry 12/2007; 103(3):871-81.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
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