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Brain aging is a naturally occurring process resulting in the decline of cognitive functions and increased vulnerability to develop age-associated disorders. Fluctuation in lipid species is crucial for normal brain development and function. However, impaired lipid metabolism and changes in lipid composition in the brain have been increasingly recognized to play a crucial role in physiological aging, as well as in several neurodegenerative diseases. In the last decades, the role of sexual dimorphism in the vulnerability to develop age-related neurodegeneration has increased. However, further studies are warranted for detailed assessment of how age, sex, and additional non-biological factors may influence the lipid changes in brains. The aim of this work is to address the presence of sex differences in the brain lipid changes that occur along aging, and in the two most common age-related neurodegenerative disorders (Alzheimer's and Parkinson's diseases). We included the studies that assessed lipid-related alterations in the brain of both humans and experimental models. Additionally, we explored the influence of sex on lipid-lowering therapies. We conclude that sex exerts a notable effect on lipid modifications occurring with age and neurodegeneration, and in lipid-reducing interventions. Therefore, the application of sex as an experimental variable is strongly encouraged for future research in the field of precision medicine approach., (© 2023 The Authors. Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry.)

Epilepsy is a common neurological disorder associated with alterations of excitation-inhibition balance within brain neuronal networks. GABA A receptor neurotransmission is the most prevalent form of inhibitory neurotransmission and is strongly implicated in both the pathophysiology and treatment of epilepsy, serving as a primary target for antiseizure medications for over a century. It is now established that GABA exerts a multifaceted influence through an array of GABA A receptor subtypes that extends far beyond simply negating excitatory activity. As the role of GABA A neurotransmission within inhibitory circuits is elaborated, this will enable the development of precision therapies that correct the network dysfunction underlying epileptic pathology., (© 2023 International Society for Neurochemistry.)

The most obvious difference in science publishing between 'then' and 'now' is the dramatic change in the communication of data and in their interpretation. The democratization of science via the Internet has brought not only benefits but also challenges to publishing including fraudulent behavior and plagiarism, data and statistics reporting standards, authorship confirmation and other issues which affect authors, readers, and publishers in different ways. The wide accessibility of data on a global scale permits acquisition and meta-analysis to mine for novel synergies, and has created a highly commercialized environment. As we illustrate here, identifying unacceptable practices leads to changes in the standards for data reporting. [ABSTRACT FROM AUTHOR]

Microdialysis is a method to study the extracellular space in vivo, based on the principle of diffusion. It can be used to measure various small molecules including the neuroregulator adenosine. Baseline levels of the compounds measured with microdialysis vary over studies. We systematically reviewed the literature to investigate the full range of reported baseline concentrations of adenosine and adenosine monophosphate in microdialysates. We performed a meta‐regression analysis to study the influence of flow rate, probe membrane surface area, species, brain area and anaesthesia versus freely behaving, on the adenosine concentration. Baseline adenosine concentrations in microdialysates ranged from 0.8 to 2100 nM. There was limited evidence on baseline adenosine monophosphate concentrations in microdialysates. Across studies, we found effects of flow rate and anaesthesia versus freely behaving on dialysate adenosine concentrations (p ≤ 0.001), but not of probe membrane surface, species, or brain area (p ≥ 0.14). With increasing flow rate, adenosine concentrations decreased. With anaesthesia, adenosine concentrations increased. The effect of other predictor variables on baseline adenosine concentrations, for example, post‐surgical recovery time, could not be analysed because of a lack of reported data. This study shows that meta‐regression can be used as an alternative to new animal experiments to answer research questions in the field of neurochemistry. However, current levels of reporting of primary studies are insufficient to reach the full potential of this approach; 63 out of 133 studies could not be included in the analysis because of insufficient reporting, and several potentially relevant factors had to be excluded from the analyses. The level of reporting of experimental detail needs to improve. Microdialysis has long been used to measure neurotransmitters, with overwhelming variations in experimental designs. A systematic literature review is the optimal method to acquire a complete overview. We systematically reviewed the literature for baseline concentrations of adenosine in microdialysates. We then performed a meta‐regression analysis to study the effects of variations in experimental design. This study shows that meta‐regression can be used as an alternative to new animal experiments to answer research questions in the field of neurochemistry. However, current levels of reporting of primary studies are insufficient to reach the full potential of this approach; 63 out of 133 studies could not be included in the analysis because of insufficient reporting, and several potentially relevant factors had to be excluded from the analyses. Therefore, the standard of experimental detail reporting needs to improve. Picture by Julia M.L. Menon, syringe and vial adapted from Servier medical art. [ABSTRACT FROM AUTHOR]

Many journals, including the Journal of Neurochemistry, enable authors to list peer reviewers as 'preferred' or 'opposed' suggestions to the editor. At the Journal of Neurochemistry, the handling editor (HE) may follow recommendations or select non-author-suggested reviewers (non-ASRs). We investigated whether selection of authorsuggested reviewers (ASRs) influenced decisions on a paper, and whether differences might be related to a reviewer's, editor's or manuscript's geographical location. In this retrospective analysis, we compared original research articles submitted to the Journal of Neurochemistry from 2013 through 2016 that were either reviewed exclusively by non-ASRs, by at least one ASR, by at least one reviewer marked by the author as 'opposed' or none. Manuscript outcome, reviewer rating of manuscript quality, rating of the reviewers' performance by the editor (R-score), time to review, and the country of the editor, reviewers and manuscript author were analyzed using non-parametric rank-based comparisons, chisquare (x2) analysis, multivariate linear regression, one-way analysis of variance, and inter-rater reliability determination. Original research articles that had been reviewed by at least one ASR stood a higher chance of being accepted (525/1006 = 52%) than papers that had been reviewed by non-ASRs only (579/1800 = 32%). An article was 2.4 times more likely to be accepted than rejected by an ASR compared to a non-ASR (Pearson's x2(1) = 181.3, p < 0.05). At decision, the editor did not simply follow the reviewers' recommendation but had a balancing role: Rates of recommendation from reviewers for rejection were 11.2% (139/1241) with ASRs versus 29.0% (1379/4755) with non-ASRs (this is a ratio of 0.39 where 1 means no difference between rejection rates for both groups), whereas the proportion of final decisions to reject was 24.7% (248/1006) versus 45.7% (822/1800) (a ratio of 0.54, considerably closer to 1). Recommendations by non-ASRs were more favorable for manuscripts from USA/Canada and Europe than for Asia/Pacific or Other countries. ASRs judged North American manuscripts most favorably, and judged papers generally more positively (mean: 2.54 on a 1-5 scale) than did non-ASRs (mean: 3.16) reviewers, whereas time for review (13.28 vs. 13.20 days) did not differ significantly between these groups. We also found that editors preferably assigned reviewers from their own geographical region, but there was no tendency for reviewers to judge papers from their own region more favorably. Our findings strongly confirm a bias toward lower rejection rates when ASRs assess a paper, which led to the decision to abandon the option to recommend reviewers at the Journal of Neurochemistry. [ABSTRACT FROM AUTHOR]

This review reflects on the origins, development, publishing trends, and scientific directions of the Journal of Neurochemistry over its 60 year lifespan as seen by key contributors to the Journal's production. The Journal first appeared in May 1956 with just two issues published in that inaugural year. By 1963, it appeared monthly and, by 2002, 24 hard copy issues were published yearly. In 2014, the Journal became online only. For much of its time, the Journal was managed through two separate editorial offices each with their respective Chief Editor (the 'Western' and 'Eastern' hemispheres). The Journal was restructured to operate through a single editorial office and Editor-in-Chief from 2013. Scientifically, the Journal progressed through distinct scientific eras with the first two decades generally centered around developments in methodology followed by a period when publications delved deeper into underlying mechanisms. By the late 1980s, the Journal had entered the age of genetics and beyond, with an increasing focus on neurodegenerative diseases. Reviews have played a regular part in the success of J Neurochem with focused special and virtual issues being a highlight of recent years. Today, 60 years and onwards, J Neurochem continues to be a leading source of top-quality, original and review articles in neuroscience. We look forward to its continued success at the forefront of neurochemistry in the decades to come. [ABSTRACT FROM AUTHOR]

Hypoxia‐inducible factor (HIF‐1) as the primary factor mediating gene‐dependent cellular responses to hypoxia represents an attractive target for the therapeutic interventions. The current Editorial comments on an as yet underestimated facet of HIF‐1–related research. The activity of HIF‐1 is being regulated by the availability of its α‐subunit HIF‐1α, which undergoes quick degradation. The process of degradation is initiated by prolyl 4‐hydroxylase (PHD). PHD is an oxygen‐dependent enzyme and therefore is inactivated in hypoxia, in turn resulting in HIF‐1α stabilization, its dimerization with HIF‐1β subunit thereby producing the transcriptionally active factor. It has been suggested that pharmacological inhibition of PHD activity might give the same results. Indeed, a large body of evidence on beneficial effects of PHD inhibitors has been accumulated in multiple laboratory and clinical trials. In addition to them, a paper by Li and colleagues published in this issue of Journal of Neurochemistry also reports that inhibition of PHD by adaptaquin reduces hypoxic‐ischemic brain injury in a neonatal mouse model. When dissecting the underlying molecular mechanisms, Li and colleagues surprisingly found that the observed effects appear to be independent of HIF‐1. These findings draw attention back to the question about possible HIF‐1 effects independent of PHD inhibitors, which has been raised several years ago but has not received sufficient attention so far, and is being discussed in this Editorial. One of the possible mechanisms might be ascribed to the ferroptosis pathway affected by PHD inhibitors but this question needs further careful studies, as well as clarification of other mechanisms possibly involved. Even if they represent a prospective therapeutic strategy, the lack of current knowledge about endogenous targets of PHD inhibitors, except for PHD, calls for a careful and balanced approach toward their clinical use. [ABSTRACT FROM AUTHOR]

This section presents abstracts of research papers related to neurochemistry, including "Selective Up-regulation of Functional mu-opioid Receptor Splice Variants by Chronic Opioids," "Acute Selective Serotonin Reuptake Inhibitors Regulate the Dorsal Raphe Nucleus Causing Amplification of Terminal Serotonin Release" and "Docosahexaeonic Acid (DHA) Prevents Corticosterone-Induced Changes in Astrocyte Morphology and Function".

l-glutamate (Glu) is the main excitatory neurotransmitter in the central nervous system (CNS) and is associated with motor behavior and sensory perception. While microdialysis methods have been used to record tonic levels of Glu, little is known about the more rapid changes in Glu signals that may be observed in awake rats. We have reported acute recording methods using enzyme-based microelectrode arrays (MEA) with fast response time and low detection levels of Glu in anesthetized animals with minimal interference. The current paper concerns modification of the MEA design to allow for reliable measures in the brain of conscious rats. In this study, we characterized the effects of chronic implantation of the MEA into the brains of rats. We were capable of measuring Glu levels for 7 days without loss of sensitivity. We performed studies of tail-pinch induced stress, which caused a robust biphasic increase in Glu. Histological data show chronic implantation of the MEAs caused minimal injury to the CNS. Taken together, our data show that chronic recordings of tonic and phasic Glu can be carried out in awake rats for up to 17 days in vivo allowing longer term studies of Glu regulation in behaving rats.

The author reflects on the N-acetylaspartylglutamate (NAAG) which is a widely peptide transmitter found in the mammalian brain and spinal cord. According to the author, this study was performed in a number of animal models. The author also mentions that glutamate contamination of commercial NAAG might be responsible for the activation on type 3 metabotropic glutamate receptor (mGluR3) by NAAG in high concentrations.

Opiate drugs, such as codeine, morphine, and heroin, are powerful analgesics, but also are used as drugs of abuse because of their psychogenic properties. Many studies have shown that opiates impact on cellular proliferation in the adult and developing brain, although anatomical pathologies are lacking in in utero exposed infants and opioid knockout mice. Recent research has defined a context-dependent role for the opioid system in neurogenesis in the adult hippocampus with exercise. Opioids have been shown to interact with proliferating cells of the postnatal subventricular zone of the lateral ventricles. The subventricular zone is also a region of adult neurogenesis, a fact that was not well established at the time this earlier research was conducted. Although a relationship between opioids and fetal neurogenesis has yet to be firmly established, many studies have implicated the opioid system in this process. One common factor that links neurogenesis in adult, postnatal, and fetal structures is the involvement of neuronal progenitor cells of the astrocytic lineage. It is therefore of interest that opioids have been consistently shown to impact upon astrocytic proliferation. It is the intention of this paper to review the literature that has established a role for the opioid system in neurogenesis in vivo in fetal, postnatal, and adult animals and to examine the links of opioids to modulation of astrocytic proliferation. [ABSTRACT FROM AUTHOR]

It is now well established that plasma membranes, such as the myelin sheath, are made of different microdomains with different lipid and protein composition. Lipid rafts are made mainly of sphingolipids and cholesterol, whereas the non-raft regions are made mainly of phosphoglycerides. Most myelin proteins may distribute themselves in raft and non-raft microdomains but the driving force that gives rise to their different distribution is not known yet. In this paper, we have studied the distribution of protein zero (P0), the most representative protein of PNS myelin, in the membrane microdomains. To this end, we have purified P0 from both non-raft (soluble P0, P0-S) and raft (P0-R) regions of PNS. Purified proteins were analyzed by two-dimensional gel electrophoresis and identified and characterized by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. A detailed structural description of the two P0 forms is given in terms of amino acid sequence, post-translational modifications, and composition of associated lipids. Our findings suggest that structural differences between the two proteins, mainly related to the glycogroups, might be responsible for their different localization. [ABSTRACT FROM AUTHOR]

In this paper, we further develop the general theory of microdialysis by extending the linear model of Bungay et al. to provide a theoretical basis for in vitro and in vivo microdialysis. Specifically, we considered the effect of active clearance processes on in vivo microdialysis, and thereby elaborated the theory of Benveniste et al. to endogenous compounds. We examined the use of steady state tissue diffusion resistance with negligible clearance processes to interpret microdialysis data. The influence of the tissue properties on the in vitro and in vivo recoveries in dual-probe microdialysis was analyzed and we simulated the effect of the operating parameters on dual probe microdialysis performance. We estimated that the minimum clearance rate constant detectable by microdialysis in a quasi-steady state is about 5.5 × 10[sup -5] s[sup -1]. This minimum rate constant establishes a criterion, below which inhibition of the active clearance processes does not show detectable influences on the microdialysis extraction efficiency. [ABSTRACT FROM AUTHOR]

Steady-state microdialysis is a widely used technique to monitor the concentration changes and distributions of substances in tissues. To obtain more information about brain tissue properties from microdialysis, a dual-probe approach was applied to infuse and sample the radiotracer, [[sup 3]H]mannitol, simultaneously both in agar gel and in the rat striatum. Because the molecules released by one probe and collected by the other must diffuse through the interstitial space, the concentration profile exhibits dynamic behavior that permits the assessment of the diffusion characteristics in the brain extracellular space and the clearance characteristics. In this paper a mathematical model for dual-probe microdialysis was developed to study brain interstitial diffusion and clearance processes. Theoretical expressions for the spatial distribution of the infused tracer in the brain extracellular space and the temporal concentration at the probe outlet were derived. A fitting program was developed using the simplex algorithm, which finds local minima of the standard deviations between experiments and theory by adjusting the relevant parameters. The theoretical curves accurately fitted the experimental data and generated realistic diffusion parameters, implying that the mathematical model is capable of predicting the interstitial diffusion behavior of [[sup 3]H]mannitol and that it will be a valuable quantitative tool in dual-probe microdialysis. [ABSTRACT FROM AUTHOR]

The article presents abstracts of research papers related to cell death. The papers were presented at a poster session held at the joint meeting of the International Society for Neurochemistry and the American Society for Neurochemistry, in Buenos Aires, Argentina from August 26-31, 2001. They include "Caspase-3 in brain: role in adaptive plasticity," "ICER-evoked cell death of different types of neurons," and "Incidence of different cell death types in the newborn rat retina."

3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) is widely used for cell viability and cytotoxicity assays, but cell biological effects of MTT itself have not been investigated. In this paper we show that MTT induces a morphological change in an intracellular membranous compartment labeled with anti-Rab5 antibody, dissociation of early endosomal auto-antigen (EEA1) from the membrane fraction, and phosphorylation of Akt probably through a phosphatidylinositol-3-OH kinase [PI(3)K] pathway in cultured rat astrocytes. These findings suggest that MTT affects cellular functions and conditions to some extent, and such effects of MTT may cause some discrepancies of measurement of cell viability using MTT assay and other assays. That is, the effects of MTT on cells could influence the results of cell viability assay. Moreover, MTT or other tetrazolium salts could be used as interesting activators of Akt to investigate the mechanism by which Akt or PI(3)K is activated. [ABSTRACT FROM AUTHOR]

Front cover: We provide evidence that the circadian clock gene Period1 (Per1) regulates CREB phosphorylation in the mouse hippocampus, sculpturing time‐of‐day‐dependent memory formation. This molecular mechanism constitutes the functional link between circadian rhythms and learning efficiency. In hippocampal neurons of wild type mice, pP90RSK translocates into the nucleus upon stimulation with forskolin (see Figure 6A in the paper), whereas in Period1‐knockout (Per1‐/‐) mice (shown in the cover image) the kinase is trapped at the nuclear periphery, unable to efficiently phosphorylate nuclear CREB. Consequently, the presence of PER1 in hippocampal neurons is a prerequisite for the time‐of‐daydependent phosphorylation of CREB, as it regulates the shuttling of pP90RSK into the nucleus. The immunofluorescence image shows cAMP‐signaling in response to forskolin stimulation in a representative dorsal hippocampal neuron of a Per1‐/‐ mouse, stained for the neuronal marker NeuN (red), the nuclear marker DAPI (blue) and the activated CREB kinase pP90RSK (green). The image was taken 2 hours after light onset, at the peak of CREB phosphorylation in WT mouse hippocampus. Magnification: 100x. Read the full article ‘Period1 gates the circadian modulation of memory‐relevant signaling in mouse hippocampus by regulating the nuclear shuttling of the CREB kinase pP90RSK’ by O. Rawashdeh, A. Jilg, E. Maronde, J. Fahrenkrug and J. H. Stehle (J. Neurochem. 2016, vol. 138 (5), pp. 731–745) on doi: 10.1111/jnc.13689 [ABSTRACT FROM AUTHOR]

Analyses of samples of articles in the Journal of Neurochemistry between 1956 (the year of its foundation) and 1990 were used to obtain numerical indices of the history of neurochemistry. Data suggest that the acceleration of neurochemical research did not merely reflect the increase of biochemical research in general and that it involved progressive decreases and increases of interest in major constituents and transmitters, respectively, as indicated by both numbers and citations of papers. Papers on all classes of transmitters increased steadily and in the order of amines > amino acids, acetylcholine > peptides. Within the field of brain metabolism, papers on energy metabolism decreased markedly. Use of techniques other than those of biochemistry/neurochemistry altered strikingly with decreases of histological, electrophysiological, and pharmacological methods and increases of chemical, immunological, and tissue culture methods. Citations by neuroscience core journals between 1975 and 1988 suggest that the relative prominence of neurochemistry within neuroscience has remained constant. Analyses indicate that the influence of the U.S.A. relative to that of other regions has remained fairly steady between 1956 and 1990, but that number of papers from the U.K. has declined, whereas the influences of Western Europe and other areas appear to have recently increased substantially. Sociological changes have been the virtual disappearance of single-author papers, an increase of multiauthorship (> 3), and a recent striking increase of assertive sentence titles.

This preface introduces the Journal of Neurochemistry Special Issue on Brain Proteostasis. Adequate control of protein homeostasis, or proteostasis, has been at the center stage of brain physiology, and its deregulation may contribute to brain diseases, including several neuropsychiatric and neurodegenerative conditions. Therefore, delineating the processes underlying protein synthesis, folding, stability, function, and degradation in brain cells is key to promoting brain function and identifying effective therapeutic options for neurological disorders. This special issue comprises four review articles and four original articles covering the roles of protein homeostasis in several mechanisms that are of relevance to sleep, depression, stroke, dementia, and COVID‐19. Thus, these articles highlight different aspects of proteostasis regulation in the brain and present important evidence on this growing and exciting field. [ABSTRACT FROM AUTHOR]

Epilepsy is a common neurological disorder associated with alterations of excitation‐inhibition balance within brain neuronal networks. GABAA receptor neurotransmission is the most prevalent form of inhibitory neurotransmission and is strongly implicated in both the pathophysiology and treatment of epilepsy, serving as a primary target for antiseizure medications for over a century. It is now established that GABA exerts a multifaceted influence through an array of GABAA receptor subtypes that extends far beyond simply negating excitatory activity. As the role of GABAA neurotransmission within inhibitory circuits is elaborated, this will enable the development of precision therapies that correct the network dysfunction underlying epileptic pathology. [ABSTRACT FROM AUTHOR]

The article presents information about the "Journal of Neurochemistry" including the members of the editorial team, copyright and photocopying, and summaries of papers in the May 2016 issue.

In this editorial, we are happy to connect with our community to explain the changes introduced to the Journal of Neurochemistry over the last year and provide some insights into new developments and exciting opportunities. We anticipate these developments, which are strongly guided to increase transparency and support early career researchers, will increase the value of the Journal of Neurochemistry for the authors and readers. Ultimately, we hope to improve the author experience with the Journal of Neurochemistry and continue to be the leading venue for fast dissemination of exciting new research focusing on how molecules, cells and circuits regulate the nervous system in health and disease. [ABSTRACT FROM AUTHOR]

News Journal of Neurochemistry is happy to announce the 2015 winner Yuda Huo for the paper '' Journal of Neurochemistry 134(6): 1067-1080, Yuda Huo, Natasha Khatri, Qingming Hou, James Gilbert, Guan Wang and Heng-Ye Man. DOI: , With this important contribution to our understanding of ubiquitination processes, the award goes again to a highly deserving candidate. Dr. Huo will present his work at the 26th Biennial ISN Conference in Paris in 2017 (see below). The Journal of Neurochemistry is celebrating its , Upcoming on Frontotemporal Dementia, Parkinson disease and the of the Journal [ABSTRACT FROM AUTHOR]

Presents a corrected version of the article "The production of hydrogen sulfide is regulated by testosterone and S-adenosyl-l-methionine in mouse brain," by Ko Eto and Hideo Kimura.

The article presents abstracts of research papers related to hormones, ions and lipids. They include "Role of hypothalamic proline-rich polypeptide in the regulation of phospholipide and carbohydrate metabolism," "Influence of phospholipids on neurosteroid modulation of solubilized GABA receptor," and "The peptide mapping of human hypothalamus."

The article presents abstracts of papers related to oligodendrocytes, which were presented at a poster session at a meeting of the International Society for Neurochemistry and the American Society for Neurochemistry. The abstracts include "De-differentiation of Schwann cells in culture is not prevented by transferrin," "Apotransferrin decreases oligodendroglial progenitor cell migration and enhances differentiation," and "In vivo and in vitro effects of apoTf on oligodendroglial maturation."

The article presents an abstract of the research paper "Neonatal hypoglycaemia and brain development." In preterm infants and in developing country populations, neonatal hypoglycaemia remains a common problem. To reduce moderate hypoglycaemia in healthy infants, the promotion of early feeding is important.

The article presents an abstract of the research paper "Diet, lipids and brain development." Formation of a myelin sheath is one of the fundamental and necessary events in the normal development of the central nervous system in vertebrates. Myelinogenesis is basically a postnatal process in rodents.

The article presents an abstract of the medical research paper "Neural Activity Affects Cultured Cerebellar Granule Cells Morphology." The paper explores the effect of high potassium (K) and GABA on cerebellar granule cell morphology measuring the fractal dimension (D) of cells plated in low density cultures.

The article presents an abstract of the medical research paper "Neurotrophin and Semaphorin Interactions During Sensory Axon Growth and Branching." The paper examines expression of neuropilin during trigeminal tract development in embryonic (E) rats and the effects of neurotrophins NGF and NT-3 on central trigeminal axon growth patterns in wholemount explant and dissociated trigeminal ganglion (TG) cell cultures.

The article presents an abstract of the medical research paper "Mitogen Activated Protein Kinase is Involved in Nerve Growth Factor Stimulated Outgrowth of Injured Mouse Sensory Axons." The paper investigates, by employing PD98059, a highly specific inhibitor of the MAPkinase kinase (MEK), the role of the mitogen activated protein kinase (MAPkinase) in the outgrowth of adult sensory axons in vitro.

The article presents an abstract of the medical research paper "Mouse and Human APOE and Estrogen Modulate Mossy Fiber Sprouting in Organotypic Hippocampal Slice Culture." The paper discusses the function of apolipoprotein E (ApoE) in neuronal sprouting. ApoE may contribute to its isotype-specific risk for Alzheimer's disease. The paper analyzes that ApoE in vitro organotypic hippocampal slice culture (OHSC) system shows granule cell mossy fiber sprouting in response to deafferentation.

Presents abstracts of papers featured in the "Journal of Neurochemistry" that deal with pharmacology, drugs and herbal compounds. "Effects of sodium/calcium exchanger inhibitors on catecholamine secretion from cultured bovine adrenal chromaffin cells"; Aspirin curtails the acetaminophen-induced rise in rat forebrain norepinephrine levels, but not of serotonin".

Presents abstracts of papers featured in the "Journal of Neurochemistry" that deal with novel methodologies, techniques and technologies. "Buffer composition affects the test sensitivity of radiochemical assay of tyrosine hydroxylase in mouse brain"; "Immunostaining of citruline may not necessarily identify nos activity: the pitfall peptidylarginine deiminase".

At the 2017 joint meeting of the International Society for Neurochemistry (ISN) and the European Society for Neurochemistry, 150 years of neurochemistry – the 50th anniversary of ISN, 40 years of European Society for Neurochemistry, and 60 years of the Journal of Neurochemistry (JNC) – was celebrated with a historical symposium that explored the foundations of neurochemical societies, key international figures in the discipline of neurochemistry, and the pre‐eminent role of the JNC. The foundations of neurochemistry were laid in Europe, notably France and Germany, in the late 18th and early 19th centuries. Neurochemists in the United Kingdom made globally relevant contributions before and after the Second World War, and Swedish contributions were especially prominent in the 1950s and 1960s. As neurochemistry is a truly international branch of neuroscience, the important contributions of neurochemists in the Americas and the Asia‐Pacific were also recognized, as were the seminal roles of the American, Asia‐Pacific, and Japanese Societies of Neurochemistry. Although ISN was only formed in 1967, earlier international meetings in Europe and the Americas reflected the growing recognition of the importance of chemistry and biochemistry for understanding and responding to the pathophysiology of clinical conditions and diseases of the central and peripheral nervous systems. JNC was first published in 1956, but the ISN only assumed complete ownership of the journal under tempestuous circumstances in 1970. The ISN‐JNC interface and the sterling work of the JNC Editors has meant that the income generated by the journal has allowed the ISN Council to implement diverse programs for supporting neurochemistry internationally, including sustaining regional neurochemical societies, and supporting neurochemists in the developing world and schools of neurochemistry. [ABSTRACT FROM AUTHOR]

The article presents abstracts of research papers related to neurochemistry. They include "Retinal ganglion cells in culture obtained from chick embryos are circadian oscillators," "Regulation of phospholipid metabolism in cultured fibroblasts by a circadian clock," and "A novel point mutation detection in the p53 gene in grade II astrocytomas by polymerase chain reaction-single strand conformation polymorphism."

In this editorial we explain how the Journal of Neurochemistry will embrace Transparent Peer Review. Our goal is to enhance the experience for authors, readers, reviewers, and handling editors and to provide a sound platform for neurochemistry publications. This development is part of our ongoing drive to maintain and further increase the value of the Journal of Neurochemistry for the scientific community. [ABSTRACT FROM AUTHOR]

The article presents abstracts of several papers related to neurochemistry including "Nedd4-mediated AMPA receptor ubiquitination regulates receptor turnover and trafficking," "Effects of chronic nicotine on heteromeric neuronal nicotinic receptors in rat primary cultured neurons," and "A novel flow cytometry-based technique to measure adult neurogenesis in the brain."

The article offers information on the issues related to neurochemistry such as depression, Hypothalamic Sim1 neurons and Wnt-induced activation of glucose metabolism along with periodical editors such as Anirban Basu, Jan Albrecht and Michael Koch, and copyright and copying information.

A correction to the article "Mu-opioid receptors are involved in the tolerance to nicotine antinociception," that was published in the 2006 issue is presented.

The article presents an abstract of a research paper related to neuromuscular diseases. The paper was presented at the meeting of the International Society for Neurochemistry and the American Society for Neurochemistry, which was held in Buenos Aires, Argentina from August 26-31, 2001. The title of the paper was "Neuromuscular diseases: a peptide-DNA vector for targeting mitochondria."

The article presents an abstract of a research paper related to Parkinson's disease, which was presented at the meeting of the International Society for Neurochemistry and the American Society for Neurochemistry, held in Buenos Aires, Argentina from August 26-31, 2001. The title of the paper was "Accumulation of detergent-insoluble &x03B1;-synuclein in Lewy body diseases and transgenic mice."

The article presents an abstract of a paper related to microglia, which was presented at a poster session at the meeting of the International Society for Neurochemistry and the American Society for Neurochemistry, held in Buenos Aires, Argentina from August 26-31, 2001. The title of the paper was "Osmolality modulates nitric oxide activity in control and dibutyryl cyclic amp (dBcAMP)-treated microglia."

The article presents an abstract of the research paper "The Amp-Activated Protein Kinase Sustains Ketone Body Production by Astrocytes During Hypoxia." The paper focuses on the role played by the AMP-activated protein kinase (AMPK) in regulating the ketone body production by astrocytes. In rat cortical astrocytes several AMPK isoforms were presented. Result of the study concluded that ketone bodies which are produced by astrocytes might be a substrate for neuronal oxidative metabolism.

The article presents an abstract of the research paper "Dietary Arachidonic and Docosahexaenoic Acid are Involved in the Normal Metabolism of Monoaminergic Neurotransmitters in Developing Brain." The paper ascertained how dietary arachidonic and docosahexaenoic acid affect on growing frontal cortex dopaminergic and serotininergic neurotransmitters.

The article presents an abstract of the medical research paper "Translocation of PKC Isoforms Towards PSD After Cerebral Ischemia." This paper is to be discussed in the Seventeenth Biennial Meeting of the International Society for Neurochemistry (ISN) and the Thirteenth General Meeting of the European Society for Neurochemistry (ESN) to be held at Berlin, Germany from August 8-14, 1999. This paper is to discuss the role of PKC in pathological nerve cell function.

The article presents an abstract of the medical research paper "Tyrosine-Hydroxylase Protein Levels in N-Methyl-Norsalsolinol Lesioned Rats." This paper is to be discussed in the Seventeenth Biennial Meeting of the International Society for Neurochemistry (ISN) and the Thirteenth General Meeting of the European Society for Neurochemistry (ESN) to be held at Berlin, Germany from August 8-14, 1999.

The article presents an abstract of the medical research paper "Changes in Protein Phosphatase 2A Activity During Global Brain Reperfusion." This paper is to be discussed in the Seventeenth Meeting of the International Society for Neurochemistry (ISN) and the Thirteenth General Meeting of the European Society for Neurochemistry (ESN) to be held at Berlin, Germany from August 8-14, 1999.

The article presents an abstract of the research paper "Ascorbate Causes Apoptosis in PC12 Cells Via Oxidative Stress." A hypothesis was proposed to explain the oxidative action of ascorbate. The observations suggest that the toxic effect of ascorbate is due to oxidative stress. The paper will be presented in the joint meeting of the International Society for Neurochemistry and the European Society of Neurochemistry that will be held in Berlin, Germany from August 8-14, 1999.