The Journal of Neurochemistry is dedicated to disseminating research covering all aspects of neurochemistry including molecular, cellular, biochemical and behavioural aspects of the nervous system, with a focus on pathogenesis, biomarkers and treatment of neurological and psychiatric disorders. We prioritize original research that demonstrates a mechanistic advance as well as critical reviews that highlight progression of knowledge in the field. We are owned by the International Society for Neurochemistry.

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Articles

ORIGINAL ARTICLE

Differential regulation of G protein‐coupled receptor‐associated proteins in the caudate and the putamen of cynomolgus macaques following chronic ethanol drinking

  •  23 May 2024

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The caudate nucleus and the putamen in human and non-human primates are functionally distinct and regulate different aspects of drug-related behavior. We found that long-term ethanol drinking in male cynomolgus macaques results in reduced expression of numerous proteins involved in G protein-coupled receptor trafficking and function in the caudate but not in the putamen. Our data underscore the unique vulnerability of the caudate nucleus to adaptations induced by chronic ethanol exposure.

ORIGINAL ARTICLE

Characterization of tritiated JNJ-GluN2B-5 (3-[3H] 1-(azetidin-1-yl)-2-(6-(4-fluoro-3-methyl-phenyl)pyrrolo[3,2-b]pyridin-1-yl)ethanone), a high affinity GluN2B radioligand with selectivity over sigma receptors

  •  21 May 2024

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In this article, Jeffrey Schoellerman and colleagues describe a new radioligand selective for GluN2B-containing NMDA receptors, which play an important role in brain physiology and are potential drug targets for neuropsychiatric and neurodegenerative disorders. [3H]-JNJ-GluN2B-5 is more selective than previous GluN2B radioligands and allows for better visualization of these receptors and measuring receptor occupancy ex vivo.

ORIGINAL ARTICLE
Open access

Mechanisms of synapse-to-nucleus calcium signalling in striatal neurons and impairments in Huntington's disease

  •  21 May 2024

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Huntington disease (HD) is an inherited neurodegenerative disorder affecting movement, mood and cognition, and striatal neurons show highest vulnerability to dysfunction and death. Calcium, a key messenger for transmitting external stimuli to the cell's nucleus, helps coordinate new protein expression that ultimately regulates neuronal health and connectivity in the brain. Here, we use a model system to explore the mechanisms of calcium signalling to the nucleus in striatal neurons, revealing critical roles for N-methyl-D-aspartate receptors and ryanodine receptors, and demonstrating early impairment in this pathway in HD.

ORIGINAL ARTICLE

Inhibition of reactive oxygen species production accompanying alternatively activated microglia by risperidone in a mouse ketamine model of schizophrenia

  •  21 May 2024

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The effects of the second-generation antipsychotic risperidone (RIS) on reactive oxygen species (ROS) and microglia were analyzed using a mouse ketamine (KET) model of schizophrenia. Compared to KET-treated mice, KET/RIS-treated mice exhibited lower gene expression of the ROS-generating enzyme (Nox2), and higher expression of antioxidant enzymes (Ho-1 and Gclc). Three types of microglia were defined by hierarchical cluster analysis: resting-ramified (type I) in control mice, moderately ramified (type II) in KET-treated mice, and hyper-ramified (type III) in KET/RIS-treated mice. In vitro ROS assay showed that RIS reduced the production of microglial ROS induced by KET. Notably, antioxidant compounds (N-Acetyl-L-cysteine [NAC] and GSK 2795039 [GSK]) alleviated schizophrenia-like behaviors induced by KET, suggesting a promising direction for the development of novel treatments for schizophrenia.

ORIGINAL ARTICLE
Open access

Exploring the kynurenine pathway in mild traumatic brain injury: A longitudinal study

  •  21 May 2024

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(Neuro)inflammation in response to mild traumatic brain injury (mTBI) may lead to the degradation of tryptophan into metabolites of the kynurenine pathway. In this study, we provide evidence for decreases of tryptophan relative to healthy controls in the acute and subacute phase of mTBI. Acute tryptophan concentrations were related to recovery at six-months post-mTBI. Furthermore, we found evidence for decreased levels of the kynurenines xanthurenic and picolinic acid that are implicated in the glutamate system. We propose that tryptophan and metabolites or enzymes of the kynurenine pathway may form novel targets for therapeutic supplementation or modulation in mTBI.

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