Dopamine transmission in the tail striatum: Regional variation and contribution of dopamine clearance mechanisms
We recorded evoked dopamine release in the four tail striatum divisions (dorsal and trilaminar medial, intermediate and lateral) and the dorsolateral striatum, using fast-scan cyclic voltammetry in rat brain slices. Clearance mechanisms were investigated using dopamine transporter knockout (DAT-KO) rats, pharmacological transporter inhibitors and dextran. Dopamine release in all tail divisions was smaller amplitude than in the dorsolateral striatum and, importantly, regional variation was observed. The intermediate division exhibited uniquely low-peak dopamine clearance velocity and high sensitivity to DAT removal. Our fin...
Source: Journal of Neurochemistry - February 4, 2024 Category: Neuroscience Authors: Bronwyn Riley,
Emily Gould,
Jordan Lloyd,
Luke E. Hallum,
Srdjan Vlajkovic,
Kathryn Todd,
Peter S. Freestone Tags: ORIGINAL ARTICLE Source Type: research
HIV ‐1 Tat and morphine interactions dynamically shift striatal monoamine levels and exploratory behaviors over time
To examine the relationship between opioid and HIV-1-induced alterations in striatal monoamine concentrations and behavior, morphine was administered to HIV-1 Tat transgenic mice for 2 weeks or 2 months. Morphine and Tat interacted to alter levels of dopamine, dopamine metabolites, norepinephrine, and 5-hydroxyindoleacetic acid depending on the duration of exposure and neurotransmitter/metabolite assayed. Co-exposure to Tat and morphine disrupted locomotor activity in a time- dependent manner. Alternatively, Tat alone inhibited social exploratory behavior, whereas morphine alone tended to increase novelty-seeking beha...
Source: Journal of Neurochemistry - February 3, 2024 Category: Neuroscience Authors: Arianna R. S. Lark,
Sara R. Nass,
Yun K. Hahn,
Benlian Gao,
Ginger L. Milne,
Pamela E. Knapp,
Kurt F. Hauser Tags: ORIGINAL ARTICLE Source Type: research
Synaptic adhesion molecule protocadherin ‐γC5 mediates β‐amyloid‐induced neuronal hyperactivity and cognitive deficits in Alzheimer's disease
We propose the following mechanism in Alzheimer's disease pathogenesis: β-Amyloid (Aβ) triggers Ca2+ influx and enhanced synaptic adhesion molecule protocadherin- γC5 (Pcdh-γC5) expression in a Ca2+-dependent manner. The cleaved carboxy terminal fragment (CTF) of Pcdh- γC5 enters the nucleus, further promoting its transcription and various synaptic proteins. Sustained neuronal hyperactivity will eventually induce vesicle depletion and synaptic dysfunction in Alzheimer's disease. AbstractNeuronal hyperactivity induced by β-amyloid (Aβ) is an early pathological feature in Alzheimer's disease (AD) and contributes to co...
Source: Journal of Neurochemistry - February 3, 2024 Category: Neuroscience Authors: Min Su,
Erying Xuan,
Xiangyi Sun,
Gaojie Pan,
Dandan Li,
Honghua Zheng,
Yun ‐wu Zhang,
Yanfang Li Tags: ORIGINAL ARTICLE Source Type: research
Bioenergetic and excitotoxic determinants of cofilactin rod formation
Cofilactin rod (CAR) formation leads to neurite degeneration after brain ischemia, but whether CAR formation is a direct result of ATP depletion or a more indirect effect of ischemic conditions has been uncertain. Here, we show that in neuronal cultures, the CAR formation induced by oxygen –glucose deprivation (OGD) is blocked by glutamate (GLU) receptor blockers, NADPH oxidase inhibition, or a free radical scavenger, despite ATP depletion. Conversely, exposure to GLU or hydrogen peroxide (H2O2) induces CAR formation in the absence of ATP depletion. Excitotoxic oxidative stress is thus the proximate cause of CAR formatio...
Source: Journal of Neurochemistry - February 2, 2024 Category: Neuroscience Authors: Nguyen Mai,
Long Wu,
G ökhan Uruk,
Ebony Mocanu,
Raymond A. Swanson Tags: ORIGINAL ARTICLE Source Type: research
The antiseizure medication valproate increases hemichannel activity found in brain cells, which could worsen disease outcomes
During seizures, the activity of neurons and hemichannels (HCs) of reactive glia are high. More glutamate and ATP are released via HCs and valproate enhances the HC activity. An HC blocker could stop this feedforward loop reducing the neuronal activity. AbstractGlial cells play relevant roles in neuroinflammation caused by epilepsy. Elevated hemichannel (HC) activity formed by connexins (Cxs) or pannexin1 (Panx1) largely explains brain dysfunctions commonly caused by neuroinflammation. Glia express HCs formed by Cxs 43, 30, or 26, while glia and neurons both express HCs formed by Panx1. Cx43 HCs allow for the influx of Ca2...
Source: Journal of Neurochemistry - January 31, 2024 Category: Neuroscience Authors: Claudia Garc ía‐Rodríguez,
Yorley Duarte,
Álvaro O. Ardiles,
Juan C. Sáez Tags: ORIGINAL ARTICLE Source Type: research
Engineering, applications, and future perspectives of GPCR ‐based genetically encoded fluorescent indicators for neuromodulators
This study provides a comprehensive review of genetically encoded fluorescent indicators (GEFIs) based on G-protein-coupled receptors (GPCRs). It discusses the development, structure, and engineering strategies of GEFIs, emphasizing the importance of both sensing (GPCR structure and activation) and reporting (fluorescent protein structure and modulation) domains. The review highlights the applications in measuring neuromodulators with high specificity and spatiotemporal resolution, addresses current limitations and misconceptions in the field, and suggests future directions for enhancing ligand-binding properties and spect...
Source: Journal of Neurochemistry - January 30, 2024 Category: Neuroscience Authors: Valentin Lu Rohner,
Paul J. Lamothe ‐Molina,
Tommaso Patriarchi Tags: REVIEW Source Type: research
Sex ‐specific pleiotropic changes in emotional behavior and alcohol consumption in human α‐synuclein A53T transgenic mice during early adulthood
In this study, we investigated whether the familial PD point mutationA53T is associated with changes in alcohol consumption behavior and emotional states at ages not yet characterized by α-synuclein accumulation. TheA53T gene mutation was shown to be associated with sex-specific diverse changes in emotional states and alcohol consumption behavior long before the onset of PD. These alterations in behavior may be linked to changes in brain ceramide metabolism. AbstractPoint mutations in the α-synuclein coding gene may lead to the development of Parkinson's disease (PD). PD is often accompanied by other psychiatric conditio...
Source: Journal of Neurochemistry - January 30, 2024 Category: Neuroscience Authors: Liubov S. Kalinichenko,
Zacharias Kohl,
Christiane M ühle,
Zurina Hassan,
Agnes Hahn,
Eva‐Maria Schmitt,
Kilian Macht,
Lyubomir Stoyanov,
Schayan Moghaddami,
Roberto Bilbao,
Volker Eulenburg,
Jürgen Winkler,
Johannes Kornhuber,
Christian Tags: ORIGINAL ARTICLE Source Type: research
Role of transcription factors, noncoding RNAs, epitranscriptomics, and epigenetics in post ‐ischemic neuroinflammation
Transcription factors, noncoding RNAs, and epitranscriptomic and epigenetic modifications collectively orchestrate the post-stroke inflammation that plays a significant role in secondary brain damage and functional outcomes. AbstractPost-stroke neuroinflammation is pivotal in brain repair, yet persistent inflammation can aggravate ischemic brain damage and hamper recovery. Following stroke, specific molecules released from brain cells attract and activate central and peripheral immune cells. These immune cells subsequently release diverse inflammatory molecules within the ischemic brain, initiating a sequence of events, in...
Source: Journal of Neurochemistry - January 27, 2024 Category: Neuroscience Authors: Suresh L. Mehta,
Vijay Arruri,
Raghu Vemuganti Tags: REVIEW Source Type: research
Acetylated tau exacerbates apoptosis by disturbing mitochondrial dynamics in HEK293 cells
Mitochondrial dynamics include two processes: mitochondrial fission and fusion. TauKQ induced mitochondrial fission by decreasing mitochondrial fusion proteins, which aggravated mitochondrial dysfunction and apoptosis. BGP-15 reversed TauKQ-induced mitochondrial dysfunctions and apoptosis by improving mitochondrial dynamics. AbstractAn increase in tau acetylation at K274 and K281 and abnormal mitochondrial dynamics have been observed in the brains of Alzheimer's disease (AD) patients. Here, we constructed three types of tau plasmids, TauKQ (acetylated tau mutant, by mutating its K274/K281 into glutamine to mimic disease-as...
Source: Journal of Neurochemistry - January 26, 2024 Category: Neuroscience Authors: Jun ‐Fei Zhang,
Zhi‐Ting Fang,
Jun‐Ning Zhao,
Gong‐Ping Liu,
Xin Shen,
Gao‐Feng Jiang,
Qian Liu Tags: ORIGINAL ARTICLE Source Type: research
Issue Information
Front coverIncreasing NAA synthase (Nat8L) via AAV-mediated overexpression in a model of Alzheimer's Disease compromises mitochondrial energy metabolism. Sequestration of mitochondrial aspartate by NAA is incompatible with pathological energetic crisis, accelerates associated cognitive decline and presents a rationale for the active reduction of NAA in a broad clinical spectrum of neurodegenerative disease.Image contentOverexpression of NAA synthase (Nat8L) in hippocampal Neurons of 5xFAD mice compounds phenotypic energy deficit and accelerates cognitive decline.Read the full article‘Over-expression of N-acetylaspartate ...
Source: Journal of Neurochemistry - January 25, 2024 Category: Neuroscience Tags: ISSUE INFORMATION Source Type: research
Neurobiological mechanisms of electroconvulsive therapy for depression: Insights into hippocampal volumetric increases from clinical and preclinical studies
Clinical MRI studies have consistently shown an increased volume of the hippocampus following electroconvulsive therapy (ECT) in severe, pharmacotherapy-resistant depression. However, the working mechanism of ECT for depression remains to be elucidated. This narrative review brings together evidence from animal models and human studies, discussing the clinical implications and the specific histological significance of the hippocampal volumetric increases. We also explore the importance of translation research that integrates human and animal models, as well as future directions needed to understand the biological mechanism...
Source: Journal of Neurochemistry - January 19, 2024 Category: Neuroscience Authors: Yoshifumi Abe,
Vera J. Erchinger,
Olga Therese Ousdal,
Leif Oltedal,
Kenji F. Tanaka,
Akihiro Takamiya Tags: REVIEW Source Type: research
Molecular prognostic of nine parthanatos death ‐related genes in glioma, particularly in COL8A1 identification
A total of 11 parthanatos genes from ParthanatosCluster database were used to obtain the 9 ParthanatosScore prognostic genes combination. ParthanatosScore was verified by 656 patients and 979 patients in TCGA and CGGA-LGG/GBM datasets. COL8A1 was screened from nine ParthanatosScore prognostic genes through the glioma cell lines and survival analysis. Silencing COL8A1 inhibited the malignant characterization. Temozolomide and AZD3759 inhibited COL8A1 expression and cell viability and promoted apoptosis and parthanatos gene expression, which is a target to improve glioma. CGGA, Chinese Glioma Genome Atlas; GBM, Glioblastoma;...
Source: Journal of Neurochemistry - January 16, 2024 Category: Neuroscience Authors: Shuangshi Fan,
Hao Li,
Kun Liu Tags: ORIGINAL ARTICLE Source Type: research
FMRP regulation of aggrecan mRNA translation controls perineuronal net development
Fragile X Messenger Ribonucleoprotein (FMRP) regulates translational efficiency of aggrecan mRNA through the protection of its poly(A) tail. Loss of FMRP leads to a reduction of aggrecan mRNA poly(A) tail length, which decreases the number of ribosomes that bind the mRNA to initiate translation. The reduction in Aggrecan protein levels results in a delay in formation of perineuronal nets (PNNs). PNNs are necessary for the excitatory/inhibitory (E/I) balance in the brain, which is disrupted in mouse models of Fragile X Syndrome (FXS), a neurodevelopmental disorder caused by the loss of FMRP. AbstractPerineuronal nets (PNNs)...
Source: Journal of Neurochemistry - January 16, 2024 Category: Neuroscience Authors: Heleen M. van't Spijker,
Joel D. Richter Tags: ORIGINAL ARTICLE Source Type: research
Serum amyloid A facilitates expansion of CD4+ T cell and CD19+ B cell subsets implicated in the severity of myasthenia gravis patients
This study aimed to explore the SAA levels in a cohort of patients with myasthenia gravis (MG) in relation to disease-related clinical parameters and myasthenic crisis (MC) and elucidate the effects of SAA on immune response. A total of 82 MG patients including 50 new-onset MG patients and 32 MC patients were enrolled in this study. Baseline data and laboratory parameters of all enrolled MG patients were routinely recorded through electronic medical systems. SAA levels were measured by enzyme-linked immunosorbent assay (ELISA) kit. CD4+ T and CD19+ B cell subsets were analyzed by flow cytometry. In vitro, human recombina...
Source: Journal of Neurochemistry - January 13, 2024 Category: Neuroscience Authors: Xiaoyu Huang,
Xueting An,
Xue Gao,
Ningning Wang,
Jia Liu,
Yong Zhang,
Guoyan Qi,
Chao Zhang Tags: ORIGINAL ARTICLE Source Type: research
Arrestin ‐3 binds parkin and enhances parkin‐dependent mitophagy
E3 ubiquitin ligase parkin induces mitophagy via ubiquitination of mitochondrial proteins. Parkin exists in closed autoinhibited conformation with the catalytic site on RING2 (brown circle) and E2 binding site on RING1 (blue ellipse) occluded. The ligase function of parkin activated following its phosphorylation by PINK1 and the binding of phospho-ubiquitin is further regulated by numerous partners. Arrestin-3 binds RING0 and RING1 domains of parkin, promoting its transition to open active conformation with both catalytic and E2 binding site accessible (yellow circles – phosphates; pUb – phosphorylated ubiquitin). Thus...
Source: Journal of Neurochemistry - January 10, 2024 Category: Neuroscience Authors: Chen Zheng,
Kevin K. Nguyen,
Sergey A. Vishnivetskiy,
Vsevolod V. Gurevich,
Eugenia V. Gurevich Tags: ORIGINAL ARTICLE Source Type: research
