5,974 results match your criteria Neurochemistry International[Journal]


Streptozotocin causes acute responses on hippocampal S100B and BDNF proteins linked to glucose metabolism alterations.

Neurochem Int 2019 Apr 19. Epub 2019 Apr 19.

Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.

Streptozotocin (STZ) is a glucosamine-nitrosourea commonly used to induce long-lasting models of diabetes mellitus and Alzheimer's disease. Direct toxicity of STZ on the pancreas and kidneys has been well characterized, but the acute effect of this compound on brain tissue has received less attention. Herein, we investigated the acute and direct toxicity of STZ on fresh hippocampal slices, measuring changes in BDNF and S100B secretion (two widely-used peripheral markers of brain injury), as well as glucose metabolism. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.04.013DOI Listing

Differential expression patterns of sodium potassium ATPase alpha and beta subunit isoforms in mouse brain during postnatal development.

Neurochem Int 2019 Apr 19. Epub 2019 Apr 19.

Ruhr University Bochum, Faculty of Chemistry and Biochemistry, Biochemistry II, Bochum, Germany; Ruhr University Bochum, International Graduate School for Neuroscience, Germany. Electronic address:

The sodium potassium ATPase (Na/K ATPase) is essential for the maintenance of a low intracellular Na and a high intracellular K concentration. Loss of function of the Na/K ATPase due to mutations in Na/K ATPase genes, anoxic conditions, depletion of ATP or inhibition of the Na/K ATPase function using cardiac glycosides such as digitalis, causes a depolarization of the resting membrane potential. While in non-excitable cells, the uptake of glucose and amino acids is decreased if the function of the Na/K ATPase is compromised, in excitable cells the symptoms range from local hyper-excitability to inactivating depolarization. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.04.009DOI Listing
April 2019
1 Read

Exendin-4 attenuates brain mitochondrial toxicity through PI3K/Akt-dependent pathway in amyloid beta (1-42)-induced cognitive deficit rats.

Neurochem Int 2019 Apr 17;128:39-49. Epub 2019 Apr 17.

Division of Pharmacology, Institute of Pharmaceutical Research, GLA University, Mathura, 281 406, India.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory loss, disorientation and gradual deterioration of intellectual ability. In the pharmacotherapy of AD, the mitochondrial protective activity of Exendin-4 in experimental studies is yet to be established though its effectiveness is demonstrated in these patients. Therefore, the mitochondria protective activity of Exendin-4 (5 μg/kg, i. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S01970186193002
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http://dx.doi.org/10.1016/j.neuint.2019.04.006DOI Listing
April 2019
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Blood-to-brain communication in the hypothalamus for energy intake regulation.

Neurochem Int 2019 Apr 16. Epub 2019 Apr 16.

Department of Anatomy & Neuroscience, Faculty of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara ,634-8521, Japan.

The arcuate nucleus (Arc) integrates circulating hormonal and metabolic signals to control energy expenditure and intake. One of the most important routes that enables the Arc to sense circulating molecules is through the median eminence (ME), which lacks a typical blood-brain barrier. However, the mechanism by which circulating molecules reach the Arc neurons remains unclear. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S01970186183060
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http://dx.doi.org/10.1016/j.neuint.2019.04.007DOI Listing
April 2019
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GLP-1: Molecular mechanisms and outcomes of a complex signaling system.

Neurochem Int 2019 Apr 16. Epub 2019 Apr 16.

Department of Surgery, Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address:

Meal ingestion provokes the release of hormones and transmitters, which in turn regulate energy homeostasis and feeding behavior. One such hormone, glucagon-like peptide-1 (GLP-1), has received significant attention in the treatment of obesity and diabetes due to its potent incretin effect. In addition to the peripheral actions of GLP-1, this hormone is able to alter behavior through the modulation of multiple neural circuits. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.04.010DOI Listing
April 2019
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Blonanserin ameliorates social deficit through dopamine-D receptor antagonism in mice administered phencyclidine as an animal model of schizophrenia.

Neurochem Int 2019 Apr 15. Epub 2019 Apr 15.

Division of Clinical Sciences and Neuropsychopharmacology, Faculty of Pharmacy, Meijo University, Nagoya, 468-8503, Japan; Division of Clinical Sciences and Neuropsychopharmacology, Graduate School of Pharmacy, Meijo University, Nagoya, 468-8503, Japan; Department of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, 466-8560, Japan. Electronic address:

Blonanserin differs from other antipsychotic drugs, such as risperidone and olanzapine and exhibits a higher affinity for dopamine-D receptors than for serotonin 5-HT receptors. We investigated the involvement of dopamine-D receptors in the effect of blonanserin on the social deficit observed in an animal model of schizophrenia and sought to elucidate the molecular mechanism underlying its action. Mice received phencyclidine (PCP: 10 mg/kg/day, s. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.04.008DOI Listing

Garcinol, a multifaceted sword for the treatment of Parkinson's disease.

Neurochem Int 2019 Apr 12;128:50-57. Epub 2019 Apr 12.

Cellular and Molecular Neurobiology Laboratory, Department of Life Science and Bioinformatics, Assam University, Silchar, 788011, Assam, India. Electronic address:

Garcinol, the principal phytoconstituent of plants belonging to the genus Garcinia, is known for its anti-oxidant as well as anti-inflammatory properties, which can be extended to its possible neuroprotective role. Recent reports disseminate the capacity of garcinol to influence neuronal growth and survival, alter the neurochemical status in brain, as well as regulate memory and cognition. The concomitant neuro-rescue property of garcinol may render it as an effective compound in Parkinson's disease (PD) therapeutics since it is capable of ameliorating the related pathophysiological changes. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.04.004DOI Listing
April 2019
3 Reads

Astrocyte dysfunction and neurovascular impairment in neurological disorders: Correlation or causation?

Neurochem Int 2019 Apr 12. Epub 2019 Apr 12.

Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, United States. Electronic address:

The neurovascular unit, consisting of neurons, astrocytes, and vascular cells, has become the focus of much discussion in the last two decades and emerging literature now suggests an association between neurovascular dysfunction and neurological disorders. In this review, we synthesize the known and suspected contributions of astrocytes to neurovascular dysfunction in disease. Throughout the brain, astrocytes are centrally positioned to dynamically mediate interactions between neurons and the cerebral vasculature, and play key roles in blood-brain barrier maintenance and neurovascular coupling. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.04.005DOI Listing

Role of the BDNF-TrkB pathway in KCC2 regulation and rehabilitation following neuronal injury: A mini review.

Neurochem Int 2019 Apr 12;128:32-38. Epub 2019 Apr 12.

Department of Rehabilitation Sciences, Graduate School of Medicine, Nagoya University, 1-1-20, Daiko-minami Higashi-ku, Nagoya-shi, Aichi, 461-8673, Japan. Electronic address:

In most mature neurons, low levels of intracellular Cl concentrations ([Cl]) are maintained by channels and transporters, particularly the K-Cl cotransporter 2 (KCC2), which is the only Cl extruder in most neurons. Recent studies have implicated KCC2 expression in the molecular mechanisms underlying neuronal disorders, such as spasticity, epilepsy and neuropathic pain. Alterations in KCC2 expression have been associated with brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB). Read More

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http://dx.doi.org/10.1016/j.neuint.2019.04.003DOI Listing
April 2019
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Long-term exposure of 2450 MHz electromagnetic radiation induces stress and anxiety like behavior in rats.

Neurochem Int 2019 Apr 4;128:1-13. Epub 2019 Apr 4.

Neurotherapeutics Laboratory, Department of Pharmaceutical Engineering and Technology, Indian Institute of Technology (Banaras Hindu University), Varanasi, 221005, U.P., India. Electronic address:

Long term exposure of electromagnetic radiations (EMR) from cell phones and Wi-Fi hold greater propensity to cause anxiety disorders. However, the studies investigating the effects of repeated exposure of EMR are limited. Therefore, we investigated the effects of repeated exposure of discrete frequencies of EMR in experimental animals. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.04.001DOI Listing
April 2019
1 Read
3.603 Impact Factor

Therapeutic strategy against ischemic stroke with the concept of neurovascular unit.

Neurochem Int 2019 Jun 1;126:246-251. Epub 2019 Apr 1.

Department of Neurosurgery, Graduate School of Medicine, Osaka University, Japan.

Stroke is one of the leading causes of death and disability globally. Although thrombolytic therapy by t-PA and mechanical thrombectomy have improved outcomes of ischemic stroke patients, both of these approaches are applicable to limited numbers of patients owing to their time constraints. Therefore, development of other treatment approaches such as developing neuroprotective drugs and nerve regeneration therapy is required to overcome ischemic stroke. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.022DOI Listing

PPAR-γ agonist GL516 reduces oxidative stress and apoptosis occurrence in a rat astrocyte cell line.

Neurochem Int 2019 Jun 1;126:239-245. Epub 2019 Apr 1.

Department of Pharmacy, University G. d'Annunzio, Chieti-Pescara, via dei Vestini 31, Chieti Scalo, Italy.

Aims: The worldwide increase in aging population is prevalently associated with the increase of neurodegenerative diseases. Peroxisome Proliferator-Activated Receptors (PPARs) are ligand-modulated transcriptional factors which belong to the nuclear hormone receptor superfamily which regulates peroxisome proliferation. The PPAR-γ is the most extensively studied among the three isoforms and the neuroprotective effects of PPAR-γ agonists have been recently demonstrated in a variety of preclinical models of neurological disorders. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.021DOI Listing
June 2019
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Pathological changes in mice with long term cuprizone administration.

Neurochem Int 2019 Jun 30;126:229-238. Epub 2019 Mar 30.

Department of Functional Anatomy and Neuroscience, Asahikawa Medical University, Midorigaoka-higashi 2-1-1-1, Asahikawa, Hokkaido, 078-8510, Japan.

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). In MS, a long disease duration is known to be a strong risk factor for converting the clinical course of the disease from relapse remitting MS to secondary progressing MS. There is a hypothesis that long sustained demyelination may exhaust neurons, however, pathological changes induced in neurons following demyelination remain unknown. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.018DOI Listing
June 2019
3 Reads

Metabotropic glutamate receptor 5 ablation accelerates age-related neurodegeneration and neuroinflammation.

Neurochem Int 2019 Jun 29;126:218-228. Epub 2019 Mar 29.

Department of Biochemistry and Immunology, Institute of Biological Sciences (ICB), Universidade Federal de Minas Gerais, Belo Horizonte, MG, 31270-901, Brazil. Electronic address:

The growing elderly population world widely prompts the need for studies regarding aged brain and its susceptibility to neurodegenerative diseases. It has been shown that aged brain exhibits several alterations, including neuroinflammation, which prone this organ to neurodegenerative processes. Metabotropic glutamate receptor 5 (mGlu receptor) has a role in neuronal cell loss and inflammation. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.020DOI Listing
June 2019
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Increased REDD1 facilitates neuronal damage after subarachnoid hemorrhage.

Neurochem Int 2019 Mar 29;128:14-20. Epub 2019 Mar 29.

Department of Neurochemistry, Institute of Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China. Electronic address:

Regulated in development and DNA damage responses 1 (REDD1) is a highly conserved stress-response protein and can be induced by hypoxia/ischemia and DNA damage. However, it is not known whether REDD1 involves in neuronal damage caused by subarachnoid hemorrhage (SAH) that is known as one of the most important causes of disability and death worldwide. Here, we first found that SAH markedly induced the increase of REDD1 (35. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.019DOI Listing
March 2019
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The importance of choosing a preclinical model that reflects what happens in Parkinson's disease.

Neurochem Int 2019 Jun 25;126:203-209. Epub 2019 Mar 25.

Molecular and Clinical Pharmacology, ICBM, Faculty of Medicine, University of Chile, Independencia 1027, 8350453, Independencia, Santiago, Chile. Electronic address:

One of the major problems in the translation of successful preclinical results to clinical studies and new therapies in Parkinson's disease is the use of preclinical models based on exogenous neurotoxins that do not replicate what happens in the disease. The loss of dopaminergic neurons containing neuromelanin in Parkinson´s disease takes years, contrasting the very rapid degeneration induced by exogenous neurotoxins. We discuss the role of endogenous neurotoxins generated during dopamine oxidation and its possible use as new preclinical models for Parkinson´s disease. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.016DOI Listing

Highly aggressive behavior induced by social stress is associated to reduced cytochrome c oxidase activity in mice brain cortex.

Neurochem Int 2019 Jun 26;126:210-217. Epub 2019 Mar 26.

Laboratory of Innovations in Therapies, Education and Bioproducts, Instituto Oswaldo Cruz/FIOCRUZ, Av. Brasil 4365, 21045-900, Manguinhos, Rio de Janeiro, Brazil. Electronic address:

Violence and aggression represent severe social problems, with profound impacts on public health. Despite the development of experimental models to study aggressive behavior is highly appreciated, the underlying mechanisms remain poorly understood. Given the key contribution of mitochondria to central nervous system bioenergetics, we hypothesized that mitochondrial function in brain would be altered by social stress. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.017DOI Listing
June 2019
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Can magnesium reduce central neurodegeneration in Alzheimer's disease? Basic evidences and research needs.

Neurochem Int 2019 Jun 22;126:195-202. Epub 2019 Mar 22.

Department of Neurology, CHUN Fann, Dakar, Senegal.

Magnesium (Mg) is a crucial divalent cation with more than 300 cellular functions. This ion shows therapeutic properties in several neurological diseases. Although there are numerous basic evidences showing that Mg can inhibit pathological processes involved in neuroglial degeneration, this low-cost option is not well-considered in clinical research and practice for now. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.014DOI Listing

c-Fos expression response to olanzapine, amisulpride, aripiprazole, and quetiapine single administration in the rat forebrain: Effect of a mild stress preconditioning.

Neurochem Int 2019 Jun 21;126:187-194. Epub 2019 Mar 21.

Department of Psychiatry, Faculty of Medicine in Bratislava, Comenius University, Mickiewiczova 13, 81369, Bratislava, Slovakia.

Antipsychotics have been shown to stimulate different forebrain areas, whereas some of them are sensitive to stress. In the present study, effect of a single administration of olanzapine (OLA), amisulpride (AMI), aripiprazole (ARI), and quetiapine (QUE) on the activity of cells in the striatal dorsolateral (stDL) area, the periventricular zone (peVZ), the septal ventrolateral (seVL) nucleus, and the accumbens nucleus shell (shACC) and core (coACC) was investigated in male rats preconditioned with a mild stress complex (CMS) for 20 days. The objective of the study was to extend the anatomical-functional knowledge on the mechanism of selected antipsychotics with the goals: 1) to analyze the ability of the selected antipsychotics to induce c-Fos protein expression in the above mentioned forebrain structures and to map the pattern of their topography and 2) to find out whether longer-lasting mild stress preconditioning may modify the impact of the selected antipsychotics on the activity of cells in the forebrain areas in adult rats. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.015DOI Listing

Poloxamer 188 rescues MPTP-induced lysosomal membrane integrity impairment in cellular and mouse models of Parkinson's disease.

Neurochem Int 2019 Jun 20;126:178-186. Epub 2019 Mar 20.

Department of Pharmacology, School of Pharmacy, Nantong University, 19 Qixiu Road, Nantong, 226001, Jiangsu, China. Electronic address:

Parkinson's disease (PD) is the second most common neurodegenerative disorder characterized by the progressive loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). Rupture of lysosome is a major cellular stress condition leading to cell death in PD. We have previously shown that environmental oxidative toxins could impair autophagic flux and lysosomal functions in PD. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.013DOI Listing
June 2019
2 Reads

The Receptor for Advanced Glycation End Products (RAGE) and DIAPH1: Implications for vascular and neuroinflammatory dysfunction in disorders of the central nervous system.

Neurochem Int 2019 Jun 20;126:154-164. Epub 2019 Mar 20.

Diabetes Research Program, Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, New York University School of Medicine, New York, NY, 10016, USA. Electronic address:

The Receptor for Advanced Glycation End Products (RAGE) is expressed by multiple cell types in the brain and spinal cord that are linked to the pathogenesis of neurovascular and neurodegenerative disorders, including neurons, glia (microglia and astrocytes) and vascular cells (endothelial cells, smooth muscle cells and pericytes). Mounting structural and functional evidence implicates the interaction of the RAGE cytoplasmic domain with the formin, Diaphanous1 (DIAPH1), as the key cytoplasmic hub for RAGE ligand-mediated activation of cellular signaling. In aging and diabetes, the ligands of the receptor abound, both in the central nervous system (CNS) and in the periphery. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.012DOI Listing
June 2019
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Cerebrovascular inflammation: A critical trigger for neurovascular injury?

Neurochem Int 2019 Jun 16;126:165-177. Epub 2019 Mar 16.

Key Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing, 211166, Jiangsu Province, PR China. Electronic address:

The cerebrovascular system is not only inert bystandard that support the metabolic demands of the brain but also elicit the barrier functions against risk factors mediated neurovascular injury. The onsets of cerebrovascular inflammation are considered as stimuli that can provoke the host defense system and trigger the development of neurological disorders. Homeostasis of the brain function is regulated by the movement of endothelial, glial, and neuronal cells within the neurovascular unit (NVU), which acts as a "platform" for the coordinated action of anti- and pro-inflammatory mechanisms. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.011DOI Listing
June 2019
3.092 Impact Factor

Inflammatory domains modulate autism spectrum disorder susceptibility during maternal nutritional programming.

Neurochem Int 2019 Jun 15;126:109-117. Epub 2019 Mar 15.

Universidad Autónoma de Nuevo Leon, Facultad de Medicina, Biochemistry Department, Mexico; Universidad Autónoma de Nuevo Leon, Centro de Investigación y Desarrollo en Ciencias de la Salud, Neurometabolism Unit, Mexico. Electronic address:

Autism spectrum disorder (ASD) is a complex neurodevelopmental disease which involves functional and structural defects in selective central nervous system (CNS) regions harming capability to process and respond to external stimuli. In addition to genetic background, etiological causes of ASD have not been fully clarified. Maternal immune activation (MIA) during pregnancy have been proposed as a potential etiological cause leading to aberrant synaptic pruning and microglia-mediated neurogenesis impairment. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.009DOI Listing

Neuro-protective effect of monomethyl fumarate on ischemia reperfusion injury in rats: Role of Nrf2/HO1 pathway in peri-infarct region.

Neurochem Int 2019 Jun 14;126:96-108. Epub 2019 Mar 14.

Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, India.

Post stroke recanalization has been associated with increased risk of oxidative stress. Stimulating endogenous antioxidant pathway by activation of nuclear factor erythroid-2-related factor-2 (Nrf2) plays a key role in neuronal defense against inflammation and oxidative stress in penumbra. Here, we explored whether monomethyl fumarate (MMF) could produce neuro-protection after ischemia/reperfusion (I/R) injury via Nrf2/HO1 activation. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.010DOI Listing
June 2019
2 Reads

Therapeutic hypothermia protects photoreceptors through activating Cirbp pathway.

Neurochem Int 2019 Jun 14;126:86-95. Epub 2019 Mar 14.

Department of Ophthalmology, Second Hospital of Jilin University, Changchun, PR China. Electronic address:

Therapeutic hypothermia as a physical method to lower the brain temperature of patients has been widely used in clinics as an effective and necessary step during the treatment of acute brain injury or edema. However, due to limitations of the ocular structure, the application of hypothermia in retinal neuroprotection still has an obvious barrier. Here, the neuroprotective mechanism produced by hypothermia in the retina was investigated, with the hopes of deciphering the key molecular targets of the signaling pathway to finally realize the ocular neuroprotection by regulating specific molecular targets. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.006DOI Listing
June 2019
1 Read

Adenosine A1 receptors modulate the Na-Hypertonicity induced glutamate release in hypothalamic glial cells.

Neurochem Int 2019 Jun 12;126:64-68. Epub 2019 Mar 12.

Instituto de Ciências Biológicas, Universidade Federal do Pará, Belém, Pará, Brazil. Electronic address:

Glutamate release in response to a hypertonic stimulus is a well described phenomenon in the hypothalamus. Evidence suggests that hypothalamic glial cells release glutamate into the extracellular environment in hypertonic conditions. In the current study, we described autocrine regulation of adenosine on glutamate release induced by Nahypertonicity in hypothalamic glial cell cultures. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.013DOI Listing

Pharmacological HIF inhibition prevents retinal neovascularization with improved visual function in a murine oxygen-induced retinopathy model.

Neurochem Int 2019 Mar 11;128:21-31. Epub 2019 Mar 11.

Laboratory of Photobiology, Keio University School of Medicine, Tokyo, Japan; Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan. Electronic address:

Neovascular retinal diseases are the leading causes of blindness in advanced countries. To date, anti-VEGF (vascular endothelial growth factor) drugs are clinically effective and widely used for these diseases. However, recent animal and clinical studies reported that potent and long-term VEGF antagonism may induce chorioretinal atrophy. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.008DOI Listing

Neuroprotective effects of targeting BET proteins for degradation with dBET1 in aged mice subjected to ischemic stroke.

Neurochem Int 2019 Mar 11. Epub 2019 Mar 11.

Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville, FL, USA. Electronic address:

Neuroinflammation after stroke significantly contributes to neuronal cell death. Bromodomain and Extra Terminal Domain (BET) proteins are essential to inflammatory gene transcription. BET proteins (BRD2, BRD3, BRD4, and BRDT) have varied effects including chromatin remodeling, histone acetyltransferase activity, and as scaffolds to recruit transcription factors; they couple chromatin remodeling with transcription. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.004DOI Listing
March 2019
1 Read

Oligodendrocyte degeneration and concomitant microglia activation directs peripheral immune cells into the forebrain.

Neurochem Int 2019 Jun 10;126:139-153. Epub 2019 Mar 10.

Institute of Anatomy, Medical University of Rostock, Rostock, Germany. Electronic address:

Brain-intrinsic degenerative cascades are a proposed factor driving inflammatory lesion formation in multiple sclerosis (MS) patients. We recently showed that encephalitogenic lymphocytes are recruited to the sites of active demyelination induced by cuprizone. Here, we investigated whether cuprizone-induced oligodendrocyte and myelin pathology is sufficient to trigger peripheral immune cell recruitment into the forebrain. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.005DOI Listing
June 2019
2 Reads

Autism genes and the leukocyte transcriptome in autistic toddlers relate to pathogen interactomes, infection and the immune system. A role for excess neurotrophic sAPPα and reduced antimicrobial Aβ.

Authors:
C J Carter

Neurochem Int 2019 Jun 9;126:36-58. Epub 2019 Mar 9.

PolygenicPathways, 41C Marina, Saint Leonard's on Sea, TN38 0BU, East Sussex, UK. Electronic address:

Prenatal and early childhood infections have been implicated in autism. Many autism susceptibility genes (206 Autworks genes) are localised in the immune system and are related to immune/infection pathways. They are enriched in the host/pathogen interactomes of 18 separate microbes (bacteria/viruses and fungi) and to the genes regulated by bacterial toxins, mycotoxins and Toll-like receptor ligands. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.007DOI Listing
June 2019
2 Reads

Prolonged activation of CXCR4 hampers the release-regulating activity of presynaptic NMDA receptors in rat hippocampal synaptosomes.

Neurochem Int 2019 Jun 8;126:59-63. Epub 2019 Mar 8.

Department of Pharmacy, DiFAR, Center of Excellence for Biomedical Research, Viale Cembrano 4, 16148, University of Genoa, Genoa, Italy; IRCCS Ospedale Policlinico San Martino, Genoa, Italy. Electronic address:

We investigated the impact of the prolonged exposure of rat hippocampal synaptosomes to CXCL12 (3 nM) on the NMDA-mediated release of [H]D-aspartate ([H]D-Asp) or [H]noradrenaline ([H]NA). Synaptosomes were stimulated twice with NMDA/CXCL12 and the amount of the NMDA-evoked tritium release (S1 and S2) quantified to calculate the S2/S1 ratio. The S2/S1 ratio for both transmitters was drastically decreased by 3 nM CXCL12 between the two stimuli (CXCL12-treated synaptosomes) in a AMD3100-sensitive manner. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.003DOI Listing

Defective vascular signaling & prospective therapeutic targets in brain arteriovenous malformations.

Neurochem Int 2019 Jun 8;126:126-138. Epub 2019 Mar 8.

Department of Neurological Surgery, University of California San Francisco, San Francisco, CA, USA.

The neurovascular unit is composed of endothelial cells, vascular smooth muscle cells, pericytes, astrocytes and neurons. Through tightly regulated multi-directional cell signaling, the neurovascular unit is responsible for the numerous functionalities of the cerebrovasculature - including the regulation of molecular and cellular transport across the blood-brain barrier, angiogenesis, blood flow responses to brain activation and neuroinflammation. Historically, the study of the brain vasculature focused on endothelial cells; however, recent work has demonstrated that pericytes and vascular smooth muscle cells - collectively known as mural cells - play critical roles in many of these functions. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.002DOI Listing
June 2019
3.092 Impact Factor

Blood vessels as a scaffold for neuronal migration.

Neurochem Int 2019 Jun 6;126:69-73. Epub 2019 Mar 6.

Department of Developmental and Regenerative Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi, 467-8601, Japan; Division of Neural Development and Regeneration, National Institute for Physiological Sciences, Okazaki, Aichi, 444-8585, Japan. Electronic address:

Neurogenesis and angiogenesis share regulatory factors that contribute to the formation of vascular networks and neuronal circuits in the brain. While crosstalk mechanisms between neural stem cells (NSCs) and the vasculature have been extensively investigated, recent studies have provided evidence that blood vessels also play an essential role in neuronal migration in the brain during development and regeneration. The mechanisms of the neuronal migration along blood vessels, referred to as "vascular-guided migration," are now being elucidated. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.03.001DOI Listing

Oral administration of carvacrol/β-cyclodextrin complex protects against 6-hydroxydopamine-induced dopaminergic denervation.

Neurochem Int 2019 Jun 5;126:27-35. Epub 2019 Mar 5.

Centro de Estudos em Estresse Oxidativo, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.

Carvacrol (CARV) presents valuable biological properties such as anti-inflammatory and antioxidant activities. However, pharmacological uses of CARV are largely limited due to disadvantages related to solubility, bioavailability, preparation and storage processes. The complexation of monoterpenes with β-cyclodextrin (β-CD) increases their stability, solubility and oral bioavailability. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.021DOI Listing
June 2019
2 Reads
3.092 Impact Factor

Signaling by hydrogen sulfide (HS) and polysulfides (HS) in the central nervous system.

Authors:
Hideo Kimura

Neurochem Int 2019 Jun 6;126:118-125. Epub 2019 Mar 6.

National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, 187-8502, Japan. Electronic address:

Hydrogen sulfide (HS) is a signaling molecule used to modify neuronal transmission, regulate vascular tone, protect tissues from oxidative stress, sense oxygen, and generate ATP. Hydrogen polysulfides (HS) have recently been identified as signaling molecules that mediate the activation of ion channels, regulation of tumor growth, and the transcriptional regulation of oxidative stress; some of which were previously ascribed to HS. Cystathionine β-synthetase (CBS), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfurtransferase (3MST) are known as HS-producing enzymes. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.01.027DOI Listing
June 2019
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Virtual screening identification of novel chemical inhibitors for aberrant interactions between pathogenic mutant SOD1 and tubulin.

Neurochem Int 2019 Jun 1;126:19-26. Epub 2019 Mar 1.

Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-Higashi, Kodaira, Tokyo, 187-8502, Japan. Electronic address:

Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease caused by selective motor neuron death. Mutations in the gene encoding copper/zinc superoxide dismutase (SOD1) belong to one of the four major mutation clusters responsible for pathogenesis of ALS. Toxic gain-of-function (not loss-of-function) of SOD1 mutants causes motor neuron degeneration. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.020DOI Listing
June 2019
5 Reads

Contribution of cholinergic interneurons to striatal pathophysiology in Parkinson's disease.

Neurochem Int 2019 Jun 27;126:1-10. Epub 2019 Feb 27.

Aix Marseille Univ, CNRS, LNC, FR3C, Marseille, France. Electronic address:

Parkinson's disease (PD) is a neurodegenerative disorder caused by the loss of nigral dopaminergic neurons innervating the striatum, the main input structure of the basal ganglia. This creates an imbalance between dopaminergic inputs and cholinergic interneurons (ChIs) within the striatum. The efficacy of anticholinergic drugs, one of the earliest therapy for PD before the discovery of L-3,4-dihydroxyphenylalanine (L-DOPA) suggests an increased cholinergic tone in this disease. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.019DOI Listing
June 2019
2 Reads

Correlative study using structural MRI and super-resolution microscopy to detect structural alterations induced by long-term optogenetic stimulation of striatal medium spiny neurons.

Neurochem Int 2019 May 27;125:163-174. Epub 2019 Feb 27.

Department of Neuropsychiatry, Keio University School of Medicine, Japan.

Striatal medium spiny neurons (MSNs) control motor function. Hyper- or hypo-activity of MSNs coincides with basal ganglia-related movement disorders. Based on the assumption that lasting alterations in neuronal activity lead to structural changes in the brain, understanding these structural alterations may be used to infer MSN functional abnormalities. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.017DOI Listing
May 2019
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Blue light exacerbates and red light counteracts negative insults to retinal ganglion cells in situ and R28 cells in vitro.

Neurochem Int 2019 May 27;125:187-196. Epub 2019 Feb 27.

Fundación de Investigación Oftalmológica, Avda. Doctores Fernández-Vega 34, E-33012, Oviedo, Asturias, Spain. Electronic address:

Neurones are dependent on their mitochondria to produce the necessary amounts of ATP for survival. Retinal ganglion cells (RGCs) have a particularly large number of mitochondria which-unlike neurones in the brain-are exposed to visual light of 400-850 nm. Here we demonstrate that short wavelength visual blue light negatively affects mitochondrial function, causing oxidative stress and decreased cell survival. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.018DOI Listing
May 2019
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Metabolomic analyses of vigabatrin (VGB)-treated mice: GABA-transaminase inhibition significantly alters amino acid profiles in murine neural and non-neural tissues.

Neurochem Int 2019 May 26;125:151-162. Epub 2019 Feb 26.

Department of Pharmacotherapy, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA, USA. Electronic address:

The anticonvulsant vigabatrin (VGB; Sabril) irreversibly inhibits GABA transaminase to increase neural GABA, yet its mechanism of retinal toxicity remains unclear. VGB is suggested to alter several amino acids, including homocarnosine, β-alanine, ornithine, glycine, taurine, and 2-aminoadipic acid (AADA), the latter a homologue of glutamic acid. Here, we evaluate the effect of VGB on amino acid concentrations in mice, employing a continuous VGB infusion (subcutaneously implanted osmotic minipumps), dose-escalation paradigm (35-140 mg/kg/d, 12 days), and amino acid quantitation in eye, visual and prefrontal cortex, total brain, liver and plasma. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6414070PMC
May 2019
2 Reads

Neurovascular interactions in skin wound healing.

Neurochem Int 2019 May 25;125:144-150. Epub 2019 Feb 25.

Department of Plastic Surgery, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Skin wound healing is a complex and dynamic biological process that involves many different cell types, the extracellular matrix, and mediators, such as neuropeptides, growth factors, and cytokines. Similar to diseases of the central nervous system, neurovascular interactions have been shown to play a pivotal role in skin wound healing, for example, as seen in the delayed healing of denervated skin. In aspects involving neurovascular interactions, while angiogenesis is considered important, physiological and pathological roles of these interactions in skin wound healing remain unclear. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.014DOI Listing
May 2019
4 Reads

GLAST (GLutamate and ASpartate Transporter) in human prefrontal cortex; interactome in healthy brains and the expression of GLAST in brains of chronic alcoholics.

Neurochem Int 2019 May 25;125:111-116. Epub 2019 Feb 25.

School of Medical Sciences, Bosch Institute, Faculty of Health and Medicine, The University of Sydney, Sydney, NSW, 2006, Australia. Electronic address:

We have analysed post-mortem samples of prefrontal cortex from control and alcoholic human brains by the technique of Western blotting to estimate and compare the expressions of glutamate transporter GLAST (Excitatory Amino Acid Transporter One; EAAT1). Furthermore, using the non-alcoholic prefrontal cortex and custom-made GLAST (EAAT1) antibody we determined GLAST (EAAT1) "interactome" i.e. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S01970186183061
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http://dx.doi.org/10.1016/j.neuint.2019.02.009DOI Listing
May 2019
5 Reads

Preproenkephalin-expressing ventral pallidal neurons control inhibitory avoidance learning.

Neurochem Int 2019 Jun 21;126:11-18. Epub 2019 Feb 21.

Laboratory for Advanced Brain Functions, Institute for Protein Research, Osaka University, Japan. Electronic address:

The ventral pallidum (VP) is a critical component of the basal ganglia neurocircuitry regulating learning and decision making; however, its precise role in controlling associative learning of environmental stimuli conditioned to appetitive or aversive outcomes is still unclear. Here, we investigated the expression of preproenkephalin, a polypeptide hormone previously shown to be expressed in nucleus accumbens neurons controlling aversive learning, within GABAergic and glutamatergic VP neurons. Next, we explored the behavioral consequences of chemicogenetic inhibition or excitation of preproenkephalin-expressing VP neurons on associative learning of reward- or aversion-paired stimuli in autoshaping and inhibitory avoidance tasks, respectively. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.011DOI Listing

Iron-induced oxidative stress contributes to α-synuclein phosphorylation and up-regulation via polo-like kinase 2 and casein kinase 2.

Neurochem Int 2019 May 22;125:127-135. Epub 2019 Feb 22.

Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders, Medical College of Qingdao University, Qingdao, 266071, China; Institute of Brain Science and Disease, Qingdao University, Qingdao, 266071, China. Electronic address:

α-Synuclein plays a central role in synucleinopathies pathogenesis such as Parkinson's disease (PD). Phosphorylation is the most common and important protein modification linked to α-synuclein pathologies. There is mounting evidence suggested iron and α-synuclein are closely related in PD. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.016DOI Listing
May 2019
1 Read
3.092 Impact Factor

Echinacoside selectively rescues complex I inhibition-induced mitochondrial respiratory impairment via enhancing complex II activity.

Neurochem Int 2019 May 21;125:136-143. Epub 2019 Feb 21.

Laboratory of Neurophysiology and Neuropathology, Department of Integrative Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. Electronic address:

Previous investigations have implicated mitochondrial dysfunction characterized by Complex I deficiency in the death of dopaminergic neurons in Parkinson's disease (PD). To date, there are no efficient therapeutic approaches to rescue mitochondrial respiratory impairment or prevent neurodegeneration in PD. The beneficial effects of echinacoside (ECH) on neurodegeneration have been reported in both in vivo and in vitro studies, yet the mechanisms underlying remain elusive and little has been investigated concerning the influences of ECH on mitochondrial respiratory impairment. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.012DOI Listing
May 2019
2 Reads

Protein and surface expression of HCN2 and HCN4 subunits in mesocorticolimbic areas after cocaine sensitization.

Neurochem Int 2019 May 19;125:91-98. Epub 2019 Feb 19.

Physiology Department, University of Puerto Rico, School of Medicine, Medical Sciences Campus, San Juan, 00936-5067, Puerto Rico. Electronic address:

The I is a mixed depolarizing current present in neurons which, upon activation by hyperpolarization, modulates neuronal excitability in the mesocorticolimbic (MCL) system, an area which regulates emotions such as pleasure, reward, and motivation. Its biophysical properties are determined by HCN protein expression profiles, specifically HCN subunits 1-4. Previously, we reported that cocaine-induced behavioral sensitization increases HCN2 protein expression in all MCL areas with the Ventral Tegmental Area (VTA) showing the most significant increase. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.004DOI Listing
May 2019
2 Reads
3.092 Impact Factor

Propagermanium, a CCR2 inhibitor, attenuates cerebral ischemia/reperfusion injury through inhibiting inflammatory response induced by microglia.

Neurochem Int 2019 May 19;125:99-110. Epub 2019 Feb 19.

State Key Laboratory of Natural Medicines, School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu, 210009, China. Electronic address:

CCR2 could recruit immune cells migrating into brain after ischemic stroke. It is unclear whether and why Propagermanium (PG, a CCR2 inhibitor) is able to protect against ischemic injury. Middle cerebral artery occlusion (MCAO) and reperfusion injury in C57BL/6 J male mice were performed in vivo to mimic ischemic stroke. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.010DOI Listing
May 2019
1 Read
3.092 Impact Factor

Activation of anti-oxidant of curcumin pyrazole derivatives through preservation of mitochondria function and Nrf2 signaling pathway.

Neurochem Int 2019 May 13;125:82-90. Epub 2019 Feb 13.

Department of Medicinal Chemistry, School of Pharmaceutical Science, Sun Yat-sen University, Guangzhou, 510006, PR China. Electronic address:

Oxidative stress is an important cause of neurodegenerative diseases. Antioxidant is an potential important method to treat such diseases. The aim of this study is to discover new and effective antioxidants and their mechanism. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.01.026DOI Listing

Abuse potential of 2-(4-iodo-2, 5-dimethoxyphenyl)N-(2-methoxybenzyl)ethanamine (25INBOMe); in vivo and ex vivo approaches.

Neurochem Int 2019 May 13;125:74-81. Epub 2019 Feb 13.

National Institute of Drug and Safety Evaluation, Ministry of Food and Drug Safety, Osong, Cheongju, Republic of Korea. Electronic address:

25INBOMe ("25-I", "N-Bomb"), one of new psychoactive substances (NPSs), is being abused for recreational purpose. However, the liability for abuse or dependence has not been systematically studied yet. The objective of the present study was to evaluate rewarding and reinforcing effects of 25INBOMe using conditioned place preference (CPP) and self-administration (SA) paradigms. Read More

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http://dx.doi.org/10.1016/j.neuint.2019.02.007DOI Listing
May 2019
1 Read