Neurobehavioral and cytotoxic effects of vanadium during oligodendrocyte maturation: A protective role for erythropoietin

Mustapha, O. A.; Oke, B. O.; Offen, Nils; Sirén, Anna‐Leena; Olopade, James Olukayode

doi:10.1016/j.etap.2014.05.001

Cited by 43 publications

(63 citation statements)

References 42 publications

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“…Briefly, the frontal, parietal and temporal bones were removed to expose the brain which was gently scooped out, post-fixed for 4 h in the same solution, then processed and embedded in paraffin blocks as described by Mustapha et al (2014). Sections were cut on a standard microtome at 5-μm thickness from paraffin embedded tissue, sectioned at Sagittal level 17, (Bregma lateral coordinates 0.675 μm, from Allen reference Mouse Brain Atlas, 2016), containing the neocortex, basal ganglia, midbrain and brain-stem.…”

Section: Methodsmentioning

confidence: 99%

“…Earlier studies have shown that vanadium crosses the blood brain barrier (García et al, 2004) to induce neuropathology including neurobehavioral (Li et al, 2013; Saxena et al, 2013; Mustapha et al, 2014; Folarin et al, 2016), neurochemical (Sasi et al, 1994; García et al, 2004) and neurocellular (Domingo, 1996; Garcia et al, 2005; Avila-Costa et al, 2006) changes. In humans, features of acute neurotoxicity include central nervous system (CNS) perturbations, (CNS) depression, tremor, impaired conditioned reflexes, as well as congestion of brain and spinal cord (Haider et al, 1998; Soazo and Garcia, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Brain Metal Distribution and Neuro-Inflammatory Profiles after Chronic Vanadium Administration and Withdrawal in Mice

et al. 2017

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Vanadium is a potentially toxic environmental pollutant and induces oxidative damage in biological systems including the central nervous system (CNS). Its deposition in brain tissue may be involved in the pathogenesis of certain neurological disorders which after prolonged exposure can culminate into more severe pathology. Most studies on vanadium neurotoxicity have been done after acute exposure but in reality some populations are exposed for a lifetime. This work was designed to ascertain neurodegenerative consequences of chronic vanadium administration and to investigate the progressive changes in the brain after withdrawal from vanadium treatment. A total of 85 male BALB/c mice were used for the experiment and divided into three major groups of vanadium treated (intraperitoneally (i.p.) injected with 3 mg/kg body weight of sodium metavanadate and sacrificed every 3 months till 18 months); matched controls; and animals that were exposed to vanadium for 3 months and thereafter the metal was withdrawn. Brain tissues were obtained after animal sacrifice. Sagittal cut sections of paraffin embedded tissue (5 μm) were analyzed by the Laser ablation-inductively coupled plasma-mass spectrometry (LA–ICP–MS) to show the absorption and distribution of vanadium metal. Also, Haematoxylin and Eosin (H&E) staining of brain sections, and immunohistochemistry for Microglia (Iba-1), Astrocytes (GFAP), Neurons (Neu-N) and Neu-N + 4′,6-diamidine-2′-pheynylindole dihydrochloride (Dapi) Immunofluorescent labeling were observed for morphological and morphometric parameters. The LA–ICP–MS results showed progressive increase in vanadium uptake with time in different brain regions with prediction for regions like the olfactory bulb, brain stem and cerebellum. The withdrawal brains still show presence of vanadium metal in the brain slightly more than the controls. There were morphological alterations (of the layering profile, nuclear shrinkage) in the prefrontal cortex, cellular degeneration (loss of dendritic arborization) and cell death in the Hippocampal CA1 pyramidal cells and Purkinje cells of the cerebellum, including astrocytic and microglial activation in vanadium exposed brains which were all attenuated in the withdrawal group. With exposure into old age, the evident neuropathology was microgliosis, while progressive astrogliosis became more attenuated. We have shown that chronic administration of vanadium over a lifetime in mice resulted in metal accumulation which showed regional variabilities with time. The metal profile and pathological effects were not completely eliminated from the brain even after a long time withdrawal from vanadium metal.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Brain Metal Distribution and Neuro-Inflammatory Profiles after Chronic Vanadium Administration and Withdrawal in Mice

et al. 2017

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“…Behavioral variables which were measured in the open field test include the following:

Line crossings: frequency with which the rat crossed a grid line with all four paws. A high frequency of this behavior indicates increased locomotion and exploration and/or a lower level of anxiety [29]

Grooming and grooming time: frequency and duration with which the rats scratched, licked, or bit their coat, whiskers, feet, or tail. A high frequency and time of this behavior indicate higher level of anxiety [30]…”

Section: Methodsmentioning

confidence: 99%

“…A high frequency of this behavior indicates increased locomotion and exploration and/or a lower level of anxiety [29]…”

Section: Methodsmentioning

confidence: 99%

The Role of Hippocampal Estradiol Receptor‐α in a Perimenopausal Affective Disorders‐Like Rat Model and Attenuating of Anxiety by Electroacupuncture

Wang

Huang

Yuan

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Hormone replacement therapy is the principal treatment for perimenopausal affective disorders which can cause severe side effects. The present study compared the effects of electroacupuncture (EA) and estradiol treatment on perimenopausal affective disorders at the behavioral and cellular levels. In this randomized experimental in vivo study, adult female rats were divided into intact, ovariectomy, chronic unpredictable stress (CUS), and ovariectomy and CUS combination groups. After week 6, all groups were subdivided to three subgroups of control, EA, and estradiol treatment. The behavioral parameters in the open field and the elevated plus maze tests were assessed before and after treatments. Alterations of serum steroid hormones and changes of estradiol receptor-α (ER-α) immunofluorescence neurons in the hippocampus sections were evaluated. EA treatment caused more antianxiety effects than estradiol treatment in CUS group (P < 0.05). Notably, estradiol and EA treatments had better significant behavioral effects when the models were not estrogen-deficient. Importantly, within each group, compared to the control group, the numbers of ER-α-positive neurons were significantly larger in EA subgroups. Therefore, EA had antianxiety effects on perimenopausal affective disorders caused by CUS but not by estrogen deficiency and upregulation of hippocampus ER-α neurons may contribute to its mechanism of action.

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“…CNPase is one of the most abundant proteins in CNS myelin and a possible auto-antigen in MS (Rosener et al, 1997). The appearance of CNPase is one of the earliest events of oligodendrocyte differentiation and is thought to play a critical role in the events leading up to myelination (Mustapha et al, 2014). The absence of CNPase causes premature death through axonal swelling.…”

Section: Discussionmentioning

confidence: 99%

Total glucosides of peony attenuates experimental autoimmune encephalomyelitis in C57BL/6 mice

Huang

Zhu

et al. 2015

Journal of Neuroimmunology

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Neurobehavioral and cytotoxic effects of vanadium during oligodendrocyte maturation: A protective role for erythropoietin

Cited by 43 publications

References 42 publications

Brain Metal Distribution and Neuro-Inflammatory Profiles after Chronic Vanadium Administration and Withdrawal in Mice

Brain Metal Distribution and Neuro-Inflammatory Profiles after Chronic Vanadium Administration and Withdrawal in Mice

The Role of Hippocampal Estradiol Receptor‐α in a Perimenopausal Affective Disorders‐Like Rat Model and Attenuating of Anxiety by Electroacupuncture

Total glucosides of peony attenuates experimental autoimmune encephalomyelitis in C57BL/6 mice

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