Developmental cuprizone exposure impairs oligodendrocyte lineages differentially in cortical and white matter tissues and suppresses glutamatergic neurogenesis signals and synaptic plasticity in the hippocampal dentate gyrus of rats

Abe, Hajime; Saito, Fumiyo; Tanaka, Takeshi; Mizukami, Sayaka; Hasegawa-Baba, Yasuko; Imatanaka, Nobuya; Akahori, Yumi; Yoshida, Toshinori; Shibutani, Makoto

doi:10.1016/j.taap.2015.11.006

Cited by 19 publications

(12 citation statements)

References 47 publications

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“…Histological findings in this study support reports that CPZ extensively destroys hippocampal neurons (25, 26) and induces neurotoxicity in the brain, as indicated by the observed cellular clusters with pyknotic characteristics, which were observed in the PFC layers, the CA4 region of the hippocampus, and the poorly stained granule cells in the granular layer of the dentate gyrus of groups treated with CPZ. Further histological analysis suggests that treatment of rats with Kv prevented CPZ-induced neuronal degeneration, especially when given before CPZ rather than after CPZ.…”

Section: Discussionsupporting

confidence: 91%

Kolaviron Protects the Prefrontal Cortex and Hippocampus against Histomorphological and Neurobehavioural Changes in Cuprizone Model of Multiple Sclerosis

Omotoso

Olajide

Gbadamosi

et al. 2018

MJMS

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To cite this article: Omotoso GO, Olajide OJ, Gbadamosi IT, Rasheed MA, Izuogu CT. Kolaviron protects the prefrontal cortex and hippocampus against histomorphological and neurobehavioural changes in cuprizone model of multiple sclerosis. Malays J Med Sci. 2018;25(2) Abstract Background: This study explored the efficacy of kolaviron-a biflavonoid complex isolated from the seeds of Garcinia kola-in protecting against cuprizone (CPZ)-induced demyelination in both the prefrontal cortex and the hippocampus of Wistar rats.Methodology: Thirty rats were treated to receive 0.5 mL phosphate-buffered saline (group A, control), 0.5 mL corn oil (group B), 0.2% CPZ (group C), for 6 weeks, 0.2% CPZ for 3 weeks and then 200 mg/kg of Kv for 3 weeks (group D), or 200 mg/kg of Kv for 3 weeks followed by 0.2% CPZ for 3 weeks (group E). Rats were assessed for exploratory functions and anxiety-like behaviour before being euthanised and perfused transcardially with 4% paraformaldehyde. Prefrontal and hippocampal thin sections were stained in hematoxylin and eosin and cresyl fast violet stains.Results: CPZ-induced demyelination resulted in behavioural impairment as seen by reduced exploratory activities, rearing behaviour, stretch attend posture, center square entry, and anxiogenic characteristics. Degenerative changes including pyknosis, karyorrhexis, neuronal hypertrophy, and reduced Nissl integrity were also seen. Animals treated with Kv showed significant improvement in behavioural outcomes and a comparatively normal cytoarchitectural profile.Conclusion: Kv provides protective roles against CPZ-induced neurotoxicity through prevention of ribosomal protein degradation.

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Section: Discussionsupporting

confidence: 91%

Kolaviron Protects the Prefrontal Cortex and Hippocampus against Histomorphological and Neurobehavioural Changes in Cuprizone Model of Multiple Sclerosis

Omotoso

Olajide

Gbadamosi

et al. 2018

MJMS

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“…Histochemical findings in this study support previous reports that CPZ extensively damages hippocampal neurons [ 32 33 ]. Nissl stain findings in the present study revealed that CPZ compromised the integrity of neuronal cells within the PFC and hippocampus of experimental animals.…”

Section: Discussionsupporting

confidence: 92%

Ameliorative effects of Moringa on cuprizone-induced memory decline in rat model of multiple sclerosis

et al. 2018

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Cuprizone is a neurotoxin with copper-chelating ability used in animal model of multiple sclerosis in which oxidative stress has been documented as one of the cascade in the pathogenesis. Moringa oleifera is a phytomedicinal plant with antioxidant and neuroprotective properties. This study aimed at evaluating the ameliorative capability of M. oleifera in cuprizone-induced behavioral and histopathological alterations in the prefrontal cortex and hippocampus of Wistar rats. Four groups of rats were treated with normal saline, cuprizone, M. oleifera and a combination of M. oleifera and cuprizone, for five weeks. The rats were subjected to Morris water maze and Y-maze to assess long and short-term memory respectively. The animals were sacrificed, and brain tissues were removed for histochemical and enzyme lysate immunosorbent assay for catalase, superoxide dismutase, and nitric oxide. Cuprizone significantly induced oxidative and nitrosative stress coupled with memory decline and cortico-hippocampal neuronal deficits; however, administration of M. oleifera significantly reversed the neuropathological deficits induced by cuprizone.

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“…For example, more environmental signals that inhibit OPC proliferation and arrest their differentiation are present in GM than in WM, although it is unknown where these signals originate [30,94,116]. When developing rats are exposed to cuprizone, a copper chelator that causes specific depletion of OLGs, via a maternal diet from gestational day 6 to postnatal day 21, the density of oligodendroglial lineage cells is widely impaired in cortical regions at postnatal day 21, whereas only mature OLGs are affected in the corpus callosum [117]. An increased expression of the anti-aging protein Klotho may protect wmOPCs from cuprizone toxicity [118].…”

Section: Heterogeneity Of Oligodendrocyte Progenitor Cells In Grey Anmentioning

confidence: 99%

Macroglial diversity: white and grey areas and relevance to remyelination

Werkman

Lentferink

Baron

2020

Cell. Mol. Life Sci.

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Macroglia, comprising astrocytes and oligodendroglial lineage cells, have long been regarded as uniform cell types of the central nervous system (CNS). Although regional morphological differences between these cell types were initially described after their identification a century ago, these differences were largely ignored. Recently, accumulating evidence suggests that macroglial cells form distinct populations throughout the CNS, based on both functional and morphological features. Moreover, with the use of refined techniques including single-cell and single-nucleus RNA sequencing, additional evidence is emerging for regional macroglial heterogeneity at the transcriptional level. In parallel, several studies revealed the existence of regional differences in remyelination capacity between CNS grey and white matter areas, both in experimental models for successful remyelination as well as in the chronic demyelinating disease multiple sclerosis (MS). In this review, we provide an overview of the diversity in oligodendroglial lineage cells and astrocytes from the grey and white matter, as well as their interplay in health and upon demyelination and successful remyelination. In addition, we discuss the implications of regional macroglial diversity for remyelination in light of its failure in MS. Since the etiology of MS remains unknown and only disease-modifying treatments altering the immune response are available for MS, the elucidation of macroglial diversity in grey and white matter and its putative contribution to the observed difference in remyelination efficiency between these regions may open therapeutic avenues aimed at enhancing endogenous remyelination in either area.

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Developmental cuprizone exposure impairs oligodendrocyte lineages differentially in cortical and white matter tissues and suppresses glutamatergic neurogenesis signals and synaptic plasticity in the hippocampal dentate gyrus of rats

Cited by 19 publications

References 47 publications

Kolaviron Protects the Prefrontal Cortex and Hippocampus against Histomorphological and Neurobehavioural Changes in Cuprizone Model of Multiple Sclerosis

Kolaviron Protects the Prefrontal Cortex and Hippocampus against Histomorphological and Neurobehavioural Changes in Cuprizone Model of Multiple Sclerosis

Ameliorative effects of Moringa on cuprizone-induced memory decline in rat model of multiple sclerosis

Macroglial diversity: white and grey areas and relevance to remyelination

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