Oligodendrocyte

AdilijiangbLyndaKongbJunhuiWangbJimingKongcQingrongTanaXin-MinLiabc Show more https://doi.org/10.1016/j.brainres.2012.06.003Get rights and content Abstract Increasing evidence supports an important role of oligodendrocytes and myelination in the pathogenesis of schizophrenia. Oligodendrocytes are the myelin-producing cells in the central nervous system. To test the myelination dysfunction hypothesis of schizophrenia, possible myelination dysfunction was evaluated in a phencyclidine (PCP)-induced

As aforementioned, due to high metabolic demands, oligodendrocytes are specifically vulnerable to oxidative stress in the mitochondria, as well as ER stress. A prominent example is the cuprizone animal model, which uses cuprizone as a oligodendrocytes-specific neurotoxin that induces CNS demyelination in mice, specifically in the corpus callosum (Torkildsen, Brunborg, Myhr, & Bo, 2008). Importantly, cuprizone acts as a chopper chelator that interferes with complex IV of the mitochondrial respiratory

Differential effects of antipsychotics on the development of rat oligodendrocyte precursor cells exposed to cuprizone Abstract Cuprizone (CPZ) is a copper-chelating agent and has been shown to induce white matter damage in mice and rats. The compromised white matter and oligodendrocytes (OLs) respond to some antipsychotics in vivo. However, little is known about the effects of antipsychotics on cultured OLs in the presence of CPZ. The aim of this study was to examine effects of some antipsychotics

Abstract Myelin and oligodendrocyte dysfunctions have been consistently found in patients with schizophrenia. The effect of antipsychotics on myelin disturbances is unknown. The present study examined the effects of quetiapine on oligodendrocyte regeneration and myelin repair in a demyelination animal model. C57BL/6 mice were fed with cuprizone (0.2% w/w) for 12 weeks to induce chronic demyelination and oligodendrocyte degeneration, after which cuprizone was withdrawn to allow recovery. Quetiapine

The lineage of rodent oligodendrocyte has been very well characterized in vitro studies. In fact, the oligodendrocyte formation is very crucial in embryogenesis as well as in the postnatal development of the individual. To be more specific, these cells are essential for myelinating neuronal axons in the central nervous system and thus allowing fast conduction of electric impulses along the neurve fibres. Oligodendrocyte death leads to demyelination process, a pathological feature of neurological

may result in cognitive impairments such as deficits in learning and memory. White matter lesions (WML) have also been linked to increasing the risk of post-stroke dementia. Cerebral white matter damage has been widely overlooked. Comprised of oligodendrocytes that form the insulating myelin in the CNS, white matter is evidentially just as vulnerable to ischemia as gray matter.

igodendrocyteÊlineageÊtranscriptionÊfactorsÊ1ÊandÊ2. Abstract Aims Oligodendrocyte/myelin abnormalities may be an important component of the pathogenesis found in schizophrenia. The aim of this current study was to examine the possible effects of the antipsychotic drugs (APDs) haloperidol (HAL), olanzapine (OLA), and quetiapine (QUE) on the development of oligodendroglial lineage cells. Main methods CG4 cells, an oligodendrocyte progenitor cell line, were treated with various concentrations of HAL

Ionotropic receptors is a binding site that opens when an ion attaches to the binding site. The ionotropic receptor is also a direct method to the ion channels. Ionotropic receptors has a channel where molecules move in and out of the ion channel. The ions that goes into the ion channel are made out of sodium which cause the membrane to become small. Metabotropic receptors is receptor that is a part of the binding site of a neurotransmitter. Metabotropic is indirect and complex method to the ion

expression is specific to terminally differentiated oligodendrocytes (Cahoy et al., 2008; Heiman et al., 2008). Importantly, knockdown of MRF in oligodendrocytes by RNA interference downregulates expression of the majority CNS myelin genes (Emery et al., 2009). In contrast, overexpression of MRF in in vitro cultured OPCs can promote myelin gene expression. Oligodendrocyte lineage-specific MRF knockout mice show normal premyelinating oligodendrocytes but they display severe myelin gene expression deficits

However, studies have shown that human embryonic stem cell derived oligodendrocyte progenitor cells can help in neuroprotection, homeostatic maintenance, suppressing inflammation, and promoting the regeneration of axons. (Sharp et al., 2010). Most of the neural stem cell potential is in ependymal cells (Meletis et al., 2008). Transplanting these oligodendrocyte progenitor cells just one week after the injury showed widespread oligodendrocyte remyelination throughout the white matter (Keirstead et al.