NMDA receptors expressed in oligodendrocytes

Wong, Richard W.

doi:10.1002/bies.20402

Cited by 24 publications

(13 citation statements)

References 22 publications

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“…In addition to presence of NMDARs in neuronal population, a report suggests the presence of NMDARs in development, ischemia and post-ischemic events (Zhou et al, 2010). The studies on animal subjects clearly indicate the involvement of astrocytic glutamate receptor in glial cell signaling (Schipke et al, 2001; Wong, 2006). In our study, although we observed alterations in NR1, NR2A and NR2B transcripts following IR-insult in mice; however, only NR1 levels were recovered to a significant extent with the use of MESC-exo cur .…”

Section: Discussionmentioning

confidence: 99%

Curcumin-loaded embryonic stem cell exosomes restored neurovascular unit following ischemia-reperfusion injury

Kalani

Chaturvedi

Kamat

et al. 2016

The International Journal of Biochemistry & Cell Biology

199

141

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We tested whether the combined nano-formulation, prepared with curcumin (anti-inflammatory and neuroprotective molecule) and embryonic stem cell exosomes (MESC-exocur), restored neurovascular loss following an ischemia reperfusion (IR) injury in mice. IR-injury was created in 8–10 weeks old mice and divided into two groups. Out of two IR-injured groups, one group received intranasal administration of MESC-exocur for 7 days. Similarly, two sham groups were made and one group received MESC-exocur treatment. The study determined MESC-exocur reduced neurological score, infarct volume and edema following IR-injury. As compared to untreated IR group, MESC-exocur treated-IR group showed reduced inflammation and N-methyl-D-aspartate receptor expression. Treatment of MESC-exocur also reduced astrocytic GFAP expression and alleviated the expression of NeuN positive neurons in IR-injured mice. In addition, MESC-exocur treatment restored vascular endothelial tight (claudin-5 and occludin) and adherent (VE-cadherin) junction proteins in IR-injured mice as compared to untreated IR-injured mice. These results suggest that combining the potentials of embryonic stem cell exosomes and curcumin can help neurovascular restoration following ischemia-reperfusion injury in mice.

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Section: Discussionmentioning

confidence: 99%

Curcumin-loaded embryonic stem cell exosomes restored neurovascular unit following ischemia-reperfusion injury

Kalani

Chaturvedi

Kamat

et al. 2016

The International Journal of Biochemistry & Cell Biology

199

141

View full text Add to dashboard Cite

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“…Oligodendrocytes and NG2+ precursor cells are known to express NMDA, AMPA and kainate receptors, similar to neurons and astrocytes, which coexpress ErbB4 with these glutamate receptors (Wong, 2006; Verkhratsky and Kirchhoff, 2007). Since NRG1/ErbB signalling has been implicated in the subcellular targeting and endocytosis of synaptic glutamate receptors (Gu et al, 2005; Kwon et al, 2005), it may serve a similar function for glutamate receptors on oligodendrocytes.…”

Section: Discussionmentioning

confidence: 99%

Neuregulin-1/ErbB Signaling Serves Distinct Functions in Myelination of the Peripheral and Central Nervous System

Brinkmann

Agarwal

Sereda

et al. 2008

Neuron

337

348

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Understanding the control of myelin formation by oligodendrocytes is essential for treating demyelinating diseases. Neuregulin-1 (NRG1) type III, an EGF-like growth factor, is essential for myelination in the PNS. It is thus thought that NRG1/ErbB signaling also regulates CNS myelination, a view suggested by in vitro studies and the overexpression of dominant-negative ErbB receptors. To directly test this hypothesis, we generated a series of conditional null mutants that completely lack NRG1 beginning at different stages of neural development. Unexpectedly, these mice assemble normal amounts of myelin. In addition, double-mutants lacking oligodendroglial ErbB3 and ErbB4 become myelinated in the absence of any stimulation by neuregulins. In contrast, a significant hypermyelination is achieved by transgenic overexpression of NRG1 type I or NRG1 type III. Thus, NRG1/ErbB signaling is markedly different between Schwann cells and oligodendrocytes that have evolved a NRG/ErbB-independent mechanism of myelination control.

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“…In neurons, NMDARs play an important role in facilitating learning and memory [3]. However, recent studies have revealed that these membrane proteins may also exist in other cell types [4], [5], [6], [7].…”

Section: Introductionmentioning

confidence: 99%

Characterisation of the Expression of NMDA Receptors in Human Astrocytes

et al. 2010

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Astrocytes have long been perceived only as structural and supporting cells within the central nervous system (CNS). However, the discovery that these glial cells may potentially express receptors capable of responding to endogenous neurotransmitters has resulted in the need to reassess astrocytic physiology. The aim of the current study was to characterise the expression of NMDA receptors (NMDARs) in primary human astrocytes, and investigate their response to physiological and excitotoxic concentrations of the known endogenous NMDAR agonists, glutamate and quinolinic acid (QUIN). Primary cultures of human astrocytes were used to examine expression of these receptors at the mRNA level using RT-PCR and qPCR, and at the protein level using immunocytochemistry. The functionality role of the receptors was assessed using intracellular calcium influx experiments and measuring extracellular lactate dehydrogenase (LDH) activity in primary cultures of human astrocytes treated with glutamate and QUIN. We found that all seven currently known NMDAR subunits (NR1, NR2A, NR2B, NR2C, NR2D, NR3A and NR3B) are expressed in astrocytes, but at different levels. Calcium influx studies revealed that both glutamate and QUIN could activate astrocytic NMDARs, which stimulates Ca2+ influx into the cell and can result in dysfunction and death of astrocytes. Our data also show that the NMDAR ion channel blockers, MK801, and memantine can attenuate glutamate and QUIN mediated cell excitotoxicity. This suggests that the mechanism of glutamate and QUIN gliotoxicity is at least partially mediated by excessive stimulation of NMDARs. The present study is the first to provide definitive evidence for the existence of functional NMDAR expression in human primary astrocytes. This discovery has significant implications for redefining the cellular interaction between glia and neurons in both physiological processes and pathological conditions.

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NMDA receptors expressed in oligodendrocytes

Cited by 24 publications

References 22 publications

Curcumin-loaded embryonic stem cell exosomes restored neurovascular unit following ischemia-reperfusion injury

Curcumin-loaded embryonic stem cell exosomes restored neurovascular unit following ischemia-reperfusion injury

Neuregulin-1/ErbB Signaling Serves Distinct Functions in Myelination of the Peripheral and Central Nervous System

Characterisation of the Expression of NMDA Receptors in Human Astrocytes

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