Effects of mGluR5 positive and negative allosteric modulators on brain damage evoked by hypoxia-ischemia in neonatal rats

Makarewicz, Dorota; Słomka, Marta; Danysz, Wojciech; Łazarewicz, Jerzy W.

doi:10.5114/fn.2015.56544

Cited by 4 publications

(3 citation statements)

References 40 publications

(75 reference statements)

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“…Moreover, mGluR5 has been shown to protect astrocytes from ischemic damage in the postnatal central nervous system (CNS) white matter (Vanzulli and Butt, 2015). However, other studies have found that antisense oligodeoxynucleotide directed to mGluR5, MPEP or MTEP, showed no neuroprotective effects against post-traumatic neuronal injury (Mukhin et al, 1996) in vitro , OGD damage (Meli et al, 2002), or hypoxia-ischemia injury in neonatal rats (Makarewicz et al, 2015). Moreover, the use of CHPG did not improve the functional and histological outcomes in a rat model of endothelin-1-induced focal ischemia (Riek-Burchardt et al, 2007).…”

Section: Roles Of Mglurs In Cerebral Ischemiamentioning

confidence: 99%

Phased Treatment Strategies for Cerebral Ischemia Based on Glutamate Receptors

Sun

Xue

Ding

et al. 2019

Front. Cell. Neurosci.

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Extracellular glutamate accumulation following cerebral ischemia leads to overactivation of glutamate receptors, thereby resulting in intracellular Ca 2+ overload and excitotoxic neuronal injury. Multiple attempts have been made to counteract such effects by reducing glutamate receptor function, but none have been successful. In this minireview, we present the available evidence regarding the role of all types of ionotropic and metabotropic glutamate receptors in cerebral ischemia and propose phased treatment strategies based on glutamate receptors in both the acute and post-acute phases of cerebral ischemia, which may help realize the clinical application of glutamate receptor antagonists.

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Section: Roles Of Mglurs In Cerebral Ischemiamentioning

confidence: 99%

Phased Treatment Strategies for Cerebral Ischemia Based on Glutamate Receptors

Sun

Xue

Ding

et al. 2019

Front. Cell. Neurosci.

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“…), others play a role in matching oligodendrocytes to the axonal surface (cell adhesion molecule L1, the polysialylated neuronal cell adhesion molecule: PSA-NCAM; Jagged 1). Similarly, neuron survival and proficient functioning strongly depends on oligodendrocytes and compact myelin sheath [ 170 – 173 ]. Keeping the above in mind, both the compounds protecting either neurons or oligodendrocytes, as well as those preserving the myelin structure, might turn out to be effective in preventing white matter damage and subsequent neurodevelopmental disorders.…”

Section: Clinical Perspectivementioning

confidence: 99%

Therapeutic Strategies for Leukodystrophic Disorders Resulting from Perinatal Asphyxia: Focus on Myelinating Oligodendrocytes

Janowska

Sypecka

2017

Mol Neurobiol

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Perinatal asphyxia results from the action of different risk factors like complications during pregnancy, preterm delivery, or long and difficult labor. Nowadays, it is still the leading cause of neonatal brain injury known as hypoxic-ischemic encephalopathy (HIE) and resulting neurological disorders. A temporal limitation of oxygen, glucose, and trophic factors supply results in alteration of neural cell differentiation and functioning and/or leads to their death. Among the affected cells are oligodendrocytes, responsible for myelinating the central nervous system (CNS) and formation of white matter. Therefore, one of the major consequences of the experienced HIE is leukodystrophic diseases resulting from oligodendrocyte deficiency or malfunctioning. The therapeutic strategies applied after perinatal asphyxia are aimed at reducing brain damage and promoting the endogenous neuroreparative mechanisms. In this review, we focus on the biology of oligodendrocytes and discuss present clinical treatments in the context of their efficiency in preserving white matter structure and preventing cognitive and behavioral deficits after perinatal asphyxia.

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“…The most effective treatment is to regain blood perfusion, which, however, may cause secondary injury on brain tissues [3,4]. Brain ischemia-reperfusion damage is associated with a complicated patho-physiology process, which includes neurodegeneration, apoptosis or necrosis of neurons [5,6]. Neurotransmitter plays a critical role in the occurrence of ischemia cerebrovascular disease [7,8].…”

Section: Introductionmentioning

confidence: 99%

The effect of dexmedetomidine on GluR2 and NR2B expression of cortical neurons after cerebral ischemia-reperfusion in rats

Li¹,

Liu²

2018

biomedicalresearch

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Objective: Neurotransmitter plays a crucial role in ischemia cerebrovascular disease. Study has shown that Dexmedetomidine (Dex) contributes to neuroprotective functions. We thus observed the regulatory effect of Dex on the expressions of Glutamate Receptor-2 (GluR2) and N-Methyl-D-Aspartic Acid (NMDA) receptor 2B (NR2B) in cerebral cortical neurons with an ischemia-reperfusion rat model. Patients and methods: Healthy male SD rats were randomly divided into sham, model and Dex treatment groups (N=20 each). Whole-brain ischemia-reperfusion model was generated by the clipping of bilateral common carotid artery with hypotension. Dex (9 μg/kg) was infused immediately after reperfusion, while the other two groups received equal volume of saline. Morris water maze was employed to detect learning and memory function of rats. Brain tissues were extracted at 6, 24 and 72 h after reperfusion. Immunohistochemistry (IHC) was used to detect GluR2 and NR2B receptor levels, the mRNA levels of which were determined by real-time PCR. Results: The longer escape latency and fewer number of crossing platform in water maze were shown in Model rats group. Cortical GluR2 expression was down-regulated while NR2B level was increased. Dex treatment inhibited escape latency and increased crossing times, along with the rise of cortical GluR2 expression and reduction of NR2B expression (p<0.05) in a time-dependent manner (p<0.05). Conclusion: Dex could alleviate ischemia-reperfusion injury of rat brain via down-regulating GluR2 while increasing NR2B expression.

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Effects of mGluR5 positive and negative allosteric modulators on brain damage evoked by hypoxia-ischemia in neonatal rats

Cited by 4 publications

References 40 publications

Phased Treatment Strategies for Cerebral Ischemia Based on Glutamate Receptors

Phased Treatment Strategies for Cerebral Ischemia Based on Glutamate Receptors

Therapeutic Strategies for Leukodystrophic Disorders Resulting from Perinatal Asphyxia: Focus on Myelinating Oligodendrocytes

The effect of dexmedetomidine on GluR2 and NR2B expression of cortical neurons after cerebral ischemia-reperfusion in rats

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