Protective Effect of the N-Methyl-D-Aspartate Receptor Antagonists, MK-801 and CPP on Cold-Induced Brain Oedema

Görgülü, Adnan; Kırış, Talat; Ünal, Faruk; Türkogˇlu, Ü.; Küçük, Mutlu; Çobanogˇlu, S.

doi:10.1007/s007010050271

Cited by 9 publications

(3 citation statements)

References 26 publications

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“…[7104] This synergism between the immune system and excitotoxic levels of glutamate, aspartate, and QUIN also have similar effects on the BBB, brain vasculature, development of edema, and metabolic changes seen with TBI. [1685108122206217]…”

Section: Role Of Microgliamentioning

confidence: 99%

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Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis

Blaylock

Maroon²

2011

Surg Neurol Int

188

180

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Some individuals suffering from mild traumatic brain injuries, especially repetitive mild concussions, are thought to develop a slowly progressive encephalopathy characterized by a number of the neuropathological elements shared with various neurodegenerative diseases. A central pathological mechanism explaining the development of progressive neurodegeneration in this subset of individuals has not been elucidated. Yet, a large number of studies indicate that a process called immunoexcitotoxicity may be playing a central role in many neurodegenerative diseases including chronic traumatic encephalopathy (CTE). The term immunoexcitotoxicity was first coined by the lead author to explain the evolving pathological and neurodevelopmental changes in autism and the Gulf War Syndrome, but it can be applied to a number of neurodegenerative disorders. The interaction between immune receptors within the central nervous system (CNS) and excitatory glutamate receptors trigger a series of events, such as extensive reactive oxygen species/reactive nitrogen species generation, accumulation of lipid peroxidation products, and prostaglandin activation, which then leads to dendritic retraction, synaptic injury, damage to microtubules, and mitochondrial suppression. In this paper, we discuss the mechanism of immunoexcitotoxicity and its link to each of the pathophysiological and neurochemical events previously described with CTE, with special emphasis on the observed accumulation of hyperphosphorylated tau.

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Section: Role Of Microgliamentioning

confidence: 99%

“…[22] Excitotoxins, also released by activated microglia, appear to be the most toxic component released by the microglia. [685108122206217]…”

Section: The Immunoexcitotoxicity Mechanismmentioning

confidence: 99%

Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis

Blaylock

Maroon²

2011

Surg Neurol Int

188

180

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“…The amount of time spent in each conditioning compartment was recorded as a measure of CPP for each phase. determined from previous studies with these drugs [10,13] .…”

Section: Place Conditioning Apparatus and Procedures Cppmentioning

confidence: 99%

Combined action of MK-801 and ceftriaxone impairs the acquisition and reinstatement of morphine-induced conditioned place preference, and delays morphine extinction in rats

et al. 2012

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The effects of memantine on lipid peroxidation following closed-head trauma in rats

Özsüer¹,

Görgülü

Kırış

et al. 2005

Neurosurg Rev

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Memantine is an uncompetitive N-methyl-D: -aspartate (NMDA) receptor antagonist. Unlike other NMDA antagonists, it has been used clinically for years for the treatment of Parkinson's disease, spasticity, and dementia without serious side effects. We aimed to investigate the therapeutic efficacy of memantine on a closed head trauma model. A total of 132 adult male Sprague-Dawley rats were randomly divided into four groups: sham-operated, control (closed head trauma), sham-vehicle (closed head trauma + saline), treatment (closed head trauma + memantine, 10 mg/kg, i.p.). A cranial impact was delivered to the skull, just in front of the coronal suture, over the left hemisphere, from the height of 7 cm. Saline or memantine were applied 15 min after trauma. Rats were euthanased 0.5, 1, 2, 6, 24, 48 h after trauma. Brain tissue samples were taken 5 mm away from the left frontal pole and also from the corresponding point of the contralateral hemispheres. Malondialdehyde activity (MDA) was considered to reflect the degree of lipid peroxidation. The MDA levels continued to increase for the first 2 h after the injury, then started to decrease gradually. Memantine treatment significantly reduced lipid peroxidation levels in the treatment group compared with other groups (P<0.01). The findings of the present study indicate that memantine provides beneficial effects after closed head trauma in rats.

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Protective Effect of the N-Methyl-D-Aspartate Receptor Antagonists, MK-801 and CPP on Cold-Induced Brain Oedema

Cited by 9 publications

References 26 publications

Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis

Immunoexcitotoxicity as a central mechanism in chronic traumatic encephalopathy-A unifying hypothesis

Combined action of MK-801 and ceftriaxone impairs the acquisition and reinstatement of morphine-induced conditioned place preference, and delays morphine extinction in rats

The effects of memantine on lipid peroxidation following closed-head trauma in rats

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