N-Methyl-d-aspartate receptor antagonist MK-801 suppresses glial pro-inflammatory cytokine expression in morphine-tolerant rats

Liu, Ching-Hang; Cherng, Chen-Hwen; Lin, Shir‐Kuan; Yeh, Chun-Chang; Wu, Ching-Tang; Tai, Yueh-Hua; Wong, Chih‐Shung

doi:10.1016/j.pbb.2011.05.016

Cited by 34 publications

(12 citation statements)

References 33 publications

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“…7,[9][10][11] Evidences from previous studies suggested that NMDA receptors are involved in the plasticity that arises from the long-term administration of morphine. [20][21][22][23][24] In the present study pretreatment with Magnesium sulfate (20,40 and 60 mg/kg, ip) 30 min before daily Morphine administration reduced tolerance and dependency of Morphine. Chronic Morphine administration induces down regulation of spinal GTs and as a result Morphine-induced GT down regulation would increase the availability of extracellular glutamate.…”

Section: Discussionsupporting

confidence: 46%

Attenuation of Morphine-Induced Tolerance and Dependency by Pretreatment with Magnesium Sulfate and Amitriptyline in Male Mice

Habibiasl¹,

Vaez²,

Aghaie³

et al. 2015

Pharm Sci

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Section: Discussionsupporting

confidence: 46%

Attenuation of Morphine-Induced Tolerance and Dependency by Pretreatment with Magnesium Sulfate and Amitriptyline in Male Mice

Habibiasl¹,

Vaez²,

Aghaie³

et al. 2015

Pharm Sci

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“…It’s worth stressing that glutamate was released by astrocyte and activated microglia during neuroinflammation [ 38 ]. In the CNS, both in vivo and in vitro, previous studies indicated that the increase in pro-inflammatory cytokines can be reduced by NMDAR antagonist MK-801 in morphine-tolerant rats [ 19 ] and by NMDAR1 siRNA in parkinsonian cell models [ 39 ]. Memantine, a well characterized NMDAR antagonist, is used to treat dementia and Parkinson’s disease in clinic [ 40 ], and it also protected neurons from some models of neurological injury such as traumatic brain injury, ischemic stroke, spinal cord ischemia or neuroinflammation [ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

“…Similar to neurons, mononuclear leukocytes and neutrophils can release glutamate, which can further exacerbate blood brain-barrier-injury [ 12 , 13 ]. Several lines of evidence indicate that NMDARs play an important role in regulating inflammation in neuronal and non-neuronal cells and tissues, such as chronic morphine-induced neuroinflammation, retinal damage, arthritis and cardiac inflammation [ 15 , 17 – 19 ]. Activation of NMDA receptors can induce acute high-permeability edema in isolated rat lungs [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

NMDA Receptor Antagonist Attenuates Bleomycin-Induced Acute Lung Injury

Liu

Peng

et al. 2015

PLoS ONE

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BackgroundGlutamate is a major neurotransmitter in the central nervous system (CNS). Large amount of glutamate can overstimulate N-methyl-D-aspartate receptor (NMDAR), causing neuronal injury and death. Recently, NMDAR has been reported to be found in the lungs. The aim of this study is to examine the effects of memantine, a NMDAR channel blocker, on bleomycin-induced lung injury mice.MethodsC57BL/6 mice were intratracheally injected with bleomycin (BLM) to induce lung injury. Mice were randomized to receive saline, memantine (Me), BLM, BLM plus Me. Lungs and BALF were harvested on day 3 or 7 for further evaluation.ResultsBLM caused leukocyte infiltration, pulmonary edema and increase in cytokines, and imposed significant oxidative stress (MDA as a marker) in lungs. Memantine significantly mitigated the oxidative stress, lung inflammatory response and acute lung injury caused by BLM. Moreover, activation of NMDAR enhances CD11b expression on neutrophils.ConclusionsMemantine mitigates oxidative stress, lung inflammatory response and acute lung injury in BLM challenged mice.

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“…Moreover, it has been demonstrated that the degree of neuroinflammation induced by neuropathy combined with chronic administration in nerve-injured rats was higher compared to the neuroinflammation induced by neuropathy alone (Raghavendra et al 2002). This suggested that neuroinflammation is a common mechanism in both neuropathy-induced and chronic morphine-induced glial activation (Raghavendra et al 2004; Liu et al 2011). In the current study, daily anti-IL-10 and HO-1 antibody injection produced significant pro-inflammatory cytokine expression and attenuated the anti-nociceptive effect of gabapentin in morphine-tolerant neuropathic pain rats.…”

Section: Discussionmentioning

confidence: 99%

Gabapentin Enhances the Morphine Anti-Nociceptive Effect in Neuropathic Pain via the Interleukin-10-Heme Oxygenase-1 Signalling Pathway in Rats

et al. 2014

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In the present study, we investigated the anti-inflammatory mechanisms by which gabapentin enhances morphine anti-nociceptive effect in neuropathic pain in rats and the interaction between the anti-nociceptive effects of gabapentin on morphine and the interleukin (IL)-10-heme-oxygenase (HO)-1 signal pathway in a rat model of neuropathic pain. The neuropathic pain model was induced via a left L5/6 spinal nerve ligation (SNL) in rats. The anti-nociceptive effect of gabapentin and IL-10 on morphine was examined over a 7-day period, and the effects of the anti-IL-10 and HO-1 inhibitor zinc protoporphyrin (ZnPP) on gabapentin/morphine co-injection were assessed. Drug administration was given over 7 days, and on day 8, both anti-inflammatory cytokine IL-10, a stress-induced protein HO-1 and pro-inflammatory cytokines IL-1β, IL-6 and TNF-α were measured. Gabapentin attenuated morphine tolerance over 7 days of co-administration, and reduced the expression of pro-inflammatory cytokines but increased IL-10 and HO-1 expression. The effect of gabapentin on morphine was partially blocked using the anti-IL-10 antibody or the HO-1 inhibitor zinc protoporphyrin. Our findings indicated that the anti-nociceptive effects of gabapentin on morphine might be caused by activation of the IL-10-HO-1 signalling pathway, which resulted in the inhibition of the expression of pro-inflammatory cytokines in neuropathic pain in the rat spinal cord.

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N-Methyl-d-aspartate receptor antagonist MK-801 suppresses glial pro-inflammatory cytokine expression in morphine-tolerant rats

Cited by 34 publications

References 33 publications

Attenuation of Morphine-Induced Tolerance and Dependency by Pretreatment with Magnesium Sulfate and Amitriptyline in Male Mice

Attenuation of Morphine-Induced Tolerance and Dependency by Pretreatment with Magnesium Sulfate and Amitriptyline in Male Mice

NMDA Receptor Antagonist Attenuates Bleomycin-Induced Acute Lung Injury

Gabapentin Enhances the Morphine Anti-Nociceptive Effect in Neuropathic Pain via the Interleukin-10-Heme Oxygenase-1 Signalling Pathway in Rats

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