2014
DOI: 10.1016/j.neuropharm.2013.09.024
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Activation of α2 adrenoceptors inhibited NMDA receptor-mediated nociceptive transmission in spinal dorsal horn of mice with inflammatory pain

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Cited by 27 publications
(24 citation statements)
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“…This increase in responsiveness leads to pain hypersensitivity. In the present study, GluN2B was found to be upregulated in RNA and protein levels after sciatic nerve ligation, consistent with the previous studies in different chronic pain models [2830], which suggests the possibility of using this mechanism as a target for the NP treatment. Previous behavioral studies have shown that systematical application of the selective GluN2B antagonists, ifenprodil and CP-101,606, produce analgesia in animals with persistent inflammatory or neuropathic pain [29, 30].…”
Section: Discussionsupporting
confidence: 92%
“…This increase in responsiveness leads to pain hypersensitivity. In the present study, GluN2B was found to be upregulated in RNA and protein levels after sciatic nerve ligation, consistent with the previous studies in different chronic pain models [2830], which suggests the possibility of using this mechanism as a target for the NP treatment. Previous behavioral studies have shown that systematical application of the selective GluN2B antagonists, ifenprodil and CP-101,606, produce analgesia in animals with persistent inflammatory or neuropathic pain [29, 30].…”
Section: Discussionsupporting
confidence: 92%
“…Based on the many different locations detailed above, there is a wide range of possibilities for novel agents to have an impact. Modulating preand postsynaptic signaling in spinal cord at the receptor level is under investigation [116]. As the genetics underlying the changes that drive LTP in peripheral and central sites become better understood, ERK1, ERK2 and MeCP2 genes will become targets for individualized pain therapy [117].…”
Section: Future Perspectivementioning
confidence: 99%
“…Inflammation may promote a series of molecular biological events, resulting in the activation of inflammatory cells from the spinal cord tissues and infiltration of the circulatory system, the release of various pro-inflammatory mediators and neurotoxins, and the generation of oxygen radicals and nitroso compounds, and consequently causing cell damage (7,8).…”
Section: Introductionmentioning
confidence: 99%