Age and meloxicam attenuate the ischemia/reperfusion-induced down-regulation in the NMDA receptor genes

Montori, Sheyla; Dos-Anjos, Severiano; Martínez-Villayandre, Beatriz; Regueiro-Purriños, Marta; Orden, José Manuel Gonzalo; Ruano, Diego; Fernández‐López, Arsenio

doi:10.1016/j.neuint.2010.03.013

Cited by 21 publications

(26 citation statements)

References 62 publications

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“…Changes in subunit composition of the NMDAR have been implicated in a number of disorders of memory and are altered in the setting of ischemia reperfusion induced inflammation 2728 . NR1 is constitutively expressed in NMDAR but the relative levels of NR2A and NR2B are variable.…”

Section: Resultsmentioning

confidence: 99%

Neutrophil depletion after subarachnoid hemorrhage improves memory via NMDA receptors

Provencio

Swank

et al. 2016

Brain, Behavior, and Immunity

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Cognitive deficits after aneurysmal subarachnoid hemorrhage (SAH) are common and disabling. Patients who experience delayed deterioration associated with vasospasm are likely to have cognitive deficits, particularly problems with executive function, verbal and spatial memory. Here, we report neurophysiological and pathological mechanisms underlying behavioral deficits in a murine model of SAH. On tests of spatial memory, animals with SAH performed worse than sham animals in the first week and one month after SAH suggesting a prolonged injury. Between three and six days after experimental hemorrhage, mice demonstrated loss of late long-term potentiation (L-LTP) due to dysfunction of the NMDA receptor. Suppression of innate immune cell activation prevents delayed vasospasm after murine SAH. We therefore explored the role of neutrophil-mediated innate inflammation on memory deficits after SAH. Depletion of neutrophils three days after SAH mitigates tissue inflammation, reverses cerebral vasoconstriction in the middle cerebral artery, and rescues L-LTP dysfunction at day 6. Spatial memory deficits in both the short and long-term are improved and associated with a shift of NMDA receptor subunit composition toward a memory sparing phenotype. This work supports further investigating suppression of innate immunity after SAH as a target for preventative therapies in SAH.

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Section: Resultsmentioning

confidence: 99%

Neutrophil depletion after subarachnoid hemorrhage improves memory via NMDA receptors

Provencio

Swank

et al. 2016

Brain, Behavior, and Immunity

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“…Primers were designed with Primer Express software (ABI, Foster City, CA). OX-42/CD11b (NM_012711; Montori et al, 2010) 0 -ACAGTGTGGGTGACCCCGTC-3 0 . Real-time PCR was performed as previously described (Baker-Herman et al, 2004;Guo et al, 2006) using a LightCycler rapid thermal cycler system (Roche Diagnostics, Mannheim, Germany) according to the manufacturer's instructions.…”

Section: Real-time Pcrmentioning

confidence: 99%

Minocycline‐induced reduction of brain‐derived neurotrophic factor expression in relation to cancer‐induced bone pain in rats

Wang

Yang

et al. 2011

J of Neuroscience Research

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Previous studies have suggested that the release of brain-derived neurotrophic factor (BDNF) from microglia in spinal cord is necessary for maintaining pain hypersensitivity after nerve injury. However, little is known about its role in cancer-induced bone pain (CIBP), which is in some ways unique. This study demonstrates a critical role of minocycline (a potent inhibitor of microglial activation)-modulated BDNF in the induction and maintenance of behavioral hypersensitivity in a rat model of CIBP. We assessed mechanical threshold and spontaneous pain of CIBP rats. Moreover, minocycline was administered intrathecally from day 4 to day 6 (early stage) or from day 10 to day 12 (later stage), after carcinoma cell inoculation. Real-time PCR, Western blots, and double immunofluorescence were used to detect the expression of OX-42 (marker of activated microglia), phosphorylated p38-MAPK (p-p38), and BDNF. We found that intrathecal minocycline could prevent CIBP at an early stage of tumor growth (from day 4 to day 6). However, at the late stage (from day 10 to day 12), intrathecal minocycline had no effect. Moreover, the expression of OX-42 and BDNF under CIBP, peaking on day 6, were all reduced after minocycline injection from day 4 to day 6. The ability of minocycline-induced reduction of BDNF in the induction of behavioral hypersensitivity could provide an opportunity for alleviating CIBP.

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“…In addition, activation of astrocytes and microglia is well known to be associated with neuronal cell death [55][56][57]. Thus, we measured neuronal cell death 7 days after ischemia by immunohistochemistry to examine the protective effects of Tat-PIM2 protein.…”

Section: Discussionmentioning

confidence: 99%

Effects of low doses of Tat-PIM2 protein against hippocampal neuronal cell survival

Woo

Shin

Kim

et al. 2015

Journal of the Neurological Sciences

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Age and meloxicam attenuate the ischemia/reperfusion-induced down-regulation in the NMDA receptor genes

Cited by 21 publications

References 62 publications

Neutrophil depletion after subarachnoid hemorrhage improves memory via NMDA receptors

Neutrophil depletion after subarachnoid hemorrhage improves memory via NMDA receptors

Minocycline‐induced reduction of brain‐derived neurotrophic factor expression in relation to cancer‐induced bone pain in rats

Effects of low doses of Tat-PIM2 protein against hippocampal neuronal cell survival

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