The Role of TNF-alpha and MAP Kinases in the Maintenance of COMT-dependent
The Role of TNF-alpha and MAP Kinases in the Maintenance of COMT-dependent
批准号:
8982961
负责人:
Jane E. Hartung
金额:
$2.96万
依托单位国家:
美国
项目类别:
财政年份:
2015
资助国家:
美国
项目状态:
已结题
起止时间:
2015-09-01 至 2016-06-29
关键词:
Adrenergic ReceptorAfferent NeuronsAmericanAnimal ModelAstrocytesBehavioralBiological AssayBiological AvailabilityCalciumCatechol O-MethyltransferaseCatecholaminesCellsCerebrospinal FluidChronicClinicalConfocal MicroscopyDataDevelopmentDrug Delivery SystemsEnzymesFibromyalgiaGeneticGenetic PolymorphismHomeostasisHourImageInflammatoryInterleukin-6InterleukinsLinkLiteratureMAPK14 geneMAPK8 geneMaintenanceMeasuresMechanicsMediatingMediator of activation proteinMicrogliaMitogen-Activated Protein KinasesMusMusculoskeletal PainNeurobiologyNeurogliaNeuronsNociceptionNociceptive StimulusNociceptorsPainPathway interactionsPatientsPeripheralPhosphotransferasesPhysiologyPlayRattusResearchRodentRoleSignal TransductionSpinal CordSpinal GangliaTechniquesTemporomandibular Joint DisordersTestingTimeTissuesTreatment EfficacyTumor Necrosis Factor-alphaWestern BlottingWorkcalcium indicatorchronic painclinically relevantcytokineextracellulargenetic varianthuman TNF proteinin vivoinhibitor/antagonistmitogen-activated protein kinase p38novelpain behaviorpublic health relevanceresponsesatellite celltemporal measurementtransmission process
中文摘要
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英文摘要
DESCRIPTION (provided by applicant):
Chronic musculoskeletal pain conditions are maladaptive and negatively impact the lives over 100 million Americans. A growing body of literature suggests that these chronic pain conditions result from imbalances in catecholamine homeostasis, which give way to increased release of pro-inflammatory molecules and increased activation of cells that transmit information about pain. Therefore, this proposal will employ a clinically-relevant animal model to [[1) determine if targeting specific pro-inflammatory molecules is able to reverse chronic pain caused by dysregulation of catecholamine homeostasis and 2) determine which cells involved in pain signal transmission play a role downstream from pro-inflammatory molecule activity.
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会议论文
Traumatic Brain Injury, Stress, and Headache
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批准号:9395336
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项目类别:
-
资助金额:$5.63万
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财政年份:2017
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负责人:Jane E. Hartung
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依托单位:
海外基金