Role of purinergic signaling and glia in TMJ nociception
嘌呤能信号和神经胶质细胞在 TMJ 伤害感受中的作用
基本信息
- 批准号:9507148
- 负责人:
- 金额:$ 47.91万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2017
- 资助国家:美国
- 起止时间:2017-08-01 至 2019-07-31
- 项目状态:已结题
- 来源:
- 关键词:AddressAffectAnatomyAnimalsArthritisBehaviorBehavioralCellsCommunicationCoupledCouplesCraniofacial PainDataDoseElectrophysiology (science)EtiologyExposure toFamilyFemaleFoodFreund&aposs AdjuvantGoalsHigh PrevalenceHumanHyperalgesiaHypertrophyInflammasomeInflammationInflammatoryInjection of therapeutic agentInjuryJawMaintenanceMasticationMasticatory musclesMethodsMicrogliaModelingMolecularMuscleNeurogliaNeuronsNociceptionOrofacial PainP2X-receptorPainPain intensityPathway interactionsPatientsPeripheralPharmacologyPhenotypePhysiologicalPlayPropertyProteinsProtocols documentationPurinergic P2 ReceptorsPurinoceptorRNA InterferenceRattusReceptor CellReceptor SignalingReflex actionReportingResearch DesignRoleSamplingSensorySignal TransductionStimulusStructure of trigeminal ganglionStudy modelsSynovial FluidTemporomandibular JointTemporomandibular Joint DisordersTemporomandibular joint disorder painTest ResultTestingTimeTissuesWomanawakebaseextracellularglial activationjaw movementmalemennerve injuryneuromechanismneuronal circuitrypressurereceptorrelating to nervous systemresponsesexsomatosensorytherapeutic targettooltreatment effect
项目摘要
Temporomandibular joint disorders (TMD) include a family of conditions that present with pain in the
temporomandibular joint (TMJ) and muscles of mastication. TMD is the most common non-dental
orofacial pain, yet the underlying physiological and cellular mechanisms are poorly understood.
Painful TMD is notable for a higher prevalence in women than men, and poor correlation between
overt signs of injury and ratings of pain intensity. Reports of elevated levels of pro-inflammatory
molecules in synovial fluid samples of non-osteoarthritic TMD patients suggest that low grade TMJ
inflammation is a common feature of TMD, but likely goes undetected without direct synovial fluid
sampling. The central hypothesis is that low grade TMJ inflammation primes trigeminal ganglion
(TG) neurons and induces persistent hyperalgesia seen as altered response properties of
spinomedullary (Vc/C1-2) neurons and jaw muscle activity. We propose that purinergic (P2)
receptors and glial cell activation play key roles in TMJ priming and maintain hyperalgesia in a
stimulus- and sex-dependent manner. The long-term goal of this project is to determine if
interference with specific P2 receptors on neurons and glia are therapeutic targets for
managing TMJ nociception and TMD pain in humans. A quantitative sensory testing (QST)
protocol is developed to assess treatment effects on TMJ-responsive neurons. Converging lines of
evidence using electrophysiological, behavioral, molecular, and anatomical approaches address
three issues: 1) is transient low grade TMJ inflammation sufficient to cause persistent changes in the
properties of TMJ-responsive TG and Vc/C1-2 neurons, jaw muscle activity and jaw movement; 2)
what is the role of purinergic receptors in TMJ priming; and 3) what is the role of glial cells in
maintenance of TMJ nociception? Unlike previous studies, this model uses a single exposure to a
non-tissue damaging inflammatory agent to prime TMJ-responsive neuronal circuits in male and
female rats and couples this insult to the responses of TMJ-responsive neurons with identified
phenotypes. Aim 1 establishes the QST protocol under TMJ primed conditions and determines the
effects of priming on the properties of TG neurons, Vc/C1-2 neurons, on MMemg activity and jaw
movement. Aim 2 determines the expression and protein levels of P2 receptors closely associated
with TG and Vc/C1-2 neurons and the role of those receptors on neural activity, jaw muscle activity
and jaw movement. Aim 3 determines the expression and protein levels of P2 receptors closely
associated with satellite glia in TG and microglia at Vc/C1-2 neurons and the role of glial cell
activation in TMJ hyperalgesia. Neuron-glia communication is a critical feature of persistent
inflammatory hyperalgesia in other models, but remains poorly defined in TMJ nociception. When
coupled with neural recording and jaw muscle reflexes, inhibition of P2 receptors closely associated
with neurons or glia, inhibition of inflammasome formation by microglia and blockade of glia-specific
secretory products by pharmacological and interference RNA approaches will enhance the
understanding of neural mechanisms underlying persistent TMJ hyperalgesia.
颞下颌关节紊乱(TMD)包括一系列以关节疼痛为表现的病症
项目成果
期刊论文数量(2)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Estrogen Status and Trigeminal Ganglion Responses to Jaw Movement.
雌激素状态和三叉神经节对下颌运动的反应。
- DOI:10.1177/00220345221077951
- 发表时间:2022
- 期刊:
- 影响因子:7.6
- 作者:Zhang,X;Rahman,M;Bereiter,DA
- 通讯作者:Bereiter,DA
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DAVID A BEREITER其他文献
DAVID A BEREITER的其他文献
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{{ truncateString('DAVID A BEREITER', 18)}}的其他基金
Trigeminal-autonomic relations in ocular homeostasis
眼稳态中的三叉神经自主关系
- 批准号:
8461195 - 财政年份:2011
- 资助金额:
$ 47.91万 - 项目类别:
Trigeminal-autonomic relations in ocular homeostasis
眼稳态中的三叉神经自主关系
- 批准号:
8130159 - 财政年份:2011
- 资助金额:
$ 47.91万 - 项目类别:
Trigeminal-autonomic relations in ocular homeostasis
眼稳态中的三叉神经自主关系
- 批准号:
8240030 - 财政年份:2011
- 资助金额:
$ 47.91万 - 项目类别:
SEX-RELATED OPIATE AND AUTONOMIC MECHANISMS IN TMD PAIN
TMD 疼痛中与性相关的阿片类药物和自主机制
- 批准号:
6176887 - 财政年份:1998
- 资助金额:
$ 47.91万 - 项目类别:
SEX-RELATED OPIATE AND AUTONOMIC MECHANISMS IN TMD PAIN
TMD 疼痛中与性相关的阿片类药物和自主机制
- 批准号:
2680135 - 财政年份:1998
- 资助金额:
$ 47.91万 - 项目类别:
SEX-RELATED OPIATE AND AUTONOMIC MECHANISMS IN TMD PAIN
TMD 疼痛中与性相关的阿片类药物和自主机制
- 批准号:
2897219 - 财政年份:1998
- 资助金额:
$ 47.91万 - 项目类别:
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