神经性疼痛和炎症PCR基因芯片 Pain: Neuropat

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Pain: Neuropathic & Inflammatory PCR Array

神经性疼痛和炎症PCR基因芯片

Product	Species	Technology	Cat. No.
Pain: Neuropathic & Inflammatory PCR Array	Human	Gene Expression	PAHS-162Z
Pain: Neuropathic & Inflammatory PCR Array	Mouse	Gene Expression	PAMM-162Z
Pain: Neuropathic & Inflammatory PCR Array	Rat	Gene Expression	PARN-162Z
Pain: Neuropathic & Inflammatory PCR Array	Rhesus Macaque	Gene Expression	PAQQ-162Z
Pain: Neuropathic & Inflammatory PCR Array	Pig	Gene Expression	PASS-162Z
Pain: Neuropathic & Inflammatory PCR Array	Chinese Hamster	Gene Expression	PAJJ-162Z

Pain: Neuropathic & Inflammatory RT² Profiler PCR Array profiles the expression of 84 genes involved in the transduction, maintenance, and modulation of pain responses. Noxious environmental stimuli, tissue damage, and disease all evoke pain. Since it afflicts up to 20% of the population at any given time, pain provides both a massive therapeutic target and a route to understanding the molecular mechanisms of nervous system function. While neuropathic pain often results from damage to the peripheral (PNS) or central nervous system (CNS), peripheral tissue damage and/or inflammation generally initiates inflammatory pain. Neuropathic and inflammatory pain both cause activation of damage-sensing neurons (nociceptors) that innervate the skin, muscle and viscera and terminate in the laminae of the spinal cord dorsal horn. Nociceptors conduct information to the CNS via neurotransmission and action potentials generated by ion channel and purinergic, opioid, and cannabinoid receptors leading to second order neuron activation. Synaptic transmission via glutamate, serotonin, and dopamine systems then follows. The transduction by nociceptors can be modulated by mediators of inflammation released by infiltrating immune cells and damaged neurons. Excitability of spinal neurons is also modulated by activation of resident microglia that release growth factors (such as BDNF), chemokines, and cytokines. Endogenous opioid peptides and arachidonic acid metabolites acting through G-protein coupled receptors also modulate neuronal excitability. A number of these pathways are currently being evaluated as potential pharmacological targets for analgesic development for pain management. Using real time PCR, research studies can easily and reliably analyze the expression of a focused panel of genes associated with neuropathic and inflammatory pain with this array.神经性疼痛和炎症PCR基因芯片可用于研究与疼痛反应的传导、维护和调节相关的84个基因的表达。有害环境刺激、组织损伤和疾病都可以引起疼痛。由于疼痛折磨着大约20％的人口，所以疼痛既提供了大量的治疗目标，同时也提供一个可以了解神经系统的功能及分子机制的途径。虽然疼痛产生的原因众多，包括外周神经系统（PNS）损伤，中枢神经系统（CNS）神经性疼痛，外周组织的损伤和/或炎症启动的炎症性疼痛，然而神经性和炎症性疼痛的根本原因在于从激活的神经元损伤检测到终止于脊髓背角的薄层的传导通路。这条通路包括：疼痛感受器收集信息，通过神经传递到中枢神经系统，并影响动作电位产生的离子通道和嘌呤、鸦片类、大麻素受体，导致二阶神经元激活，再通过谷氨酸、5-羟色胺和多巴胺系统的突触传递进行信号传导。其中，伤害性感受的传导，可以被炎症介质相关的浸润性免疫细胞和神经元受损调节。脊髓神经元的兴奋性也可以被邻近的小胶质细胞所释放的生长因子、趋化因子和细胞因子调控。内源性鸦片肽和花生四烯酸代谢产物的作用，通过G-蛋白偶联受体同样可以调节神经元的兴奋性。许多这些途径都是目前正在研究的潜在的药物镇痛疼痛治疗的发展目标。使用实时定量PCR，研究者可以方便并且可信地研究与神经性疼痛和炎症相关的基因的表达。
Conduction of Pain:
Ion Channels: TRPA1, TRPV1, TRPV3.
Sodium Channels: SCN10A, SCN11A, SCN3A, SCN9A, SLC6A2.
Potassium Channels: KCNIP3, KCNJ6, KCNQ2, KCNQ3.
Purinergic Receptors: ADORA1, P2RX3, P2RX4, P2RX7, P2RY1.
Opioid Receptors: OPRD1, OPRK1, OPRM1.
Cannabinoid Receptors: CNR1, CNR2.
Synaptic Transmission:
Glutamate Receptors: GRIN1, GRIN2B, GRM1, GRM5.
Serotonin Receptors: HTR1A, HTR2A.
Calcium Channel: CACNA1B.
Modulation of Pain Responses:
Eicosanoid Metabolism: PLA2G1B, PTGER1, PTGER3, PTGER4, PTGES, PTGES2, PTGES3, PTGS1, PTGS2.
Inflammation: ACE, ALOX5, BDKRB1, CALCA, CCK, CCKBR, CCL2, CCR2, CD200, CD4, CHRNA4, CSF1, CX3CR1, DBH, EDN1, EDNRA, FAAH, GCH1, IL10, IL18, IL1A, IL1B, IL2, IL6, ITGAM, ITGB2, MAPK1, MAPK14, MAPK3, MAPK8, PENK, PNOC, PROK2, TAC1, TACR1, TLR2, TLR4, TNF.
Neurotransmitters: ADRB2, COMT, DBH, MAOB, PDYN, PENK, PNOC.
Neurotrophins: BDNF, GDNF, NGF, NTRK1.