Pain sensation is mediated by ion channels in nerve endings, including TRPA1, TRPV1, TRPM3, and P2X receptors, which transmit pain inputs to the central nervous system through dorsal root ganglion (DRG) neurons. TRPA1, TRPV1, and TRPM3 detect noxious stimuli and trigger pain signals in peripheral nerve endings. TRPV4 contributes to mechanical hypersensitivity during inflammation, while ASIC1a, ASIC2a, and ASIC3 participate in pain perception during acidosis caused by inflammation or injury. Nav1.1, Nav1.7, Nav1.8, and Nav1.9 mediate action potentials in DRG neurons and conduct pain signals to the spinal cord. Cav2.2 contributes to neurotransmitter release at spinal synapses and modulates pain transmission. Kv1.3, Kv1.4, Kv4.2, IK, and BK regulate neuronal excitability and inflammation, offering potential targets for immune-related pain, while KCNQ2/3 helps dampen excitatory pain signals. P2X3, P2X4, and P2X7 participate in sensory signaling and inflammation and are relevant to neuropathic and inflammatory pain. nAChRα7 and NMDA receptors can modulate synaptic plasticity and pain hypersensitivity, particularly in chronic and inflammatory pain. HCN1 also modulates neuronal excitability and may contribute to chronic pain states.
Our Pain–Inflammation Ion Channel Portfolio is designed to identify and validate ion-channel targets involved in pain and inflammatory pathways. The panel includes channels implicated in central and peripheral pain signaling, hypersensitivity associated with neuropathic and inflammatory conditions, and immune regulation, providing a comprehensive tool for drug discovery.
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