About this Research Topic
Pain is a distressing feeling often caused by intense or damaging stimuli. Pain is classified into 3 categories such as nociceptive, neuropathic and inflammatory. Acute pain can be mild and last just a moment. Chronic pain is a pain that is ongoing and usually lasts longer than six months.
A wide range of different types of voltage- and ligand-gated ion channels, including sodium, calcium, and TRP channels and other channels are critically involved in the detection and processing of painful stimuli in sensory neurons.
Pain mediators such as bradykinin, serotonin, substance P and prostaglandin E2 increase Ca2+ influx through Cav leading to a significant increase in intracellular calcium ([Ca2+]i). The increased ([Ca2+]i) can contribute to increased neural activity that is relayed to the central nervous system leading to increased pain perception. Chronic changes in ion channel expression and function are thought to contribute to chronic pain states. These channels mediate cell signaling function as well as regulating membrane potential and excitability. This includes the release of neurotransmitters, the activation of calcium-dependent enzymes, and calcium-dependent changes in plasticity and gene transcription.
The aim of this Research Topic is to provide an overview of the different calcium-permeable ion channels involved in the pain pathway.
We welcome articles addressing the following, but not limited to, themes:
• state of the art methods to investigate the different Ca-p ion channels from a physiological point of view, genetic expression level differences and upstream regulation differences
• currently available tools for genetic and molecular studies
• potential targets to control for pain management
Keywords: Central nervous system, formalin, ion channels, pain, store operated calcium channels, voltage gated calcium channels
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