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• W2007337144 abstract "Acute nociceptive pain is caused by the direct action of a noxious stimulus on pain-sensitive nerve endings, whereas inflammatory pain (both acute and chronic) arises from the actions of a wide range of inflammatory mediators released following tissue injury. Neuropathic pain, which is triggered by nerve damage, is often considered to be very different in its origins, and is particularly difficult to treat effectively. Here we review recent evidence showing that members of the hyperpolarization-activated cyclic nucleotide-modulated (HCN) ion channel family – better known for their role in the pacemaker potential of the heart – play important roles in both inflammatory and neuropathic pain. Deletion of the HCN2 isoform from nociceptive neurons abolishes heat-evoked inflammatory pain and all aspects of neuropathic pain, but acute pain sensation is unaffected. This work shows that inflammatory and neuropathic pain have much in common, and suggests that selective blockers of HCN2 may have value as analgesics in the treatment of pain. Acute nociceptive pain is caused by the direct action of a noxious stimulus on pain-sensitive nerve endings, whereas inflammatory pain (both acute and chronic) arises from the actions of a wide range of inflammatory mediators released following tissue injury. Neuropathic pain, which is triggered by nerve damage, is often considered to be very different in its origins, and is particularly difficult to treat effectively. Here we review recent evidence showing that members of the hyperpolarization-activated cyclic nucleotide-modulated (HCN) ion channel family – better known for their role in the pacemaker potential of the heart – play important roles in both inflammatory and neuropathic pain. Deletion of the HCN2 isoform from nociceptive neurons abolishes heat-evoked inflammatory pain and all aspects of neuropathic pain, but acute pain sensation is unaffected. This work shows that inflammatory and neuropathic pain have much in common, and suggests that selective blockers of HCN2 may have value as analgesics in the treatment of pain." @default.
• W2007337144 created "2016-06-24" @default.
• W2007337144 creator A5012959156 @default.
• W2007337144 creator A5034556369 @default.
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• W2007337144 date "2012-08-01" @default.
• W2007337144 modified "2023-10-04" @default.
• W2007337144 title "HCN2 ion channels: an emerging role as the pacemakers of pain" @default.
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• W2007337144 doi "https://doi.org/10.1016/j.tips.2012.04.004" @default.
• W2007337144 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22613784" @default.
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