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10.1038/ncomms11697 http://scihub22266oqcxt.onion/10.1038/ncomms11697 C4895018!4895018!27241733     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2016 ; 7 (ä): ä Nephropedia Template TP {{tp|p=27241733|t=2016. BK channels in microglia are required for morphine-induced hyperalgesia |pdf=|usr=}}{{27241733}} gab.com Text BK channels in microglia are required for morphine-induced hyperalgesia JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27241733 #FOAvip Although morphine is a gold standard medication, long-term opioid use is associated with serious side effects, such as morphine-induced hyperalgesia (MIH) and anti-nociceptive tolerance. Microglia-to-neuron signalling is critically involved in pain hypersensitivity. However, molecules that control microglial cellular state under chronic morphine treatment remain unknown. Here we show that the microglia-specific subtype of Ca2+-activated K+ (BK) channel is responsible for generation of MIH and anti-nociceptive tolerance. We find that, after chronic morphine administration, an increase in arachidonic acid levels through the ?-opioid receptors leads to the sole activation of microglial BK channels in the spinal cord. Silencing BK channel auxiliary ?3 subunit significantly attenuates the generation of MIH and anti-nociceptive tolerance, and increases neurotransmission after chronic morphine administration. Therefore, microglia-specific BK channels contribute to the generation of MIH and anti-nociceptive tolerance. Twit Text FOAVip BK channels in microglia are required for morphine-induced hyperalgesia ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=27241733 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27241733 #FOAvip English Wikipedia <ref>{{Cite pmid|27241733}}</ref> BK channels in microglia are required for morphine-induced hyperalgesia #MMPMID27241733 Hayashi Y; Morinaga S; Zhang J; Satoh Y; Meredith AL; Nakata T; Wu Z; Kohsaka S; Inoue K; Nakanishi H Nat Commun 2016[]; 7 (ä): ä PMID27241733show ga Although morphine is a gold standard medication, long-term opioid use is associated with serious side effects, such as morphine-induced hyperalgesia (MIH) and anti-nociceptive tolerance. Microglia-to-neuron signalling is critically involved in pain hypersensitivity. However, molecules that control microglial cellular state under chronic morphine treatment remain unknown. Here we show that the microglia-specific subtype of Ca2+-activated K+ (BK) channel is responsible for generation of MIH and anti-nociceptive tolerance. We find that, after chronic morphine administration, an increase in arachidonic acid levels through the ?-opioid receptors leads to the sole activation of microglial BK channels in the spinal cord. Silencing BK channel auxiliary ?3 subunit significantly attenuates the generation of MIH and anti-nociceptive tolerance, and increases neurotransmission after chronic morphine administration. Therefore, microglia-specific BK channels contribute to the generation of MIH and anti-nociceptive tolerance. äBK channels in microglia are required for morphine-induced hyperalgesi(epmc).pdf DeepDyve Pubget Overpricing