Spinal microglia specific BK channels contribute to the morphine-induced hyperalgesia

Release date: 2016.06.01


Research Results Life & Health

 Although morphine is a gold standard medication, long-term opioid use is associated with serious side effects, such as morphine-induced hyperalgesia (MIH) and antinociceptive tolerance. Microglia-to-neuron signaling is critically involved in pain hypersensitivity. However, molecule that control microglial cellular state under chronic morphine treatment remains unknown.
Here we show that microglia-specific subtype of Ca2+-activated K+ (BK) channel is responsible for the generation of MIH and antinociceptive tolerance. After chronic morphine administration, there was an increase in arachidonic acid levels through the -opioid receptors, leading to the sole activation of microglial BK channels in the spinal cord. The gene silencing of BK channel auxiliary 3 subunit significantly attenuated the generation of MIH and antinociceptive tolerance and increased neurotransmission following chronic morphine administration.
Therefore, microglia-specific BK channels contribute to the generation of MIH and antinociceptive tolerance. The research achievement was published online in Nature Communications on May 31, 2016.

Fig.1 Schematic illustration of the disrupted ion homeostasis in microglia following stimulation with morphine.

Journal Reference

BK channels in microglia are required for morphine-induced hyperalgesia, ,Nature Communications, 10.1038/NCOMMS11697.

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