Figure 3: The PLA2–AA pathway triggers the current activation of BK channels in microglia following morphine treatment.
From: BK channels in microglia are required for morphine-induced hyperalgesia
(a–g) Typical traces of BK currents in MG6 after 24 h of morphine (10 μM) treatment with or without naloxone (a μ-opioid receptor inhibitor, 10 μM) (a), pertussis toxin (PTx, 10 nM) (b), AACOCF3 (10 μM) (c), indomethacin (1 μM) (d), NS398 (10 μM) (e), zileuton (100 μM) (f) and baicalein (100 μM) (g). (h) The amplitude of BK currents at +30 mV in MG6 after 24 h of morphine treatment (n=22/16/7/4/7/4/4/4/5 cells). (i) The PWT of morphine-treated mice with or without i.t. injection of AACOCF3 (100 pmol) (n=5 for Saline, n=5 for Morphine, n=6 for Morphine+AACOCF3). (j) BK currents in the lamina I spinal microglia after 5 days of morphine administration. (k) The amplitude of BK currents at +30 mV in the lamina I spinal microglia (n=5 for Saline, n=6 for Morphine, n=8 for Morphine+AACOCF3, from three mice each). The data represent the means±s.e.m. ***P=0.0001 (Cont versus Morphine), †P=0.0101, ††P=0.0027, †††P=0.0001, 0.0001, 0.0001, 0.0001 (versus Morphine), F8, 64=33.34, a one-way ANOVA followed by the Tukey’s post hoc test (h), **P=0.0021, ***P=0.0001, 0.0001, 0.0001 (Saline versus Morphine), ††P=0.0027, 0.0084 (Morphine versus Morphine+AACOCF3), (drug × time point interaction): F2, 16=33.34, a two-way ANOVA followed by the Bonferroni post hoc test (i). ***P=0.0001, 0.0001 (each column), F2, 91=52.51, a one-way ANOVA followed by the Tukey’s post hoc test (k).
