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. Author manuscript; available in PMC: 2019 May 16.
Published in final edited form as: J Neurochem. 2018 Nov 19;148(1):29–45. doi: 10.1111/jnc.14606

Fig. 2.

Fig. 2

Voltage-sensitive outflowing IKv during Vm depolarization were significantly reduced in response to acute methamphetamine (Meth) exposure. (a) Sample traces of IKv at control condition, and in response to 20, and 100 μM Meth. The vertical dashed lines indicate the time points at which the currents were measured. (b) Acute Meth exposure in vitro induced a significant decrease in the voltage-sensitive outflowing IKv (Control vs. 20 and 100 μM Meth, n = 22/18 vs. 19/12 and 9/7 cells/independent experiments, respectively; Two-way rmANOVA: treatment: F(2,47) = 2.775, p = 0.0726; voltage: F(15,705) = 106.7, p < 0.001; interaction: F(30,705) = 2.784, p < 0.001. Tukey’s post hoctest: *,**p < 0.05 or 0.01 for Control vs. Meth 20 μM, #,##,###p < 0.05, 0.01, or 0.001 for Control vs. 100 μM Meth, and &p < 0.05 for 20 μM Meth vs. 100 μM Meth). (c) Acute Meth significantly reduced the time constant (T) of IKv during the activation of Kv/Kv-like K+ channels in human fetal astrocytes compared to controls (Control: n = 20/18 vs. Meth: n = 14/10 cells/independent experiments; Two-way rmANOVA: treatment: F(1,32) = 5.377, p = 0.027; voltage: F(15,467) = 1.028, p > 0.05; interaction: F(15,467) = 1.143, p > 0.05. Newman–Keuls post hoc test: *,***p < 0.05 or 0.001).