Data for: Inflammation differentially controls transport of depolarizing Nav versus hyperpolarizing Kv channels to drive rat nociceptor activity
Data files
Mar 17, 2023 version files 119 MB
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Fig1_Activity_Data_Control_Post-ProTxII.csv
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Fig1_Activity_Data_Control_Pre-ProTxII.csv
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Fig1_Activity_Data_IMTreated_Post-ProTxII.csv
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Fig1_Activity_Data_IMTreated_Pre-ProTxII.csv
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Fig2_Current_Kv7_Data_IM.csv
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Fig2_Current_Kv7_Data_WT.csv
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Fig2_Current_Nav1.7_Data_IM.csv
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Fig2_Current_Nav1.7_Data_WT.csv
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Fig2_Surface_Expression_Data_Kv7.2.csv
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Fig2_Surface_Expression_Data_Nav1.7.csv
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Fig3_Kv7.2_Ant_Ctl_1-1.tif
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Fig3_Kv7.2_Ant_Ctl_1-2.tif
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Fig3_Kv7.2_Ant_Ctl_1-3.tif
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Fig3_Kv7.2_Ant_Ctl_1-4.tif
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Fig3_Kv7.2_Ant_Ctl_1-5.tif
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Fig3_Kv7.2_Ant_Ctl_1-6.tif
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Fig3_Kv7.2_Ant_Ctl_1-7.tif
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Fig3_Kv7.2_Ant_Ctl_1-8.tif
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Fig3_Kv7.2_Ant_Ctl_1-9.tif
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Fig3_Kv7.2_Ant_Ctl_2-1.tif
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Fig3_Kv7.2_Ant_Ctl_2-10.tif
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Fig3_Kv7.2_Ant_Ctl_2-2.tif
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Fig3_Kv7.2_Ant_Ctl_2-3.tif
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Fig3_Kv7.2_Ant_Ctl_2-4.tif
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Fig3_Kv7.2_Ant_Ctl_2-5.tif
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Fig3_Kv7.2_Ant_Ctl_2-6.tif
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Fig3_Kv7.2_Ant_Ctl_2-7.tif
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Fig3_Kv7.2_Ant_Ctl_2-8.tif
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Fig3_Kv7.2_Ant_Ctl_2-9.tif
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Fig3_Kv7.2_Ant_Ctl_3-1.tif
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Fig3_Kv7.2_Ant_Ctl_3-2.tif
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Fig3_Kv7.2_Ant_Ctl_3-3.tif
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Fig3_Kv7.2_Ant_Ctl_3-4.tif
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Fig3_Kv7.2_Ant_Ctl_3-5.tif
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Fig3_Kv7.2_Ant_Ctl_3-6.tif
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Fig3_Kv7.2_Ant_Ctl_3-7.tif
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Fig3_Kv7.2_Ant_Ctl_3-8.tif
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Fig3_Kv7.2_Ant_Ctl_3-9.tif
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Fig3_Kv7.2_Ant_Ctl_4-1.tif
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Fig3_Kv7.2_Ant_Ctl_4-2.tif
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Fig3_Kv7.2_Ant_Ctl_4-3.tif
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Fig3_Kv7.2_Ant_Ctl_4-4.tif
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Fig3_Kv7.2_Ant_Ctl_4-5.tif
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Fig3_Kv7.2_Ant_Ctl_4-6.tif
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Fig3_Kv7.2_Ant_Ctl_4-7.tif
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Fig3_Kv7.2_Ant_Ctl_4-8.tif
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Fig3_Kv7.2_Ant_Ctl_4-9.tif
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Fig3_Kv7.2_Ant_IM_1-1.tif
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Fig3_Kv7.2_Ant_IM_1-2.tif
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Fig3_Kv7.2_Ant_IM_1-3.tif
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Fig3_Kv7.2_Ant_IM_1-4.tif
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Fig3_Kv7.2_Ant_IM_1-5.tif
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Fig3_Kv7.2_Ant_IM_1-6.tif
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Fig3_Kv7.2_Ant_IM_1-7.tif
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Fig3_Kv7.2_Ant_IM_1-8.tif
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Fig3_Kv7.2_Ant_IM_1-9.tif
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Fig3_Kv7.2_Ant_IM_2-1.tif
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Fig3_Kv7.2_Ant_IM_2-10.tif
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Fig3_Kv7.2_Ant_IM_2-2.tif
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Fig3_Kv7.2_Ant_IM_2-3.tif
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Fig3_Kv7.2_Ant_IM_2-4.tif
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Fig3_Kv7.2_Ant_IM_2-5.tif
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Fig3_Kv7.2_Ant_IM_2-6.tif
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Fig3_Kv7.2_Ant_IM_2-7.tif
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Fig3_Kv7.2_Ant_IM_2-8.tif
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Fig3_Kv7.2_Ant_IM_2-9.tif
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Fig3_Kv7.2_Ant_IM_3-1.tif
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Fig3_Kv7.2_Ant_IM_3-10.tif
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Fig3_Kv7.2_Ant_IM_3-2.tif
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Fig3_Kv7.2_Ant_IM_3-3.tif
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Fig3_Kv7.2_Ant_IM_3-4.tif
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Fig3_Kv7.2_Ant_IM_3-5.tif
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Fig3_Kv7.2_Ant_IM_3-6.tif
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Fig3_Kv7.2_Ant_IM_3-7.tif
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Fig3_Kv7.2_Ant_IM_3-8.tif
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Fig3_Kv7.2_Ant_IM_3-9.tif
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Fig3_Kv7.2_Ant_IM_4-1.tif
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Fig3_Kv7.2_Ant_IM_4-2.tif
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Fig3_Kv7.2_Ant_IM_4-3.tif
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Fig3_Kv7.2_Ant_IM_4-4.tif
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Fig3_Kv7.2_Ant_IM_4-5.tif
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Fig3_Kv7.2_Ant_IM_4-6.tif
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Fig3_Kv7.2_Ant_IM_4-7.tif
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Fig3_Kv7.2_Ant_IM_4-8.tif
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Fig3_Kv7.2_Ant_IM_4-9.tif
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Fig3_Kv7.2_Anterograde_Processed_Data_Fluorescence.csv
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Fig3_Kv7.2_Anterograde_Processed_Data_Flux.csv
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Fig3_Kv7.2_Anterograde_Processed_Data_Velocity.csv
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Fig3_Kv7.2_Ret_Ctl_1-1.tif
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Fig3_Kv7.2_Ret_Ctl_1-2.tif
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Fig3_Kv7.2_Ret_Ctl_1-3.tif
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Fig3_Kv7.2_Ret_Ctl_1-4.tif
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Fig3_Kv7.2_Ret_Ctl_1-5.tif
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Fig3_Kv7.2_Ret_Ctl_1-6.tif
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Fig3_Kv7.2_Ret_Ctl_1-7.tif
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Fig3_Kv7.2_Ret_Ctl_1-8.tif
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Fig3_Kv7.2_Ret_Ctl_1-9.tif
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Fig3_Kv7.2_Ret_Ctl_2-1.tif
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Fig3_Kv7.2_Ret_Ctl_2-10.tif
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Fig3_Kv7.2_Ret_Ctl_2-2.tif
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Fig3_Kv7.2_Ret_Ctl_2-3.tif
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Fig3_Kv7.2_Ret_Ctl_2-4.tif
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Fig3_Kv7.2_Ret_Ctl_2-5.tif
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Fig3_Kv7.2_Ret_Ctl_2-6.tif
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Fig3_Kv7.2_Ret_Ctl_2-7.tif
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Fig3_Kv7.2_Ret_Ctl_2-8.tif
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Fig3_Kv7.2_Ret_Ctl_2-9.tif
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Fig3_Kv7.2_Ret_Ctl_3-1.tif
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Fig3_Kv7.2_Ret_Ctl_3-2.tif
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Fig3_Kv7.2_Ret_Ctl_3-3.tif
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Fig3_Kv7.2_Ret_Ctl_3-4.tif
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Fig3_Kv7.2_Ret_Ctl_3-5.tif
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Fig3_Kv7.2_Ret_Ctl_3-6.tif
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Fig3_Kv7.2_Ret_Ctl_3-7.tif
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Fig3_Kv7.2_Ret_Ctl_3-8.tif
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Fig3_Kv7.2_Ret_Ctl_3-9.tif
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Fig3_Kv7.2_Ret_Ctl_4-1.tif
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Fig3_Kv7.2_Ret_Ctl_4-2.tif
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Fig3_Kv7.2_Ret_Ctl_4-3.tif
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Fig3_Kv7.2_Ret_Ctl_4-4.tif
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Fig3_Kv7.2_Ret_Ctl_4-5.tif
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Fig3_Kv7.2_Ret_Ctl_4-6.tif
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Fig3_Kv7.2_Ret_Ctl_4-7.tif
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Fig3_Kv7.2_Ret_Ctl_4-8.tif
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Fig3_Kv7.2_Ret_Ctl_4-9.tif
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Fig3_Kv7.2_Ret_IM_1-1.tif
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Fig3_Kv7.2_Ret_IM_1-2.tif
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Fig3_Kv7.2_Ret_IM_1-3.tif
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Fig3_Kv7.2_Ret_IM_1-4.tif
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Fig3_Kv7.2_Ret_IM_1-6.tif
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Fig3_Kv7.2_Ret_IM_1-7.tif
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Fig3_Kv7.2_Ret_IM_1-8.tif
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Fig3_Kv7.2_Ret_IM_1-9.tif
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Fig3_Kv7.2_Ret_IM_2-1.tif
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Fig3_Kv7.2_Ret_IM_2-10.tif
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Fig3_Kv7.2_Ret_IM_2-2.tif
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Fig3_Kv7.2_Ret_IM_2-3.tif
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Fig3_Kv7.2_Ret_IM_2-4.tif
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Fig3_Kv7.2_Ret_IM_2-6.tif
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Fig3_Kv7.2_Ret_IM_2-7.tif
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Fig3_Kv7.2_Ret_IM_2-8.tif
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Fig3_Kv7.2_Ret_IM_2-9.tif
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Fig3_Kv7.2_Ret_IM_3-1.tif
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Fig3_Kv7.2_Ret_IM_3-2.tif
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Fig3_Kv7.2_Ret_IM_3-3.tif
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Fig3_Kv7.2_Ret_IM_3-4.tif
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Fig3_Kv7.2_Ret_IM_3-5.tif
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Fig3_Kv7.2_Ret_IM_3-6.tif
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Fig3_Kv7.2_Ret_IM_3-7.tif
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Fig3_Kv7.2_Ret_IM_3-8.tif
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Fig3_Kv7.2_Ret_IM_3-9.tif
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Fig3_Kv7.2_Ret_IM_4-1.tif
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Fig3_Kv7.2_Ret_IM_4-2.tif
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Fig3_Kv7.2_Ret_IM_4-3.tif
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Fig3_Kv7.2_Ret_IM_4-4.tif
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Fig3_Kv7.2_Ret_IM_4-5.tif
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Fig3_Kv7.2_Ret_IM_4-6.tif
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Fig3_Kv7.2_Ret_IM_4-7.tif
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Fig3_Kv7.2_Ret_IM_4-8.tif
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Fig3_Kv7.2_Ret_IM_4-9.tif
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Fig3_Kv7.2_Retrograde_Processed_Data_Fluorescence.csv
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Fig3_Kv7.2_Retrograde_Processed_Data_Flux.csv
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Fig3_Kv7.2_Retrograde_Processed_Data_Velocity.csv
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Fig3_Nav1.7_Ant_Ctl_1-1.tif
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Fig3_Nav1.7_Ant_Ctl_1-2.tif
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Fig3_Nav1.7_Ant_Ctl_1-8.tif
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Fig3_Nav1.7_Ant_Ctl_1-9.tif
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Fig3_Nav1.7_Ant_Ctl_2-1.tif
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Fig3_Nav1.7_Ant_Ctl_2-9.tif
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Fig3_Nav1.7_Ant_Ctl_3-1.tif
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Fig3_Nav1.7_Ant_Ctl_3-11.tif
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Fig3_Nav1.7_Ant_Ctl_3-2.tif
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Fig3_Nav1.7_Ant_Ctl_3-3.tif
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Fig3_Nav1.7_Ant_Ctl_3-4.tif
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Fig3_Nav1.7_Ant_Ctl_3-9.tif
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Fig3_Nav1.7_Ant_IM_1-1.tif
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Fig3_Nav1.7_Ant_IM_1-2.tif
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Fig3_Nav1.7_Ant_IM_2-1.tif
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Fig3_Nav1.7_Ant_IM_2-3.tif
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Fig3_Nav1.7_Ant_IM_2-8.tif
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Fig3_Nav1.7_Ant_IM_2-9.tif
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Fig3_Nav1.7_Ant_IM_3-1.tif
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Fig3_Nav1.7_Ant_IM_3-8.tif
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Fig3_Nav1.7_Ant_IM_3-9.tif
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Fig3_Nav1.7_Anterograde_Processed_Data_Fluorescence.csv
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Fig3_Nav1.7_Anterograde_Processed_Data_Flux.csv
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Fig3_Nav1.7_Anterograde_Processed_Data_Velocity.csv
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Fig3_Nav1.7_Ret_Ctl_1-1.tif
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Fig3_Nav1.7_Ret_IM_3-1.tif
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Fig3_Nav1.7_Ret_IM_3-8.tif
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Fig3_Nav1.7_Ret_IM_3-9.tif
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Fig3_Nav1.7_Retrograde_Processed_Data_Fluorescence.csv
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Fig3_Nav1.7_Retrograde_Processed_Data_Flux.csv
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Fig3_Nav1.7_Retrograde_Processed_Data_Velocity.csv
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Fig4_Kv7.2_Insertion_Data_Ctl.csv
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Fig4_Kv7.2_Insertion_Data_IM.csv
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Fig4_Kv7.2_Removal_Data_Ctl.csv
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README.md
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Abstract
Inflammation causes pain by shifting the balance of ionic currents in nociceptors towards depolarization, leading to hyperexcitability. The ensemble of ion channels within the plasma membrane is regulated by processes including biogenesis, transport, and degradation. Thus, alterations in ion channel trafficking may influence excitability. Sodium channel NaV1.7 and potassium channel KV7.2 promote and oppose excitability in nociceptors, respectively. We used live-cell imaging to investigate mechanisms by which inflammatory mediators modulate the abundance of these channels at axonal surfaces through transcription, vesicular loading, axonal transport, exocytosis, and endocytosis. Inflammatory mediators induced a NaV1.7-dependent increase in activity in distal axons. Further, inflammation increased the abundance of NaV1.7, but not of KV7.2, at axonal surfaces by selectively increasing channel loading into anterograde transport vesicles and insertion at the membrane, without affecting retrograde transport. These results uncover a cell-biological mechanism for inflammatory pain and suggest NaV1.7 trafficking as a potential therapeutic target.