Pyrethroids inhibit K2P channels and activate sensory neurons: basis of insecticide-induced paraesthesias

Created on 03.10.17

A new study has examined the effect of pyrethroids such as permethrin or tetramethrin (TM) on two-pore domain potassium (K2P) channels mainly expressed in sensory neurons and suggested that inhibition of K2P channels facilitates sensory neuron activation and increases their excitability which contributes to the generation of paraesthesias and pain after parathyroid exposure.

The study by Castellanos published in the September 2017 Pain Journal used electrophysiological and calcium imaging experiments to show that a high percentage of TM-responding neurons were nociceptors, which were also activated by TRPA1 and/or TRPV1 agonists.

The study  suggests that pyrethroids activated and enhanced the excitability of peripheral saphenous nerve fibers and produced a significant inhibition of native TRESK, TRAAK, TREK-1 and TREK-2 currents. At the behavioural level, intradermal TM injection in the mouse paw produced nocifensive responses and caused mechanical allodynia, demonstrating that the effects seen on nociceptors in culture lead to pain-associated behaviors in vivo.

In TRESK knockout mice, pain-associated behaviors elicited by TM were enhanced, providing further evidence for a role of this channel in preventing excessive neuronal activation.

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