Patch-clamp recordings find increased TREK channel activity at physiological temperature in nodose ganglion neurons, suggesting their role in thermal sensation alongside TRPs.
Temperature homeostasis is controlled by the vagus nerve. Thermal information is collected by thermoreceptors present in the viscera and driven across sensory neurons of the nodose ganglia (NG), which in turn send it to the hypothalamus. While transient receptor potential channels (TRPs) are traditionally considered for thermal transduction, TREK channels belonging to the two-pore domain K+ channels family are emerging as thermosensors, but their role in the NG remains understudied. Patch-clamp recordings revealed that increasing the temperature to physiological levels causes a hyperpolarization of the membrane potential followed by a depolarization and, despite physiological temperature increased the firing rate, we have demonstrated that TREK channels might be taking part in the excitability control by counteracting TRPs’ effects. In fact, single-channel experiments revealed an increase in TREK channel open probability and a subsequent rise in their activity in NG neurons. All this indicates that TREK channels, mainly TREK1, may be responsible along with TRPs for the maintenance of the membrane potential at physiological temperature in NG neurons.
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Rueda‐Ruzafa et al. (2025) studied this question.
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