Intrinsic Adaptive Plasticity in Mouse and Human Sensory Neurons

Here, we show that sustained depolarization (induced by 24h incubation in 30mM KCl) induces compensatory changes that decrease excitability of mouse and human sensory neurons without directly opposing membrane depolarization. Voltage clamp recordings show that sustained depolarization produces no significant alteration in voltage-gated potassium currents, but a robust reduction in voltage-gated sodium currents, likely contributing to the overall decrease in neuronal excitability. The compensatory decrease in neuronal excitability and reduction in voltage-gated sodium currents reversed completely following a 24h recovery period in normal medium. Similar adaptive changes were not observed in response to 24h of sustained action potential firing induced by optogenetic stimulation at 1Hz, indicating the need for prolonged depolarization to drive engagement of this adaptive mechanism in sensory neurons. Our findings show that mouse and human sensory neurons are capable of engaging adaptive mechanisms to regulate intrinsic excitability in response to sustained depolarization in a manner similar to that described in neurons in the central nervous system.

The data listed here show a description of the electrophysiological analysis of mouse and human sensory neurons subjected to sustained depolarization. In addition, you will find results from immunocytochemistry and cell viability assays. The data listed here also includes statistical analysis generated by Graphpad. Please refer to our manuscript for further description.

The link to the RNAseq dataset is listed below