Hydrogen sulfide regulates hippocampal neuron excitability via S-sulfhydration of Kv2.1.

ABSTRACT: Hydrogen sulfide (H₂S) is gaining interest as a mammalian signalling molecule with wide ranging effects. S-sulfhydration is one mechanism that is emerging as a key post translational modification through which H₂S acts. Ion channels and neuronal receptors are key target proteins for S-sulfhydration and this can influence a range of neuronal functions. Voltage-gated K⁺ channels, including Kv2.1, are fundamental components of neuronal excitability. Here, we show that both recombinant and native rat Kv2.1 channels are inhibited by the H₂S donors, NaHS and GYY4137. Biochemical investigations revealed that NaHS treatment leads to S-sulfhydration of the full length wild type Kv2.1 protein which was absent (as was functional regulation by H₂S

SUBMITTER: Dallas ML 

PROVIDER: S-EPMC8046973 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature