Sensory experience-induced plasticity of somatostatin interneurons occurs through two-pore potassium (K2P) channels

Abstract

GABAergic interneurons (INs) are powerful modulators of plasticity and learning in cortical networks, but plasticity of INs themselves is not well understood. We studied experience-dependent plasticity in somatostatin (SST) INs, which critically regulate dendritic integration, sensory tuning, and plasticity in pyramidal neurons in sensory cortex. Whether SST INs exhibit experience-dependent plasticity, and by what mechanisms, is unknown. We found that 3 days of whisker deprivation strongly downregulated intrinsic excitability of SST INs in L2/3 of somatosensory cortex, by reducing input resistance. Deprivation also increased mEPSCs onto SST INs. The reduction in intrinsic excitability was caused by an increase in leak potassium current through two-pore K+ (K2P) channels, without changes in HCN, KV1, or KV7 currents, which contribute to plasticity in other IN types and brain areas. Immunohistochemistry showed an increase in TRESK, but not other K2P channels, indicating a novel role for K2P channels in experience-dependent plasticity of interneuron excitability.