Open AccessPotassium channels contribute to activity‐dependent regulation of dendritic inhibition
Author(s) -
Chang Jeremy T.,
Higley Michael J.
Publication year - 2018
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13747
Subject(s) - excitatory postsynaptic potential , dendritic spike , neuroscience , gabaergic , inhibitory postsynaptic potential , neocortex , depolarization , postsynaptic potential , voltage dependent calcium channel , membrane potential , chemistry , voltage gated ion channel , calcium , calcium imaging , dendritic spine , biophysics , potassium channel , microbiology and biotechnology , biology , ion channel , receptor , biochemistry , organic chemistry , hippocampal formation
GABA ergic inhibition plays a critical role in the regulation of neuronal activity. In the neocortex, inhibitory interneurons that target the dendrites of pyramidal cells influence both electrical and biochemical postsynaptic signaling. Voltage‐gated ion channels strongly shape dendritic excitability and the integration of excitatory inputs, but their contribution to GABA ergic signaling is less well understood. By combining 2‐photon calcium imaging and focal GABA uncaging, we show that voltage‐gated potassium channels normally suppress the GABA ergic inhibition of calcium signals evoked by back‐propagating action potentials in dendritic spines and shafts of cortical pyramidal neurons. Moreover, the voltage‐dependent inactivation of these channels leads to enhancement of dendritic calcium inhibition following somatic spiking. Computational modeling reveals that the enhancement of calcium inhibition involves an increase in action potential depolarization coupled with the nonlinear relationship between membrane voltage and calcium channel activation. Overall, our findings highlight the interaction between intrinsic and synaptic properties and reveal a novel mechanism for the activity‐dependent regulation of GABA ergic inhibition.