Ca2+-activated K+ channels reduce network excitability, improving adaptability and energetics for transmitting and perceiving sensory information
Ca2+-activated K+ channels (BK and SK) are ubiquitous in synaptic circuits, but their role in network adaptation and sensory perception remains largely unknown. Using electrophysiological and behavioral assays and biophysical modelling, we discover how visual information transfer in mutants lacking the BK channel (dSlo-), SK channel (dSK-) or both (dSK-;;dSlo-) is shaped in the Drosophila R1-R6 photoreceptor-LMC circuits (R-LMC-R system) through synaptic feedforward-feedback interactions and reduced R1-R6 Shaker and Shab K+ conductances. This homeostatic compensation is specific for each mutant, leading to distinctive adaptive dynamics. We show how these dynamics inescapably increase the energy cost of information and distort the mutants motion perception, determining the true price and limits of homeostatic compensation in an in vivo genetic animal model. These results reveal why Ca2+-activated K+ channels reduce network excitability (energetics), improving neural adaptability for transmitting and perceiving sensory information.\n\nHighlightsO_LIHomeostatic plasticity in Drosophila dSlo-, dSK- and dSK-;;dSlo- null-mutants retains R1-R6 photoreceptors light information sampling while reducing other K+-conductances\nC_LIO_LIAs mutant R-LMC-R circuits rebalance synaptic loads homeostatically, R1-R6s become more depolarized, with dSK- and dSK-;;dSlo- responding faster and dSlo- slower, whilst LMC outputs oscillate, with dSK- responding faster and dSK-;;dSlo- and dSlo- slower than wild-type\nC_LIO_LIHomeostatic compensation in the mutant circuits impedes adaptation, increases the energy cost of visual information and distorts optomotor behavior\nC_LIO_LIHence, Ca2+-activated K+ channels improve adaptability and energetics for transmitting and perceiving sensory information\nC_LI