Sensory processing is dynamically tuned by internal state, yet how metabolic signals reshape the earliest stages of sensory circuits remains poorly understood. Here we identify a circuit mechanism by which satiety suppresses olfactory sensitivity at the first central synapse in the mouse olfactory bulb. Using a within-animal paradigm modelling fasted and glucose-induced sated states, we show that satiety impairs food-finding behaviour and reduces olfactory receptor neuron input to the olfactory bulb. Periglomerular (PG) cells, which co-express insulin receptors and the potassium channel Kv1.3, mediate this effect: insulin inhibits the low-voltage-activated Kv1.3 current in PG cells, increasing their spontaneous and odour-evoked activity. This heightened PG cell activity drives enhanced presynaptic inhibition of olfactory receptor neuron terminals, dampening sensory input before it reaches mitral cells. These findings establish insulin-dependent presynaptic inhibition of PG cells as a key locus of state-dependent sensory gain control. ### Competing Interest Statement The authors have declared no competing interest. Medical Research Council, https://ror.org/03x94j517, MR/V003747/1 Biotechnology and Biological Sciences Research Council, BB/ Z51679X/1

Overview of the RoleAre you an ambitious researcher looking for your next challenge? Do you have an established background in Neuroscience? Do you want to further your career in one of the UK’s leadin...

Learning-induced changes in primary sensory neurons support concentration-invariant perception of an odor.