Key points Vagal sensory inputs transmit information from the viscera to brainstem neurones located in the nucleus tractus solitarii to set physiological parameters. These excitatory synapses exhibit a CB1 endocannabinoid‐induced long‐term depression (LTD) triggered by vagal fibre stimulation. We investigated the impact of nutritional status on long‐term changes in this long‐term synaptic plasticity. Food deprivation prevents LTD induction by disrupting CB1 receptor signalling. Short‐term refeeding restores the capacity of vagal synapses to express LTD. Ghrelin and cholecystokinin, respectively released during fasting and refeeding, play a key role in the control of LTD via the activation of energy sensing pathways such as AMPK and the mTOR and ERK pathways. Abstract Communication form the viscera to the brain is essential to set physiological homoeostatic parameters but also to drive more complex behaviours such as mood, memory and emotional states. Here we investigated the impact of the nutritional status on long‐term changes in excitatory synaptic transmission in the nucleus tractus solitarii, a neural hub integrating visceral signals. These excitatory synapses exhibit a CB1 endocannabinoid (eCB)‐induced long‐term depression (LTD) triggered by vagal fibre stimulation. Since eCB signalling is known to be an important component of homoeostatic regulation of the body and is regulated during various stressful conditions, we tested the hypothesis that food deprivation alters eCB signalling in central visceral afferent fibres. Food deprivation prevents eCB‐LTD induction due to the absence of eCB signalling. This loss was reversed by blockade of ghrelin receptors. Activation of the cellular fuel sensor AMP‐activated protein kinase or inhibition of the mechanistic target of rapamycin pathway abolished eCB‐LTD in free‐fed rats. Signals associated with energy surfeit, such as short‐term refeeding, restore eCB‐LTD induction, which in turn requires activation of cholecystokinin receptors and the extracellular signal‐regulated kinase pathway. These data suggest a tight link between eCB‐LTD in the NTS and nutritional status and shed light on the key role of eCB in the integration of visceral information.