Sleep regulation depends on the complex interplay between homeostatic and circadian processes synchronized by the light/dark cycle. Sleep is also directly influenced by projections from the retina to the preoptic area (POA). Although the light-responsive POA neurons project to several wake-promoting neurons, including histaminergic neurons in the tuberomammillary nucleus (TMN), there is no functional evidence for their involvement in light-induced sleep. We used hM4Di-HDC-cre mice (HDC+/+, n=8) and histidine decarboxylase (HDC-/-, n=7) knockout mice subjected to an ultradian light/dark protocol (LD1:1h:1h over 24h), and another group of hM4Di-HDC-cre mice (HDC+/+, n=8) exposed to a 1-h light pulse. We found that light pulses during the biological night enhanced slow wave sleep and increased cortical EEG power in the delta range, and that these effects were significantly attenuated both in HDC-/- (82 vs 23 min/6h, p=0.005) under LD1 condition and in hM4Di-HDC-cre mice after acute chemogenetic inhibition of histamine neurons by the DREADD ligand deschloroclozapine (15 vs 6 min/h, p=0.0016) under a 1-h light pulse. In addition, we show that the sleep-inducing effect of light is circadian dependent, with the strongest effect at the beginning and end of the night in HDC +/+ mice. We also observe that the response dynamics to light are slowed down when lacking histamine neurotransmission. Our study provides experimental evidence that the acute sleep-inducing effects of light on sleep require histamine neurotransmission in mice.