Volatile anaesthetics have been in use for years in clinical practice, although mechanism of their action is not yet fully understud. There are many hypotheses suggesting the site of their action. With so far investigated possible involvements of GABA and NMDA receptors, recent researches indicate possible action of volatile anaesthetics on lipid signalling domains. Lipid rafts are localized lipid structures with large quantity of cholesterol and glycosphingolipids. Lipid rafts function as signalling platforms, incorporated in the fluid membrane, in the transmission of signals inside the cell. This disertation presents a research on the ability of volatile anaesthetics to act on lipid rafts signalling domains. Tests were conducted in vivo, using the B4galnt1 mouse model. This mouse model has a modified ability to produce lipid domains due to the blocked synthesis of complex gangliosides. Tests included both mice strains, C57BL/6 and C57BL/6J fed with Cuprizone. Mice were exposed to different tests before and after anaesthesia with sevoflurane and isoflurane. Tests included Visual placing response, Hindlimb extension reflex, Forelimb grip strength, RotaRod, Activity cage, modified Lashley III maze, and passive avoidance task. The induction and recovery times from anaesthesia were observed and measured. The research results suggest that B4galnt1 mice have significantly shorter induction time of anaesthesia using isoflurane (p<0.001) and sevoflurane (p<0.001), compared to the WT mice fed with Cuprizone. WT mice fed with Cuprizone had significantly longer time in maintaining RotaRod, than B4galnt1 mice before induction of anaesthesia (p<0.001). Under Passive Avoidance test, 84.6% of B4galnt1 mice and 25% of Cuprizone fed mice models postponed entrance into the dark room. B4galnt1 mice have significantly less horizontal movement in the first (p = 0.002) and fourth (p<0.001) minute, as well as significantly less vertical movement in the first (p <0.001) and fourth (p <0.001) minute before induction time of anaesthesia compared to WT mice fed with Cuprizone. The differences in the results of cognitive and motor skills tests before and after anaesthesia were caused by changes in composition of lipid domains, and not by hypomyelinisation.