It has been established in chronic experiments on rabbits that accumulation of endogenous acetylcholine (galanthamine--1 mg/kg) prevents the development of sodium hydroxybutyrate (500 mg/kg) ability to increase the excitability of the mesencephalic reticular formation and to reduce the level of frontal cortex excitability. Inhibition of the central muscarinic (metamizyl--2 mg/kg) or nicotinic (eterofen--10 mg/kg) cholinoreceptors prevents the stimulant action or sodium hydroxybutyrate on the excitability of the dorsal hippocamp and mesencephalic reticular formation. Blockade of the central N-cholinoreceptors changes the marked effect of sodium hydroxybutyrate on the blood content of the test brain structures. This may attest to the participation of N-cholinoreceptors in the effects of sodium hydroxybutyrate.