Jatamansi potentiated the effect of pentobarbital by shortening sleep latency and prolonging total sleeping time in swiss albino mice, though not as remarkable as that of diazepam. Earlier reports suggest that the increase and decrease of pentobarbitone-induced sleep time can be a useful tool for examining the stimulatory or inhibitory effects on CNS, especially for investigating influences on gamma-aminobutyric acid (GABA A ) ergic systems in CNS. [24] The previous report suggested that ethanolic extract of Jatamansi significantly altered locomotor activity. [25] Jatamansone exerted a tranquilizing effect in mice and monkeys [13] and a significant reduction in hyperactivity and improvement in restlessness and aggressiveness on hyperkinetic children similar to amphetamine. [8] Alcoholic extract of Jatamansi root increased the level of GABA on acute administration and increased the levels of most of the central biogenic amines and inhibitory neurotransmitters on chronic administration. [27] Thus, earlier studies indicate isolated compounds or extracts exert highly significant sedative activity while **data** of this study indicates    Benzodiazepines have been used for the treatment of insomnia and other CNS disorders predominantly. These drugs potentiate the effects of the inhibitory neurotransmitter of GABA, by binding to a specific site on the GABA A receptors to produce allosteric enhancement of anion flux through this ligand-gated chloride channel. [28,29] Most sedative-hypnotics used in the treatment of insomnia target the GABA A receptor. As test drug increased the duration of sleep time induced by a sub hypnotic dose of pentobarbitone, it can be stated that the drug may interact with pentobarbitone on the CNS via GABA A -ergic mechanisms in CNS.