• CNS depressants  sedation, reduction of anxiety
• Rapid acting  induction of anaesthesia (eg thiopental)
• Short acting  treat insomnia, adjunct to anaesthesia, sedative and hypnotic (eg pentobarbital, secobarbital)
• Long acting  treat insomnia and seizures (eg phenobarbital)
• suppress respiration by inhibiting the hypoxic and CO2 response of the chemoreceptors
• bind to GABA receptor-chloride channel complex and both enhance the inhibitory effect of GABA and directly mimic actions of GABA. As they mimic effects of GABA  no limit to amount of CNS depression due to exogenous administration (compared to benzodiazepines which only enhance endogenous GABA  limit to amount of CNS depression)
• metabolised in the liver and induce the cytochrome P-450 enzymes  large number of drug interactions
• have low therapeutic index  risk for overdose
• adverse effects – respiratory depression, suicide (from overdose), dependence/abuse

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