Although normal control of the sleep-wake cycle is exerted by the suprachiasmatic nucleus via melatonin receptor subtype 1 and 2 (MT1 and MT2) receptors (melatonin receptor subtype), most current pharmacologic treatments for insomnia mainly involve GABAergic (gamma-aminobutyric acid) mechanisms. Most currently prescribed sleep agents are benzodiazepine receptor agonists, which induce sleep by binding to the benzodiazepine receptor site of the gamma-aminobutyric acid-A receptor complex. Gamma-aminobutyric acid is the major inhibitory transmitter in the central nervous system, and its receptors are distributed widely throughout the brain. In addition to sleep, benzodiazepine receptor agonists can cause a wide range of ancillary effects not directly related to sleep, depending on the precise subset of gamma-aminobutyric acid-A receptors activated. These include sedative, anxiolytic, muscle-relaxant, and amnesic effects. The risk of tolerance, dependence development, and abuse potential associated with the benzodiazepine receptor agonists also may reflect effects of these drugs on the gamma-aminobutyric acid-A receptor complex.