Barbiturates, formerly very common until the 1970s, modulate GABA-A receptors by directly opening the chloride channel at high concentrations; i.e., they can keep it open even when there is no endogenous GABA available, leading to extreme respiratory depression, coma, and death. They also possess very small therapeutic margin, because the dose used to induce sedation is close to the dose that is potentially lethal, so a fairly modest overdose is lethal. Benzodiazepines, as the safer alternative, produce another type of effect: rather than opening the channel itself, they enhance the receptor's affinity for the available GABA, thereby enhancing its effect. This creates a ceiling effect beyond which there is no further increase in respiratory depression, a feature that renders overdoses by themselves infrequent to kill. In combination with other central nervous system depressants like alcohol, opioids, or barbiturates, however, they have an additive effect that can result in respiratory arrest. Valium is a trade name for diazepam, so we are dealing with a benzodiazepine.