As already noted, depressants have many features. Alcohol, barbiturates, non-barbiturate sedatives and, of course, benzodiazepines have a similar effect at equivalent dosage. In addition, there is cross tolerance between them. They can reinforce each other. There is also cross-dependence, since the appropriate dose of any depressant can be used to reduce the withdrawal symptoms caused by any other. Indeed, benzodiazepines are often used to mitigate the effects of alcohol withdrawal. Thus, reliable evidence was obtained about the generality of the mechanism of action of depressants. By the early 1970s, evidence began to accumulate that GABA (gamma-aminobutyric acid), the main inhibitory neurotransmitter of the brain, serves as a common link.

There was a problem, as there was no direct evidence that any depressant binds to the GABA neurotransmitter receptor. Then, in 1977, two laboratories, independently of each other, reported the discovery of benzodiazepine bonds to receptors, and it was consistently shown that, being special for benzodiazepines, these receptors are also part of what is called the GABA-benzodiazepine receptor complex. Apparently, the usual nervous delay caused by GABA increases greatly when the benzodiazepine receptor is activated. In addition, it was found that the third receptor in the system is responsible for barbiturates. That is, barbiturates and benzodiazepines act by increasing the neural delay in the GABA system, although they affect different receptors.

Another sensational discovery was the development of new drugs that are antagonists in benzodiazepine receptors. These drugs block the effects of benzodiazepines, but can themselves have a certain effect. This effect provoked convulsions and anxiety – symptoms opposite to the action of benzodiazepines. For example, when working with a compound called FG-7142, it was observed that it caused panic attacks and a craving for violence in three patients who took the drug. Animal studies confirmed the claim that FG-7142 causes fear or anxiety. Today, prospective studies with this drug and similar compounds can reveal important secrets of neurochemistry of anxiety. After all, benzodiazepine receptors exist in the brain for some purpose, and they are unlikely to simply wait for the discovery of benzodiazepines in the brain. Benzodiazepines are more likely to mimic some kind of natural neurotransmitter regulation of fear or anxiety.

When benzodiazepines are absorbed in the stomach, the absorption process is slow enough and therefore they have a long duration of action. However, there are significant differences in the duration of action and effects of different benzodiazepines, which are taken into account when prescribing.
Table 7-2 shows the time required for the metabolism of half the dose of some commonly used benzodiazepines. Long-acting benzodiazepines, such as Valium, are considered as the most effective when trying to maintain a constant dosage of the drug for a long period, for example, when a patient suffers from heightened anxiety. Benzodiazepines, having a short and moderate duration of action, are more suitable for treating insomnia when it is desirable that the effects of the drug disappear by the morning.