Figure 1. Excitatory and inhibitory neurotransmission. Ligand-gated ion channels, which are selectively permeable to particular cations or anions, mediate excitatory and inhibitory neurotransmission. The principal excitatory and inhibitory neurotransmitters are glutamate and -aminobutyric acid (GABA), respectively.

Figure 2. -Aminobutyric acid (GABA)ergic synapse. After being released from the nerve terminal, the neurotransmitter GABA activates GABA_A receptors located in the postsynaptic membrane. They constitute GABA-gated chloride channels ( Cl^–) whose performance is enhanced in the presence of a benzodiazepine (e.g. diazepam). The action of GABA is terminated by GABA transporters (GT), by which the neurotransmitter is taken up into the nerve terminal.

Figure 3. Diazepam, the prototypical benzodiazepine drug. The chemical structure of diazepam, a 1,4-benzodiazepine, and the pharmacological spectrum of benzodiazepine drugs. Therapeutic indications and chemical structures of various other benzodiazepine drugs are given in Table 1 and Table 2, and in Figure 4.

Figure 4. Chemical structures of benzodiazepine drugs.

Figure 5. Enhancement of the -aminobutyric acid (GABA) response by a benzodiazepine. In the presence of a benzodiazepine (e.g. diazepam), the dose–response curve of GABA is shifted to the left. The action of benzodiazepines is activity dependent and self-limiting: in the absence of GABA, the benzodiazepine has no potentiating effect (bottom left part of the curves); when the GABA response is maximal, it is not further enhanced by the benzodiazepine (top right).

Figure 6. Structure–activity relationship of the benzodiazepines. The pharmacological potency of benzodiazepines correlates closely with their affinity to the benzodiazepine-binding site. This is exemplified for the muscle relaxant activity of various benzodiazepines. Their affinity was determined by competition for the binding site with [ ³H]diazepam. The numbers refer to benzodiazepines not in clinical use. Ed_min, minimum effective dose.