The effect of benzodiazepines is associated with the allosteric modification of gamma-aminobutyric acid (GABA) receptors. Gamma-aminobutyric acid reduces the excitability of neurons by binding to GABA receptors. Benzodiazepines, allosterically interacting with GABA receptors, increase the affinity of GABA to these receptors, thereby increasing the flow of chloride ions into the neurons and increasing the inhibitory postsynaptic potential, which reduces the excitability of neurons. After binding, the benzodiazepine ligand closes the GABA receptor into a conformation in which it has a greater affinity for the GABA neurotransmitter. The opening of ion channels becomes more frequent resulting in the hyperpolarization of the postsynaptic membrane and neuronal resistance to excitation. As the inhibitory effect of GABA is potentiated, benzodiazepines result in sedative and anxiolytic effects.