Drugs have long been considered crucial targets for transmitter-gated ion channels. The majority of medications utilized to treat schizophrenia, anxiety, depression, and sleeplessness work at chemical synapses, and many of these pharmaceuticals function by binding to transmitter-gated channels. For instance, some drugs like barbiturates and tranquilizers bind to GABA receptors and enhance the inhibitory effect of GABA neurotransmitter. Thus, reduced concentration of GABA enables the opening of Cl- channels. 
Furthermore, psychoactive drugs could potentially target many other synaptic signalling machinery components. In fact, numerous neurotransmitters are released by Na+-driven carriers and are subsequently removed from the synaptic cleft. By inhibiting such carriers, synaptic transmission is strengthened as the action of the transmitter is prolonged. For example, Prozac is one of antidepressant medications that works by preventing the absorption of serotonin neurotransmitter. Also, other antidepressants operate by inhibiting the reabsorption of both serotonin and norepinephrine.