Amphetamines and cocaine: By displacing norepinephrine (N E) from the peripheral adrenergic nerve endings, these drugs probably mimic the effects of the amine. In the brain, from nerves containing NE and dophine (D A), they act to release these amines. Displacement of catecholamine from storage sites may also be a mode of action of these drugs. The use of these drugs can be self-rewarding, since they release dopamine, which is correlated with rewarding stimulation.

Alcohol: Profound alteration of central nervous system function can occur with ethanol, a depressant capable of interacting with nerve cell membranes. Upon acute administration, its acts in a biphasic, dose-dependent manner such that high doses produce the well known sedative effects, while very low doses of ethanol increases neural excitability in main brain regions. A regional hierarchy of susceptibility ranging from primary sensory neurons as least affected to association cortex and reticular formation as most affected has been supported by many laboratory studies, which has attempted to define the primary sites of ethanol’s acute effects within the brain. However, it has not been ruled out that there may be a general disruptive effect at synapses throughout the brain.