Cocaine is a natural alkaloid extracted from the leaves of the Andean shrub Erythroxylon coca (Agarwal and Sen, 2004). It is used as an ophthalmic and spinal anesthetic. It is the primary nonalcoholic drug of abuse. Its recent popularity since the 1980s has been due to the smoked form known as crack or rock. Cocaine is sold on the streets as a water-soluble hydrochloride (HCl) salt for snorting or intravenous injection. It can be injected subcutaneously or intramuscularly, but this slows absorption and does not give a rush. It can also be smoked as a free base, and is rapidly absorbed in this form through the lungs with swift penetration to the brain.
Cocaine blocks the initiation or conduction of the action potential following local application to a nerve and stimulates the central nervous system (CNS) (Agarwal and Sen, 2004). The local anesthetic effect is a direct membrane effect. Cocaine blocks initiation and conduction of electrical impulses within nerve cells by preventing the rapid increase in cell permeability to sodium ions during depolarization. The most notable effect is CNS stimulation by altering the uptake and metabolism of norepinephrine, dopamine, serotonin and acetylcholine. This blocking of the reuptake of norepinephrine and dopamine results in activation of the sympathetic nervous system, raising arterial pressure, causing tachycardia, and a predisposition to ventricular arrhythmias and seizures. It may also result in mydriasis, hyperglycemia, and hyperthermia. The effects on the dopaminergic system produce euphoria and addiction.
In the short-term, cocaine stimulates dopaminergic neurotransmission by blocking dopamine reuptake, but in the long-term, the nerve terminals become depleted of dopamine which has been theorized to contribute to the dysphoria that develops during withdrawal (Agarwal and Sen, 2004). Higher doses mediate CNS toxicity. Cocaine also causes neuropsychiatric complications...