Historical Overview

Cocaine is basically an organic compound that usually exists in plants of Northern South America. This plant is also found in minimal amount in India, Africa and Indonesia. The height of the plant may vary depending upon the elevation of the location. At higher locations, the plant may reach up to approximately 9 feet of height. The reason behind this strange concept is that at higher elevations the alkaloid content in the plant is greatly reduced because of high growth.  The reaping pattern however initially is after two years of plantation. But later on it can increase up to three times in a year. The leaves are first dried and are then converted to a paste like form which is finally used for the production of cocaine hydrochloride. The actual yield of hydrochloride from the leaves is in lesser amount then the weight of the leaves. Thus paste and other hydrochlorides that are extracted from the leaves are approximately in the ratio of one to hundred (that is for every hundred kilograms of leaves, the paste attained would be of one kilogram).

Historically the cocoa plant and its extractions are considered as a psychotropic drug. Most of the former people at Peru used to chew its leaves in their religious rituals and the Spanish habitants realized that without having the cocoa leaves they could not perform heavy labor in the mines.

The past reveals that in 19th century a chemist named Carl Wohler, who was famous for synthesizing urea for the first time, imported cocoa leaves to show his student Albert Niemann. The successful extraction of cocaine from cocoa leaves is the experiment of Albert Niemann. From its inception till date, many tonics and other organic liquids are composed by employing the cocaine and its astonishing characteristics. Medical features of cocaine are first studied by an Italian physician named Mantegazza.

The excessive use of cocaine initially enhances the brain concentration but its long term side effect includes the reduction in the normal concentrations that can cause depression and other traumas to its regular users. Cocaine protects the neurons against the harmful effects of DA and binds it to the receptors located on the nerve terminal. Furthermore the DA is re-consumed and is restrained due to the binding of sodium channels. The dissolved content of DA is transformed across the membrane of sensitive neurons that can considerably increase the DA concentrations while resulting in chronic disorders in the postsynaptic neuron.

Later in 1870’s many papers had been written regarding the potential use of cocaine to treat morphine addictions. However Sigmund Freud was the first one to discover the related drug. Carl Koller was the first physician who used cocaine as an anesthetic in ophthalmological surgery. This amazing drug is then found to have strange traits that can give power to the exhausted people, can satisfy the appetite and can cause people to forget their mishaps and ill-lucks.

Cocaine was reported for its dangerous toxicity that can cause cardiac muscle contractions and other harmful fatalities. Despite of its potential harms and fears, cocaine became more and more popular among the people. In 1914, as cocaine abuse was reported in strong words, the United States banned the direct selling of this narcotic drug. However later on by the vigilance of United Stated Controlled Substances act of 1970, it was officially declared that the drug also has some medical value. So the medical use of the drug was allowed under strict administration and only for the limited use in ear, nose and throat surgery (10 to 20%) and other ophthalmologic treatments (1 to 4 %).

Cocaine is the most prohibited drug abuse these days. Formerly it was reputed as a drug for affluent but now the cheaper version of the drugs has made this drug accessible for the less wealthy people. National Survey conducted in 2002 on the topic of Drug and Health Abuse had brought to note that approximately 34 million of Americans are addicted to this threat. However more endangering fact of this is mostly the younger people (of age less than twelve) are habitual of this narcotic. Currently the rough statistics estimate more than two million people as the recent users of this harmful substance.

Mechanism of Action

Cocaine is globally used as an anesthetic agent. Its most significant ability is its resistance against sodium block channels. Thus it increases the threshold for action against the same. There are many other harmful substances that can be blocked by using cocaine in the clinical treatments. These severe chemicals include neurotransmitters norepinephrine (NE), dopamine (DA) and serotonin (5-HT). NE is so harmful that it can cause many furious diseases such as hypertension, mydriasis and tachypnea. The natural affects of cocaine are more than the behavioral effects of cocaine. Desirable effects of cocaine may include rise in sexual excitement, gain of energy and attaining high self-esteem. There can be many unwanted effects of pertinent cocaine use such as approximate hallucinations and paranoia.

After an acute dose of cocaine, brain concentrations of DA are elevated briefly and then markedly reduced to below-normal concentrations, correlating with the central stimulators effects (rush) and depression (crash) experienced by the cocaine user. Cocaine prevents the reuptake of DA into the pre-synaptic dopaminergic neuron by binding to receptors on the DA transporter located on the dopaminergic nerve terminal This DA reuptake, mediated by sodium, chloride, and energy-dependent active transport, is inhibited when cocaine binds to the sodium binding site on the transporter and alters the chloride binding site, preventing the binding of both ions. Because translocation of DA across the membrane of the pre-synaptic neuron is inhibited, increased extracellular IDA concentrations result in chronic stimulation of the HA receptor in the postsynaptic neuron.

Positive emission tomography demonstrated that 47% of the DA transporters were engaged by cocaine before its effects were recognized, with 60 to 77% occupied after doses regular with cocaine abusers. The time course for the high in humans paralleled that of the cocaine concentration in the striatum, a region in the brain implicated in control of motivation and reward. For equivalent plasma cocaine concentrations and DA transporter blockade, smoked cocaine induced considerably superior self reports of thighs than intranasal cocaine, and showed a trend for greater effect than intravenous cocaine. The time to reach peak subjective effects is notably faster for smoked cocaine (1.4 min) than for intravenous cocaine (3.1 min) and intranasal cocaine (14.6 min). This study demonstrates the significance of rate of cocaine delivery into the brain on its reinforcing effects.

Chronic cocaine administration alters the DA transporter in the meso-limbic regions of the brain. Up-regulation of cocaine binding sites in the striatum results in the need for additional cocaine to continue experiencing its rewarding effects. Chronic cocaine users repeatedly administer cocaine to augment synaptic levels of DA. This process becomes cyclic and demonstrates how cocaine binge or “run” is followed by a crash, and why the excitement to self-medicate is so strong.

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