Cocaine is Schedule II in the United States. This means it is illegal to sell without a DEA license and illegal to buy or possess without a license or prescription.
Addictive Potential: High
Emergency Room Visits Yearly: 125,921 in 2003 more...
Mandatory Minimum Sentence: 5 years for 500 - 4999 grams mixture
Mechanism of Action: blockade of DAT, inhibits MAO uptake, inhibits the uptake of 5-HT3, MGluR5 agonist, a sigma ligand agonist, and more (see the cocaine pharmacology section below)
Cocaine (or crack in its freebase form) is a crystalline tropane alkaloid that is obtained from the leaves of the coca plant. It is a stimulant of the central nervous system and an appetite suppressant, giving rise to what has been described as a euphoric sense of happiness and increased energy. It is most often used recreationally for this effect. Nonetheless, cocaine is formally used in medicine as a topical anesthetic, specifically in eye, nose and throat surgery.
Cocaine is not a new drug. In fact, it is one of the oldest known drugs. The pure chemical, cocaine hydrochloride, has been an abused substance for more than 100 years, and coca leaves, the source of cocaine, have been ingested for thousands of years by the ancient peoples of Peru and other pre-Colombian Andean societies.
There is a long list of prominent intellectuals, artists, politicians, and musicians who have used cocaine — ranging from Sir Arthur Conan Doyle and Sigmund Freud to U.S. Presidents Ulysses S. Grant and reportedly, George W. Bush. At one time, cocaine could even be found in trace amounts in the Coca-Cola beverage, although that is no longer the case.
Cocaine’s effects appear almost immediately after a single dose, and disappear within a few minutes or hours. Taken in small amounts (up to 100 mg), cocaine usually makes the user feel euphoric, energetic, talkative, and mentally alert, especially to the sensations of sight, sound, and touch. It can also temporarily decrease the need for food and sleep. Some users find that the drug helps them perform simple physical and intellectual tasks more quickly, while others experience the opposite effect.
The duration of cocaine’s immediate euphoric effects depends upon the route of administration. The faster the absorption, the more intense the high. Also, the faster the absorption, the shorter the duration of action. The high from snorting is relatively slow in onset, and may last 15 to 30 minutes, while that from smoking may last 5 to 10 minutes.
The short-term physiological effects of cocaine include constricted blood vessels; dilated pupils; and increased temperature, heart rate, and blood pressure. Large amounts (several hundred milligrams or more) intensify the user’s high, but may also lead to bizarre, erratic, and violent behavior. These users may experience tremors, vertigo, muscle twitches, paranoia, or, with repeated doses, a toxic reaction closely resembling amphetamine poisoning. Some users of cocaine report feelings of restlessness, irritability, and anxiety. In rare instances, sudden death can occur on the first use of cocaine or unexpectedly thereafter. Cocaine-related deaths are often a result of cardiac arrest or seizures followed by respiratory arrest.
Long-Term Effects of Cocaine Use:
Cocaine is a powerfully addictive drug. Thus, an individual may have difficulty predicting or controlling the extent to which he or she will continue to want or use the drug. Cocaine’s stimulant and addictive effects are thought to be primarily a result of its ability to inhibit the reabsorption of dopamine by nerve cells. Dopamine is released as part of the brain’s reward system, and is either directly or indirectly involved in the addictive properties of every major drug of abuse.
An appreciable tolerance to cocaine’s high may develop, with many addicts reporting that they seek but fail to achieve as much pleasure as they did from their first experience. Some users will frequently increase their doses to intensify and prolong the euphoric effects. While tolerance to the high can occur, users can also become more sensitive (sensitization) to cocaine’s anesthetic and convulsant effects, without increasing the dose taken. This increased sensitivity may explain some deaths occurring after apparently low doses of cocaine.
Use of cocaine in a binge, during which the drug is taken repeatedly and at increasingly high doses, leads to a state of increasing irritability, restlessness, and paranoia. This may result in a full-blown paranoid psychosis, in which the individual loses touch with reality and experiences auditory hallucinations.
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The pharmacodynamics of cocaine involve the complex relationships of neurotransmitters, including Dopamine, Serotonin, and Glutamate, among others. The most extensively studied effect of cocaine on the central nervous system is the blockade of the dopamine transporter (DAT) protein. Dopamine transmitter released during neural signaling is normally recycled via the transporter; i.e., the transporter binds the transmitter and pumps it out of the synaptic cleft back into the presynaptic neuron, where it is taken up into storage vesicles. Cocaine binds tightly at the dopamine transporter forming a complex that blocks the transporter's function. The dopamine transporter can no longer perform its reuptake function, and thus dopamine accumulates in the synaptic cleft. This results in an enhanced and prolonged postsynaptic effect of dopaminergic signaling at dopamine receptors on the receiving neuron. Prolonged exposure to cocaine, as occurs with habitual use, leads to homeostatic dysregulation of normal (i.e. without cocaine) dopaminergic signaling via down-regulation of dopamine receptors and enhanced signal transduction. The decreased dopaminergic signaling after chronic cocaine use may contribute to depressive mood disorders and sensitize this important brain reward circuit to the reinforcing effects of cocaine (e.g. enhanced dopaminergic signaling only when cocaine is self-administered). This sensitization contributes to the intractable nature of addiction and relapse.
Cocaine's effects on serotonin (5-hydroxytryptamine, 5-HT) show across multiple serotonin receptors, and is shown to inhibit the re-uptake of 5-HT3 specifically as an important contributor to the effects of cocaine. The overabundance of 5-HT3 receptors in cocaine conditioned rats display this trait, however the exact effect of 5-HT3 in this process is unclear. The 5-HT2 receptor (particularly the subtypes 5-HT2AR, 5-HT2BR and 5-HT2CR) show influence in the evocation of hyperactivity displayed in cocaine use.
Sigma receptors are effected by cocaine, as cocaine functions as a sigma ligand agonist. Further specific receptors it has been demonstrated to function on are NMDA, the D1 dopamine receptor, and the The 5th subtype of the Metabotropic Glutamate Receptor (MGluR5). MGluR5 is an essential factor in cocaine self-administration and locomotor effects. The reinforcing properties of cocaine are absent in mice that lack MGluR5 and an MGluR5 antagonist dose dependently decreased cocaine self-administration.
Cocaine also blocks sodium channels, thereby interfering with the propagation of action potentials; thus, like novocaine, it acts as a local anesthetic. In addition to this, cocaine has some target binding to the site of the Kappa-opioid receptor and it inhibits monoamine uptake in rats with ratios of about: serotonin:dopamine = 2:3, serotonin:norepinephrine = 2:5.
Cocaine's addictive properties stem partially from its Dopamine Transporter (DAT) blocking effects. In particular, by increasing the dopaminergic transmission from ventral tegmental area neurons. However, a study has shown that mice with no dopamine transporters still exhibit the rewarding effects of cocaine administration. Later work demonstrated that a combined DAT/Serotonin Transporter (SERT) knockout eliminated the rewarding effects. Glutamate also plays a role in cocaine addiction, specifically the 5th subtype of the Metabotropic Glutamate Receptor (MGluR5).
The rewarding effects of cocaine are influenced by circadian rhythms, possibly by involving a set of genes termed "clock genes". Beyond this, there is a correlation between a variant of the CAMK4 gene and cocaine addiction; a German study found that addicts were 25% more likely to have a variant of the gene than people who did not use cocaine.
It is important to note that chronic cocaine addiction is not solely due to cocaine reward. Chronic repeated use is needed to produce cocaine-induced changes in brain reward centers and consequent chronic dysphoria. Dysphoria magnifies craving for cocaine because cocaine reward rapidly, albeit transiently, improves mood. This contributes to continued use and a self-perpetuating, worsening condition, since those addicted usually cannot appreciate that long-term effects are opposite those occurring immediately after use.
Cocaine addiction can be treated with a cocaine drug rehab which is important to counter the cocaine effects and lead addicts to recover from addiction to coke.
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History of Cocaine Use in the United States
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