Cocaine is a psychoactive alkaloid of the coca plant; it was originally used for local surgeries as an anaesthetic but has now become a recreational drug. Unlike amphetamines, which resemble the structural formula of dopamine and noradrenaline, cocaine has a similar structure to other synthetic sedatives. Cocaine is well absorbed when administered via the mucous membranes, the GI tract and IV route. Peak concentration happens within five minutes after intravenous injection, while the peak levels from smoking are usually reached within 60 minutes. Some cocaine is excreted in urine unchanged, the majority is metabolized into benzoylecgonine, ecgonine methyl ester, norcocaine and other metabolites. Although cocaine has a short half-life, the elimination half-life of the metabolites lasts longer. Studies also show that the half-life of cocaine may increase the longer it is used.
Cocaine acts by enhancing the action of dopamine, it does this by blocking its reuptake into the nerve terminal via the transporter and thus increasing the amount of dopamine available. Dopamine is a neurotransmitter that helps control the brain’s reward and pleasure centres. Dopamine also helps regulate movement and emotional responses. It is a neurotransmitter that projects in many areas of the brain. Physiologically dopamine is involved in many essential functions, these include; cognition, movement and reward. Disruption in the dopaminergic system has been shown to lead to a wide range of symptoms. For example, Parkinson’s disease like symptoms can appear, such as tremors. These symptoms are marked by a change in cognitive function and mood. Studies show that people with low dopamine may be more prone to addiction. The presence of specific dopamine receptors is also associated with sensation seeking people (Verma, 2015).
Cocaine, like other drugs has a euphoric and sustained mood elevation effect on the individuals taking them. This is because cocaine produces its psychoactive and addictive effects on the limbic system. The limbic system is a series of interconnected system in the brain that regulates pleasure and motivation. An initial short-term effect of taking the drug is euphoria caused by the build-up of dopamine, this causes the desire to take the drug again. The more dopamine molecules meet the receptors the more the electrical properties of the receiving cells are altered. To keep the cells in each region of the brain functioning at appropriate intensities, neither too high or low, the dopaminergic cells continually increase and decrease the number of molecules they produce. They further regulate the amount of dopamine by pulling some previously released dopamine into themselves.
Cocaine interferes with this control mechanism, by tying the transporter molecule that dopaminergic cells use to retrieve dopamine from the surrounding cells. As a result of this, the dopamine that would otherwise be picked up remains in action (Nestler, 2005). (About Glutamate Toxicity, 2011) found that changes involving genes occur in the limbic system, which is the main site for cocaine effects. The effects are enormous and long lasting and contribute significantly to the transition from drug abuse to addiction. Studies indicate that cocaine affects the expressions of several genes in the brain, including some that influence the important neurotransmitter glutamate and the body’s natural opioid like compounds (Nestler, 2005). Glutamate is a powerful neurotransmitter that is responsible for sending signals between nerve cells. Under normal condition it plays an essential role in learning and memory.
Cocaine increases energy, self-confidence, promotes talkativeness, alleviates fatigue and enhances mental alertness. At high doses and during chronic use, feelings of euphoria may be replaced with restlessness, excitability, sleeplessness, loss of libido, nervousness, aggression, suspicion and paranoia, hallucinations, delusional thoughts, and large dilated pupils. Chronic cocaine use may lead to a range of cardiac complications. For example, acute myocardial infarction and myocardial ischemia are common. Cocaine blocks the sodium/potassium channels, which induces abnormal depressed cardiovascular profiles. Use of cocaine together with alcohol increases cocaine levels in the blood. Cocaine stimulates the adrenergic system by binding to norepinephrine transporters. This results in an increased effects of norepinephrine effects on post synaptic receptor sites. Blocking norepinephrine reuptake induces tachycardia and hypertension. Other studies indicate that the perpetual use of cocaine is associated with an increase of CV complications such as hypertension and coronary spasms. Heart attack in constant cocaine use is thought to be caused by increased oxygen demand, vasoconstriction of the coronary artery, increased platelet aggregation and thrombus formation. Also, potential arrhythmias and dysrhythmias may occur (Kim & Park, 2019).
Other long-term complications include accelerated atherosclerosis, cardiomyocyte apoptosis, sympathoadrenal-induced myocyte damage, chronic arrhythmias, cardiac hypertrophy and dilated cardiomyopathy. Regular cocaine use has also been associated with many abnormalities in the vascular system of the brain, the most common are, haemorrhagic and thromboembolic strokes. Some people are more vulnerable to cocaine-induced excited delirium, symptoms include hyperthermia, extreme behavioral agitation and in some cases, violent behaviours. This may result in collapse or sudden cardiac death (Roberts, 2007).
Illicit use of drugs In Australia
• In 2016, around 3.1 million Australians reported using an illegal drug.
• In 2016, the most common illegal drug was cannabis, followed by misuse of pharmaceuticals, cocaine, and then ecstasy.
• While overall use of methamphetamine has decreased, use of crystal methamphetamine (ice) continues to be a problem.
• People who are using crystal methamphetamine (ice), are using it more frequently which increases the risks and harms.
Elsevier. (2018, May 31). Cocaine use alters gene expression in brain reward circuits: Study investigates transcriptome-wide alterations in response to cocaine self-administration in mice. ScienceDaily. Retrieved June 20, 2018 from http://www.sciencedaily.com/releases/2018/05/180531102706.htm
Winhusen, T. M., Lewis, D. F., Somoza, E. C., & Horn, P. (2014). Pharmacodynamics Must Inform Statistics: An Example from a Cocaine Dependence Pharmacotherapy Trial. ISRN Addiction, 2014.
About Glutamate Toxicity. (2011, June 26). HOPES Huntington’s Disease Information. https://hopes.stanford.edu/about-glutamate-toxicity/
Kim, S. T., & Park, T. (2019). Acute and Chronic Effects of Cocaine on Cardiovascular Health. International Journal of Molecular Sciences, 20(3). https://doi.org/10.3390/ijms20030584
Nestler, E. J. (2005). The Neurobiology of Cocaine Addiction. Science & Practice Perspectives, 3(1), 4–10.
Roberts, J. R. (2007). Acute Agitated Delirium from Cocaine: A Medical Emergency. Emergency Medicine News, 29(10), 18–20. https://doi.org/10.1097/01.EEM.0000296568.05338.c5
Verma, V. (2015). Classic Studies on the Interaction of Cocaine and the Dopamine Transporter. Clinical Psychopharmacology and Neuroscience, 13(3), 227–238. https://doi.org/10.9758/cpn.2015.13.3.227