Author: Gary Jackson

The Neurobiology of Cocaine Addiction PMC

Cocaine is a naturally occurring alkaloid that can be extracted from its botanical source and formulated into cocaine hydrochloride or ‘crack cocaine’. Cocaine induces its main psychoactive effects by impeding monoamine reuptake. The drug impacts several organs, such as the heart; brain; liver; kidneys; lungs; and has complex underlying mechanisms of toxicity that are herein described. The literature reports on numerous mechanisms to explain the toxicity of cocaine at the cardiovascular level. Firstly, by interfering with the reuptake of catecholamines and indirectly acting over α- and β-adrenergic receptors, cocaine can induce vasoconstriction of the coronary arteries and markedly increases oxygen demands by speeding up the heart rate and stimulating contractility of the heart. Moreover, the induced increase of endothelin-1 (a vasoconstrictor) and reduction in the production of nitric oxide (a vasodilator) creates an imbalance that favours vasoconstriction [96].

When the mixture is heated, it makes a crackling sound, hence the name. Crack producers make crack with baking soda (sodium bicarbonate) or ammonia and water, and it is heated to remove the hydrochloride. Crack is the street name for a type of cocaine that has had the hydrochloride removed, making it possible to smoke. Diluting the cocaine enables the seller to make more profit by “stretching” the amount of pure cocaine they have to sell. When Coca-Cola was first produced, it contained 9 milligrams of cocaine per glass.

Experimental Results With ΔFosB

You may develop depression, unpredictable mood changes, paranoia, or even violent behaviors toward yourself and others. You could have hallucinations, meaning you see or hear things that aren’t there. The 2021 survey found no differences in rates of cocaine use among different ethnic and racial groups in the U.S.

In summary, in this review, we have highlighted many challenges that exist in the field of CUD therapeutics, outlined evidence-based treatments, and underscored promising novel therapies.
One of the most employed methods of detection for cocaine are immunoassays, a fast method that allows a qualitative presumptive assessment of the drug in the biological matrix tested (e.g., blood, urine).
However, instead of leaving the cell that produces it and stimulating neighboring cells as dopamine does, ΔFosB remains in its original cell and stimulates certain genes.
Cocaine, also known as coke, is a powerful stimulant derived from the coca plant.
One of the genes stimulated by ΔFosB is an enzyme, cyclin-dependent kinase-5 (CDK5), which promotes nerve cell growth.
And they will try to determine the degree of your dependence and will suggest treatment options.

The results of these studies have been the subject of several excellent systematic reviews and meta-analyses.16–19 In this review article, we provide a clinically relevant overview of the current literature on CUD. We first summarize the clinical epidemiology of CUD and then follow with an overview of the neurobehavioral consequences of short- and long-term cocaine use. We then summarize the current pharmacological and behavioral treatment approaches for CUD, and discuss emerging treatment approaches.

How is cocaine addiction treated?

Cocaine is one of the most consumed stimulants throughout the world, as official sources report. It is a naturally occurring sympathomimetic tropane alkaloid derived from the leaves of Erythroxylon coca, which has been used by South American locals for millennia. Cocaine can usually be found in two forms, cocaine hydrochloride, a white powder, or ‘crack’ cocaine, the free base. While the first is commonly administered by insufflation (‘snorting’) or intravenously, the second is adapted for inhalation (smoking). Cocaine can exert local anaesthetic action by inhibiting voltage-gated sodium channels, thus halting electrical impulse propagation; cocaine also impacts neurotransmission by hindering monoamine reuptake, particularly dopamine, from the synaptic cleft. The excess of available dopamine for postsynaptic activation mediates the pleasurable effects reported by users and contributes to the addictive potential and toxic effects of the drug.