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How Cocaine Affects The Brain/Dopamine

My STEAM project studies a few various components and key structures of the nervous system by examining dopamine levels and portraying how they can change through specific substances.

We know cocaine is a drug but what is it? This substance is one of the most frequently abused drugs and responsible for being one of the major causes for emergency hospital room visits(Renato B. Pereira et al, 2015). So what does it exactly do? Cocaine can enter the brain and bloodstream through multiple intake methods: snorting, smoking, injecting. The chemicals or toxins from the substance are working in the central nervous system by creating an influx of extra stimulation in the limbic system. The limbic system is the region in the brain which controls certain sensations such as pleasure, anger, and sadness.

Within the brain are molecules that give people the “feel-good” sensation or feelings of satisfaction. These molecules are commonly referred to as dopamine, which work as neurotransmitters or chemical messengers and are healthy for individuals in regulated amounts. In a normal functioning and sober body, these dopamine molecules are removed and transported from a space called the synaptic cleft after the molecules finish performing their function. The synaptic cleft is a gap or space region between cells in a chemical synapse where neurotransmitters diffuse(J. Gordon Betts et al, 2022). Dopamine enters free-floating into the synaptic cleft and binds to receptors of receiving cells specific to them, as if they are coded or programmed to certain ones. Once attached to their special receptors, dopamine births the stimulation effects by altering electric impulses in these cells which then changes the cells’ functions(Nestler, 2005). After completing this action, dopamine is transported outside of the cleft.

This control of entering and exiting at the appropriate time and levels also helps coordinate regulation of the molecules to avoid stimulation. Dopamine originates from a set of brain cells called dopaminergic cells which are responsible for bringing them into creation and dispersing them to where they need to be(Nestler, 2005). These cells are constantly adjusting dopamine by increasing or decreasing their levels to fit the body’s needs. Sometimes, they may pull used dopamine molecules back into the synaptic cleft and reuse them for receptors to assist in regulating stimulation.

However, toxins from cocaine are harmful because they disable these transporters from performing their necessary functions by sealing or blocking them. This then disrupts the dopaminergic cells from retrieving dopamine molecules in the first place and allowing them to reach their proper location. With nowhere to go, dopamine molecules are trapped and floating around in the cleft. The dopamine molecules overstimulate or overpower the cells and brain as a result because they are stuck rebinding to receptors repetitively. Users therefore feel a “high” or euphoria-like sensation from the drug due to this extra constant build-up of dopamine, also enabling them to not really recognize pain sensations much at the time of use.

However, cocaine’s effects are very short-lived, which essentially causes users to use it more often due to building tolerance levels quickly and longing for the “high” again. This typically leads to a harmful cycle of substance abuse and addiction. This substance not only affects the “reward” pathway but other areas of the body. Common effects are increasing heart rate, blood pressure, body temperature, respiration, and can even amplify pre-existing medical conditions(Doweiko & Evans, 2023, pp. 106-109). Control of the body’s cognition abilities and voluntary movements are also affected, often causing users to often become fidgety or unable to settle down. All in all, cocaine can have a grand impact on the nervous system.

Works Cited
Betts, J. G., Desaix, P., Johnson, E., Johnson, J. E., Korol, O., Kruse, D., Poe, B., Wise, J., Womble, M. D., & Young, K. A. (2022). Anatomy and Physiology 2e. OpenStax. https://openstax.org/details/books/anatomy-and-physiology-2e?Book%20details
Doweiko, H. E., & Evans, A. (2023). Concepts of Chemical Dependency.
Cengage Learning.
Nestler E. J. (2005). The neurobiology of cocaine addiction. Science & practice perspectives,
3(1), 4–10. https://doi.org/10.1151/spp05314
Springer Nature, Pereira, R. B., Andrade, P. B., & Valentão, P. (2015, June 24). A Comprehensive View of the Neurotoxicity Mechanisms of Cocaine and Ethanol. Neurotoxicity Research, 28, 253-267. https://doi.org/10.1007/s12640-015-9536-x

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