Neurobiological Workings of Cocaine Addiction

            The increasing use of drugs and manifestation of drug addiction continues to increase in the United States. Specifically, cocaine use has grown. Its ability to elevate mood and emotions and creating a feeling of power, attracts individuals. Yet, its broad effects on the brain stemming from dopamine elevation, memory impairment and decrease in decision making, sets a foundation for a highly addictive drug that deteriorates the neurobiological system. The use of cocaine on the brain, specifically the GLP-1 receptor, is explored by Mitchell Roitman in his lecture as well as in his study, Central GLP-1 Receptor Activation Modulates Cocaine-Evoked Phasic Dopamine Signaling in the Nucleus Accumbens Core. The GLP-1 receptor is seen to produce a dopamine packed signal in response to cocaine use. further able to come to the conclusion that by inhibiting a section of the GLP-1R, there would be a limited dopamine response to cocaine, therefore potentially helping someone overcome the addiction. Roitman’s study of GLP-1 and the potential effects it could have on cocaine addiction, opens a doorway to unique manners to treat cocaine addiction though neurological developments.

            By being able to observe someone’s dopamine release level, they could also determine their biological addiction to cocaine. In a study by Eric Nestler called The Neurobiology of Cocaine Addiction, he observes cocaine’s direct effects on the brain and how it is able to develop an addictive response. It is important to understand the full biological pathway of cocaine to not only determine how it works, but also how to treat it. Nestler observes that cocaine provides a response in the brain’s limbic system. The limbic system is directly correlated towards emotions and mood. He observes similarly to Roitman’s study, that cocaine use results in a spike of dopamine levels, which is the main catalyst for providing the addiction. Simultaneously, it is observed that in the limbic region, the frontal cortex is important for the decision making. Therefore, when cocaine use is administered over a long period of time, the limbic region and the frontal cortex begin to deteriorate, causing a decrease in decision making. This allows the subject to be more likely to become addicted with the deterioration of the frontal cortex because they are potentially more likely to continuing to seek cocaine use. Another region in the limbic system is observed for Nestler, observing the region that focuses on memory. He comes to the conclusion that during a period of cocaine use, this experience is elevated and recorded in the memory as intense and different. This creates a dynamic where one has a distinct memory of that intense experience. All of these separate elements of cocaine and its effect on the brain, attribute to the addiction a nor enforcement of the drug.

            Before having observed Roitman’s lecture as well as reading Nestler’s study, the effects of long-term cocaine use were apparent. I had never studied the exact details and mechanisms of what happens during cocaine use. Through both of these studies, hypotheses can be generated regarding how to treat the addictive properties. Just like majority of addictions, the subject won’t be addicted after one use. But, with increased and consistent use of cocaine, will provide reinforcement in which the body becomes accustomed to the use and expects it. Therefore, cocaine producing a response in both dopamine increase as well as effects on mood through the limbic system, compromises the neurobiological system by providing an external factor that supplements an elevated feeling and emotion. It is important to observe the effects cocaine has on the brain, in order to determine the best manner to diminish its dopamine release as well as detrimental effects to the limbic system.

Works Cited

Nestler, Eric J. “The neurobiology of cocaine addiction.” Science & practice perspectives vol. 3,1 (2005): 4-10.

Fortin, Samantha M., and Mitchell F. Roitman. “Central GLP-1 Receptor Activation Modulates Cocaine-Evoked Phasic Dopamine Signaling in the Nucleus Accumbens Core.” Physiology & Behavior, vol. 176, 2017, pp. 17–25., doi:10.1016/j.physbeh.2017.03.019.