Drug Use and Neurotransmitters This is Your Brain on Drugs - Research Paper Example

Cocaine Use and Neurotransmitters Cocaine is identified as one of the moist addictive drugs used by humans and acts through the inhibition of neurotransmitter uptake, including serotonin, norepinephrine, and dopamine. By binding to the receptors involved in reuptake of these neurotransmitters, cocaine prevents them from being reabsorbed, leading to neurotransmitter accumulation in the synapse (Wolf 36). This results in the amplification of normal dopamine effects on the post-synaptic neuron. In turn, the modification of this group of neurons leads to more dependency as a result of excess dopamine, more energy due to excessive norepinephrine, and increased confidence as a result of excess serotonin.

Moreover, since the axons of neurons involved in norepinephrine release and reuptake in the coeruleus project into all major forebrain structures, the overall effect of cocaine is very powerful. In chronic users of cocaine, the brain becomes increasingly reliant on cocaine for the maintenance of these artificially elevated levels of serotonin, dopamine, and norepinephrine, especially those that are involved in the brain’s reward circuit. Indeed, the post-synaptic membrane could manufacture new receptors for cocaine in order to maintain high levels of neurotransmitters, leading to increased sensitivity to the drug that produces cravings and depression (Wolf 36).

The use of cocaine and its effect on neurotransmitter reuptake has a direct association with cognitive deficits, including visual memory loss. High doses of cocaine in the brains of young person’s leads to a decline in their ability to form working memories as they approach adulthood, which might indicate that cocaine damages the ability of the brain to learn during new experiences (Riezzo 5632). Moreover, the inhibitory effect of cocaine on neurons located in the amygdale, which has a high concentration of dopamine and serotonin receptors, decreases the functioning of implicit and emotional learning that form part of the emotional memory.

The high concentration of the same receptors in the hippocampus also portend negative effects for the use of cocaine on the consolidation of declarative memories, as well as the transfer of these memories to other parts of the brain on order for them to stored as long term memory. The consolidation theory, which states that permanent storage of memory is the result of physical processes that alter neurons, lends credence to the notion that physical alteration of neurotransmitter receptors in the brain regions responsible for memory formation, storage, and retrieval affects the ability of short and long term memory to function effectively (Riezzo 5632).

When the individual stops using cocaine, the amount of dopamine in the synapses declines, specifically because the brain has become dependent on cocaine to regulate the amount of neurotransmitter in the synapses (Ferris 1712). As a result, the person begins to experience feelings of fatigue, depression, and low mood, also known as withdrawal symptoms. Brain abnormalities related to neurotransmitter regulation may persist long after the individual stops using the drug, which causes carvings and feelings of discomfort as the brain still needs cocaine to regulate its neurotransmitter receptor activity.

Some of the short term consequences of cocaine use include over-confidence, depression, excessive energy for short busts, paranoia, violence, psychosis, delusions, and dependency. Long term consequences include neurological incidents like seizures and strokes due to the physical alteration of neurotransmitter pathways. Cocaine is highly addictive and these addictive properties are closely related to its impact on the reward circuit neurons. By artificially increasing dopamine release and inhibiting its reuptake, the cocaine user builds tolerance to the drug and requires higher doses to achieve their high (Ferris 1712).

Works CitedFerris, Mark J. "Cocaine self-administration produces pharmacodynamic tolerance: differential effects on the potency of dopamine transporter blockers, releasers, and methylphenidate." Neuropsychopharmacology 37.7 (2012): 1708-1716. Retrieved from: http://www.nature.com/npp/journal/v37/n7/full/npp201217a.html Riezzo, I. "Side effects of cocaine abuse: multiorgan toxicity and pathological consequences." Current medicinal chemistry 19.33 (2012): 5624-5646. Retrieved from: http://www.ingentaconnect.

com/content/ben/cmc/2012/00000019/00000033/art00007 Wolf, Marina E. "Neuroscience: behavioural effects of cocaine reversed." Nature 481.7379 (2012): 36-37. Retrieved from: http://www.nature.com/nature/journal/v481/n7379/abs/481036a.html