The Impact of Drug Abuse on Brain Function

Drug use and abuse have profound effects on the human brain, with long-term consequences that can be both physically and mentally debilitating. Control organs of the body, such as the brain that is responsible for cognitive, emotional, and motor function is also common targets of toxic substances. Some drugs, when taken over a period of time, have a toxic effect on the cells in the brain that are responsible for thought processes and basic personality structures. It has been established that substances like cocaine and methamphetamine affect the body’s normal chemistry and also stimulate dangerous changes to the basic structure of the brain, most of which cannot be undone.

This paper will scrutinize the impact of drug use on the brain, with particular emphasis on methamphetamine and cocaine. These two drugs show the strong neurological side of long-term usage and result in problems like memory impairments, lack of brain coordination, and neurological diseases.

Overview of the Brain’s Structure and Reward System

The human brain is one of the most complex structures in human beings, and it has different parts that control behavior, thinking, feeling, and body functions. Drug addiction lies in the brain reward system, which is a set of structures in the brain whose primary reward circuitry plays a crucial role in strengthening behavior through the release of happy chemicals, mainly dopamine. As parts of this incentive system, one includes the parts of the brain such as the frontal-limbic circuit that includes the prefrontal cortex, amygdala, and the nucleus accumbens required for decision-making, emotional regulation, and motivation (Baik, 2020).

In normal physiological circumstances, dopamine releases are controlled in reaction to important stimuli, such as eating and social interaction. Upon its release, dopamine unites with targeted receptors in the brain to create pleasurable sensations that enhance the potential for repeating those behaviors. The release of dopamine is tightly regulated, and excess dopamine is reabsorbed into neurons through dopamine transporters, maintaining a delicate balance.

However, this normally self-regulating process becomes disrupted when stimulations, including cocaine/methamphetamine, are taken. For instance, cocaine comes under drugs that work by inhibiting the dopamine transporters, thus permitting an increased quantity of dopamine to remain in the synaptic cleft for normal reabsorption. This flooding of dopamine triggers a more intense feeling of pleasure but has repercussions on the brain, including neuroadaptation to receptors, which makes it dormant for dopamine receptors. And just like Methamphetamine, even though both increase dopamine in the brain, methamphetamine also works through a similar mechanism in that it triggers the release of this neurotransmitter and also limits the reuptake of dopamine, meaning more dopamine accumulates in the brain.

Therefore, when applied continuously, these drugs alter the equilibrium of the brain and render it less efficient in regulating dopamine without the intervention of the aforestated drugs. This leads to tolerance, whereby the brain requires more quantities of the drug in order to provide the desired effects, which more often ends up destroying the neurons, particularly those in the dopamine reward system. Over time, it weakens the structure of the brain cells and thus results in poor intelligence and increased vulnerability to mental disease.

Cocaine and Its Mechanism of Action

Cocaine is a potent stimulant that directly affects the central nervous system (CNS), primarily by interfering with the normal function of neurotransmitters. Medically, cocaine exerts its effects by targeting the brain’s mesolimbic reward system, particularly the pathways that involve dopamine, a neurotransmitter responsible for regulating pleasure, motivation, and reward.

The exact mechanism that cocaine imposes on the body is the inhibition of the reuptake of dopamine neurotransmitters at the synaptic gap. Normally, when dopamine is released in a synapse, it binds to dopamine receptors in the next neuron and transmits a signal. The dopamine that remains in the synaptic cleft is removed via dopamine transporters present in the presynaptic neuron. Cocaine acts to block these dopamine transporters and, therefore, does not permit the reuse of dopamine. This has an effect on increasing dopamine amounts in the synaptic cleft that has a seductive impact on stimulating dopamine receptors too much. This process results in intense and rapid euphoria, increased energy, and heightened alertness.

Cocaine’s impact extends beyond dopamine. It also affects other neurotransmitter systems, including serotonin and norepinephrine, both of which play roles in mood regulation and stress responses. Chronic cocaine use leads to significant disruptions in these systems, contributing to emotional instability, anxiety, and depressive symptoms. This drug alters the typical structure and functioning of the brain, occasioning long-term effects on the neurotransmission process. It decreases brain size, especially in regions like the prefrontal cortex and amygdala, which have to do with decision-making ability, control, and emotion, respectively. Researchers employing MRI-related techniques have stated that long-term cocaine use has ‘neurotoxic’ effects that do cause ‘Grey matter loss,’ leading to ‘Cognitive’ changes. Further, the study showed that neuroinflammation, as induced by cocaine, leads to neuronal degeneration and, ultimately, the death of brain neurons.

Long-Term Effects of Cocaine on Brain Function and Behavior

The long-term use of cocaine leads to profound and often irreversible changes in brain function and behavior. Chronic exposure to the drug causes persistent alterations in the brain’s reward circuitry, resulting in significant cognitive, emotional, and behavioral impairments. Over time, these changes make it increasingly difficult for users to experience pleasure from natural stimuli, contributing to the compulsive drug-seeking behavior characteristic of addiction.

Among the adverse effects of cocaine are behavioral, cognitive, and neurocognitive change, most especially errands of executive control, memory, and decision. The dopaminergic neurons in the prefrontal cortex, the brain’s executive center for the impulse to attend and decide, might degenerate from cocaine use. Recent fMRI analysis of the brain revealed that maturing users of cocaine had considerably low activity in the prefrontal cortex, which is caused by less serotonin neurotransmitter production, thus being unable to reason and control themselves (Liśkiewicz et al., 2019).

Additionally, cocaine impacts the hippocampus, a part of the brain useful for memory. This area might undergo structural alterations resulting from neuroinflammation and oxidative stress, which result from cocaine, and it becomes difficult to memorize what was not learned before. These cognitive impairments can, however, persist even if the individual has stopped taking this substance for some time, implying that the affected nerve cells could be permanently damaged.

Behaviorally, long-term cocaine users often experience increased irritability, paranoia, and anxiety. The effect of overstimulation of dopamine receptors and consequent depletion of dopamine seen with drug use results in mood swings and increases susceptibility to mood disorders. Repeated activation of the brain’s reward center can result in the development of tolerance—a condition in which the individual requires progressively larger doses of the substance, used with increasing frequency, to achieve the same effect. This fosters a cycle of addiction, where the individual becomes both physically and emotionally dependent on cocaine to carry out daily activities.

Long-term cocaine use is also associated with an increased risk of developing psychosis. Cocaine-induced psychosis is characterized by hallucinations, delusions, and paranoia, often resembling symptoms of schizophrenia. This condition is thought to arise from the drug’s effect on both dopamine and serotonin pathways, which regulate mood and perception.

Methamphetamine and Its Mechanism of Action

Methamphetamine is a powerful stimulant that causes extensive damage to the brain through its dual action of increasing dopamine release and inhibiting dopamine reuptake. Medically, methamphetamine targets the vesicular monoamine transporter-2 (VMAT2), a protein responsible for packaging dopamine into vesicles within the presynaptic neuron. By disrupting VMAT2, methamphetamine forces dopamine out of storage and into the synaptic cleft, leading to an abnormally high release of dopamine.

Methamphetamine not only causes the over-release of dopamine but also inhibits dopamine reuptake through the inactivation of DAT and allows for the continued stimulation of dopamine receptors. This kind of stimulation enhances highly pleasurable feelings and, at the same time, results in neurotoxic effects. The sudden release and subsequent dissipation of dopamine produce reactive oxygen species (ROS) that lead to oxidative stress (National Institute on Drug Abuse, 2019). Oxidative stress impacts the neuronal membrane, mitochondria, and DNA with the subsequent demise of dopaminergic and serotoninergic neurons.

Neuropsychological consequences of methamphetamine dependence include neuronal disturbances in the various zones of the brain, such as the prefrontal cortex, hippocampus, and striatum. MRI reveals subcortical abnormalities, particularly the reduction in the volume of gray matter that is critical for memory, decision-making, and impulse control. In addition, the substance affects the glutamate system, which is directly related to the control of the plasticity of the connections between the brain cells and boasts a negative long-term impact on cognition. methamphetamine has neurotoxic effects and has been found to cause extensive and irreparable harm to the brain even after the withdrawal of the drug.

Long-Term Effects of Methamphetamine on Brain Cells and Cognitive Function

Long-term methamphetamine use results in severe and often irreversible damage to brain cells, primarily due to its neurotoxic effects. methamphetamine’s ability to induce an excessive release of dopamine not only overstimulates dopamine receptors but also causes significant oxidative stress, leading to the destruction of dopamine and serotonin-producing neurons. This destruction contributes to profound cognitive and psychological impairments in chronic users.

The areas of the brain most susceptible to the poisonous consequences of methamphetamine are the frontal regions, particularly the prefrontal cortex, responsible for decision-making, impulse control, and emotion regulation. Another technique used to show that methamphetamine users have lesser gray matter is PET scans, proving that the prefrontal cortex of such individuals lacks the capacity to control the impulse to make good decisions (Liśkiewicz et al., 2019). This creates structural changes that lead to enhanced aggression and the wrong decision-making when it comes to substance-looking-for behavior.

Besides, regarding methamphetamine consumption, neurotoxicity affects the hippocampus; this is a part of the brain that controls the learning process and memory. The general effects of long-term methamphetamine use are a deficit in short-term memory as well as long-term memory and also a deficit in general cognitive flexibility. The side effects may be loss of memory, learning problems, and attention deficit disorder, which may persist even when a user has stopped using the drug.

Methamphetamine also affects the basal ganglia; the basal ganglia are a group of structures that are involved in motor control and the processing of rewards. Injury of the basal ganglia results in motor disorder and reduced capacity to derive hedonic tone from stimuli that are normally pleasurable. This damage can remain even after a user has completely stopped using methamphetamine, an effect that permanently robs people of the capacity to derive pleasure from other aspects of life, a state diagnosed as anhedonia.

Furthermore, chronic methamphetamine use significantly increases the risk of developing psychiatric disorders. Research indicates a higher prevalence of depression, anxiety, paranoia, and psychosis among long-term users, with many exhibiting symptoms similar to schizophrenia. This is thought to be a result of both the neurodegenerative effects of methamphetamine on the brain and the dysregulation of neurotransmitters such as dopamine and serotonin.

Comparative Analysis of Cocaine and Methamphetamine’s Impact on the Brain

While both cocaine and methamphetamine are stimulants that integrate into the human brain in a similar yet different manner, cocaine mainly inhibits the reabsorption of dopamine, which leads to its buildup within the synaptic spaces. This gives brief intervals of feelings of pleasure, but with repeated administration, it causes changes in the receptor densities that ultimately cause neurological deficits and long-lasting contractions in the brain. Contrary to this, methamphetamine not only inhibits the reuptake of dopamine but also increases the release of the neurotransmitter by bringing the dopaminergic concentrations to even more toxic levels.

Despite causing considerable damage to the brain’s reward pathway, meth is worse as it usually causes widespread neuronal loss. In this connection and due to its ability to induce oxidative stress, methamphetamine results in more degradation of dopamine and serotonin neurons as compared to cocaine, which mainly affects dopamine neurons (Shrestha et al., 2022). Furthermore, with regard to the glutamate system, methamphetamine causes greater degrees of cognitive dysfunction in learning and memory.

Implications for Treatment and Recovery

The neurotoxic effects of cocaine and methamphetamine make treatment and recovery for individuals suffering from addiction particularly challenging. Both drugs cause significant structural and functional damage to the brain, particularly in areas responsible for decision-making, memory, and emotional regulation. This damage complicates the recovery process, as users not only need to overcome their physical dependence on the drug but also deal with lasting cognitive and emotional impairments.

For cocaine users, the loss of dopamine receptors and disruption of the brain’s reward system often leads to an inability to experience pleasure from natural rewards, known as anhedonia. This condition remains even after the cessation of cocaine use and increases the likelihood of relapse. Interventions to cocaine dependence mainly involve cognitive behavioral therapy to assist in changing a user’s pattern of thinking and behavior. However, medication-assisted treatments (MAT) for cocaine addiction are limited, and no drug for cocaine use disorder has been approved by the FDA (Richards and Laurin, 2020). Somatic treatments such as transcranial magnetic stimulation are under study to try and reverse the cocaine-induced changes in brain functioning in individuals with chronic cocaine dependence.

Consistently, methamphetamine users face even greater challenges in recovery due to the broader and more severe neurotoxicity associated with the drug. Dopamine and serotonin are neurotransmitters that are important to the brain’s higher functions, as well as appropriate behavior, and the reduction of these neurons leads to lower cognition, mood regulation, and impulse inhibition, which means that users struggle to refrain from having another fix (Yasaei and Saadabadi, 2023). However, since methamphetamine leads to the degeneration of the brain in all the users, recovery is normally difficult and partial; hence, many users normally have permanent impairment in the areas of memory, decision-making, and emotional well-being. The most frequently applied behavioral approaches are CBT and contingency management (CM), although the outcomes are not consistent, and rates of relapse are high.

Conclusion

In summary, cocaine and methamphetamine present profound consequences when the substance is abused for an elongated period, which is enhanced reduction in cognitive factors and neuron loss of dopamine and serotonin. Cocaine particularly affects the reuptake of dopamine, and methamphetamine releases even more dopamine but also promotes higher neurotoxicity. Chemical consequences are difficulties in such domains as memory and decision-making, as well as the ability to control personal emotions, which makes the treatment process very difficult. Alas, even if the application of CBT or new methods like transcranial magnetic stimulation is provided, the possibility of effectively tackling the addiction is rather low due to the highly toxic effect that these drugs cause in the human brain. All of these impacts have to be addressed in order to improve the therapeutic and prophylactic methods.

References

Baik, J.-H. (2020). Stress and the Dopaminergic Reward System. Experimental & Molecular Medicine, 52(12), 1879–1890. https://doi.org/10.1038/s12276-020-00532-4

Liśkiewicz, A., Przybyła, M., Park, M., Liśkiewicz, D., Nowacka-Chmielewska, M., Małecki, A., Barski, J., Lewin-Kowalik, J., & Toborek, M. (2019). Methamphetamine-associated cognitive decline is attenuated by neutralizing IL-1 signaling. Brain, Behavior, and Immunity, 80(79), 247–254. https://doi.org/10.1016/j.bbi.2019.03.016

National Institute on Drug Abuse. (2019, October). How is Methamphetamine different from other stimulants, such as cocaine? National Institute on Drug Abuse. https://nida.nih.gov/publications/research-reports/methamphetamine/how-methamphetamine-different-other-stimulants-such-cocaine

Richards, J. R., & Laurin, E. G. (2020). Cocaine. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK430769/

Shrestha, P., Katila, N., Lee, S., Seo, J. H., Jeong, J.-H., & Yook, S. (2022). Methamphetamine-induced neurotoxic diseases, molecular mechanism, and current treatment strategies. Biomedicine & Pharmacotherapy, 154(56), 113591. https://doi.org/10.1016/j.biopha.2022.113591

Yasaei, R., & Saadabadi, A. (2023, May 1). Methamphetamine. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK535356/

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• ➢ Critique or defend the concept of “we live and always will live in a society of drug use and abuse.” Discuss factors related to this statement and costs involved. Be sure to include aspects of historical overview of the use of drugs throughout history, biopsychosocial model of addiction, as well as medicinal use.
• ➢ Discuss the relationship between social structures, culture, and the use of substances throughout history. Be sure to include information about the use as medicinal substances, religious rituals, celebratory situations, and use instead of water.
• ➢ Research has shown that drug use affects the brain and that long term abuse of drugs can destroy brain cells. Discuss how drug use and abuse affect the brain. In explaining your rationale, please use at least 2 drugs of abuse to help demonstrate your statements. You can choose any 2 you desire.
• ➢ In reading recent research, please choose at least 4 drugs (or categories of drugs) that are the most abused in the area of the country in which you live. Please share current trends, as well as past statistics, to help your claims. Please also share at least 2 region-specific reasons why each drugs is abused more so than others based on appropriate sociological demographics in the region.
• ➢ At times, there is a fine line between “therapeutic use vs. abuse” in terms of prescription medications. In thinking about the difference, please research at least 5 evidence-based means of assessing whether medication(s), taken as prescribed or not, are being abused. It is also important to mention DSM-5 criteria for substance use disorders and to use peer-reviewed medical research in explaining your thoughts.