Stimulant drugs increase alertness and energy through activation of the central nervous system (Spine Universe). Some results of stimulant drug use ingestion include increased blood pressure, heart rate, respiration, and attention (Spine Universe). Drugs impact the body through neural transmission, or communication of neurons in the brain (National Institute on Drug Abuse). Stimulant drugs are classified as agonists. Agonist drug mechanism involves higher presynaptic neurotransmitter release or inhibited neurotransmitter removal within a synapse. Higher neurotransmitter numbers within a synapse lead to more bindings on the postsynaptic cell, resulting in specific drug effects on the body (National Institute on Drug Abuse).
Stimulant drugs such as cocaine and amphetamines provide the user a “euphoric” experience. High levels of dopamine are released as a result. Dopamine is a neurotransmitter involved in pleasurable and salient experiences, such as good food, laughter, or sex. The brain is wired to seek dopamine release. Dopamine release after drug use is higher than after natural experiences, wiring the brain to seek the experience again. When an individual is addicted to a stimulant drug, the initial state of euphoria fades. The drug addicted individual seeks out the heightened dopamine release from drug use over natural dopamine release experiences. (National Institute on Drug Abuse)
The “reward pathway” in the brain is heavily associated with motivated behavior and is involved in addiction of all kinds. The reward pathway lies within the limbic system, beginning at the ventral tegmental area in the midbrain and extending to the nucleus accumbens. Dopamine is the most common neurotransmitter released within the reward pathway. Activation of the reward pathway is essential to reinforcement because of the dopamine response to new or pleasurable activities. Through dopamine release and connection to emotion through the limbic system, the brain is driven to experience the same pleasure again. While stimulant drugs act on many other brain systems and neurotransmitters, dopamine and the reward pathway are certainly a component of addiction. (Powledge, 1999)
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While addiction is a risk in all drug use, a clear neural distinction lies within recreational and dependent drug users. Stimulant dependent individuals exhibit decreased impulse control and orbitofrontal cortex gray matter volume, a possible predisposition to addiction. Drug craving is associated with the orbitofrontal cortex and inhibitory control. Studying attentional bias to cocaine-related cues elicits activation of these brain areas and allows for comparison between neural structures of recreational and dependent cocaine users.
Participants included 50 stimulant-dependent individuals, 27 recreational cocaine users, and 52 healthy, non-drug users. The stimulant dependent individuals met DSM-IV criteria for stimulant dependence. Recreational users had been using cocaine for a minimum of 2 years without displaying any dependent characteristics. As brain structure similarities have been found even in drug abstinent biological family members with stimulant addicted members, the control group did not include participants with a history of familial drug use.
The Stroop task incorporating vocabulary in relation to cocaine during fMRI screening was used to evaluate attentional bias and orbitofrontal brain region activation. Stimulant dependent individuals displayed attentional bias to cocaine-cues shown by a greater number of errors and increased response times within the task. Both recreational users and drug abstinent individuals did not show attentional bias with cocaine-cues during the Stroop task.
Compared to controls, fMRI imaging displayed a significant decrease in activity in the right inferior frontal gyrus and right orbitofrontal cortex in recreational users. However, fMRI imaging displayed an increase in activity in the right inferior frontal gyrus for stimulant-dependent users. The inferior frontal gyrus is associated with cognitive control and inhibition. Differing activation levels in the right inferior frontal gyrus and right orbitofrontal cortex may be due to salience of cocaine-cue words and effort required to look beyond the words.
Enlarged orbitofrontal cortex in recreational users may cause less cortical activity during the Stroop task performance, as it employs cognitive processing in the frontal lobe. Enlarged orbitofrontal cortex could also be serving as a protective factor against development of dependence for recreational users. Decision-making is also associated with the orbitofrontal cortex. Stimulant dependent drug users show dysfunction in decision making due to abnormalities in the orbitofrontal region, leading to compulsivity towards drug use. Overall, predisposing brain abnormalities for stimulant use and orbitofrontal cortex volume contributes to recreational versus dependent drug use. (Smith, D. G., Simon Jones, P., Bullmore, E. T., Robbins, T. W., & Ersche, K. D. 2014).
Compulsivity and impulsivity are key components in drug dependence. Striatal-cortical neural connections are critical for reward, decision-making, motivation, and habit learning. Striatal-cortical neural network abnormalities are observed in cocaine-addicted individuals.
Increased understanding of striatal circuits and their relation to drug dependence may ultimately inform treatment. 56 cocaine dependent individuals and 56 healthy, drug abstinent individuals were included in this study. fMRI imaging displayed striatal circuit function. Impulsivity was measured using the BIS-11.
Altered striatal-cortical connections were observed in cocaine dependent users compared to controls. Cocaine dependent individuals exhibited decreased striatal-cingulate, striatal-insula, and striatal-striatum connectivity strength and increased striatal-frontal connectivity strength compared to controls. Cocaine dependent individuals displayed a decreased resting state functional connectivity (rsFC) between the ventral striatum inferior area, dorsal anterior cingulate cortex, and the superior temporal gyrus. However, the cocaine using group displayed increased rsFC between the dorsal striatum and dorsal lateral prefrontal cortex. In regard to the putamen, cocaine-users displayed decreased connectivity in the dorsal striatum, cingulate, and insula.
Compulsivity of drug use was positively predicted by the connectivity strength difference between both the right ventral striatum and left anterior prefrontal cortex/orbitofrontal cortex, and between the right ventral striatum inferior and dorsal anterior cingulate cortex. Elevated striatal and dorsal lateral prefrontal cortex connectivity strength was positively correlated with recent cocaine use and BIS-11 scores. Furthermore, a positive correlation between rsFC and loss of control was observed. Increased impulsivity in cocaine dependent users compared to healthy controls was consistent with other studies. (Salmeron, B. J., Hu, Y., Gu, H., Yang, Y., & Elliot, S. 2015).
The reward pathway and dopamine reinforcement lies at the center of stimulant drug addiction, however, there are many neural factors predisposing and sustaining drug addiction. Orbitofrontal cortex volume impacts inhibitory control and decision making, contributing to the compulsivity factor of drug addiction (Smith et al., 2014). Connectivity strength and resting activity between the striatum and cortical regions of the brain varies between cocaine dependent individuals and drug abstinent individuals (Salmeron et al., 2015)
Various neurologically based findings on stimulant drug addiction all point to the structural differences in the brain related to addiction. Drug addiction is considered a chronic disorder due to the structural differences in the brain and elevated dopamine thresholds. Recovery from addiction is complex relapse is not surprising considering the various neurological differences in an addicted person.
Going into this paper, I thought I was going to write about the reward pathway and dopamine reinforcement in drug abuse. Although very challenging, I am thrilled that I have learned about the various neurological aspects of stimulant drug addiction. I enjoyed learning about predisposition to stimulant drug use. Predisposition does not lead to drug addiction by any means, but it is important to understand that neurological structure and functioning is genetically altered by familial stimulant drug abuse. I also have a better understanding of the complexity in treatment of stimulant addiction. Research on this topic was particularly challenging, as many articles were reviews, or part of a single line of research. Lay articles were focused on dopamine and reward, while current research articles have surpassed that finding and are focused on further neurologic correlates to drug abuse.
