Honours Human Behaviour, Class of 2022, McMaster University
Drug addiction or “dependence” is typically defined by three cognitive criteria: compulsive need to take the drug, reduced control in limiting intake, and a negative affective state during withdrawal.1 The reinforcement/reward model effectively describes the neurobiological mechanisms that drive addictive behaviours. Dopaminergic pathways are central to this model, which include regions of the midbrain such as the substantia nigra, striatum, nucleus accumbens, and the ventral tegmental area.1 Drugs, such as cocaine, will prolong dopamine neurotransmitter activity by preventing its reuptake from neurons in the system. Since dopamine is associated with reward behaviours, this effect reinforces an individual’s motivation to seek out and take the drug.1 Several other drugs also activate the dopaminergic system, such as marijuana (THC), alcohol, and opiates. Additional features of the reinforcement model describe the substances’ ability to produce a negative affective state during abstinence, mediated by central and peripheral noradrenergic pathways.1,2 Activation of these coinciding reinforcement pathways are what make compulsive drug use highly potent.
The following review aims to identify different neurological processes involved in the development of drug addiction, and its relationship to adolescence. Research articles were gathered by searching PubMed and ScienceDirect databases. Various search terms were used to identify peer-reviewed papers discussing the developmental changes that occur for adolescents and increase their susceptibility to drug addiction, the neurological consequences of substance abuse, and effective treatment mechanisms.
Based on complex cognitive interactions that arise during drug use, substances operate as an alluring stimulus for many individuals. Those who are more inclined to “sensation-seeking” have an increased likelihood of using drugs.3 This term is defined by the desire to obtain novel and complex sensations, often involving physical and social risks. Adolescents have a particular proclivity to sensation-seeking behaviors, associated with increased recklessness while obtaining the intended goal.3 Adolescent development is simultaneously marked by other physiological factors such as puberty and later development of frontal brain regions.4 Neurological changes that occur across adolescence elucidate the inclination for individuals to engage in rewarding behaviours and subsequently, their increased vulnerability to substance abuse.
Many studies have shown that drastic increases in drug use patterns and drug dependency occur during adolescence.2 Overall, adolescents have higher rates of substance abuse compared to children and older adults. Different neurobiological changes that occur during adolescent development, such as decreases in grey matter volume and cortical thickness, mediate this increase in substance abuse. The former is also known as “synaptic pruning” and its changes move from posterior to anterior regions of the brain, with the prefrontal cortex (PFC) maturing later in adolescence.2 As prefrontal regions aid cognitive control, adolescents will lack important forethought into the potential consequences of their actions, and instead focus on the immediate benefits. Conversely, midbrain regions mature earlier for adolescents and facilitate the automatic processing of rewards. This is evident in the activity of their striatum, a brain region of the dopaminergic system which shows an increased response to rewards.5 Overall, developmental patterns of synaptic pruning lead to decreased control processing and enhanced reward responses in adolescents, making it difficult for them to deflect their motivation to seek appetitive stimuli. Thus, adolescents become more inclined to seek fast-acting and accessible rewards, such as drugs, without considering their detrimental effects. Other developmental changes that occur throughout adolescence include alterations of the dopaminergic and GABAergic systems.2 Both neurotransmitter pathways are triggered during drug use. While these reward systems are noted to mature early in adolescence, the amygdala comparatively matures later, and facilitates harm-avoidance behaviours.2 Thus, differential development in these three systems will regulate adolescent vulnerability to drug use, such that:
- Reward pathways mature faster and are therefore overactive compared to other neural regions. According to reward models of addiction, these pathways are central to reinforce drug-taking and drug-seeking behaviours.
- Cognitive control systems are underdeveloped due to delayed maturation, resulting in teenagers being more susceptible to rash decisions and deviant behaviour.
- The harm-avoidance system (amygdala) is weak and therefore limits adolescents’ understanding of the consequences of substance use.
These neurobiological changes also interact with other cognitive and sociological factors that adolescents are particularly vulnerable to, further mediating their susceptibility to drug abuse. Examples of these factors can be external or internal, including peer pressure, depression, and anxiety.2,4 Adolescent drug dependency also leads to an unconscious and habitual triggering of attentional cues related to substances, such as a specific environment where one repeatedly used drugs.5 This further attenuates one’s ability to control their substance use.
Drug abuse subsequently damages the neural systems initially involved in the development of that dependency.2 For example, prefrontal cortex and hippocampal volumes are reduced in adolescents who regularly binge drink compared to adolescents who do not use substances. Generally, heavy drinking overaccelerates synaptic pruning in frontal regions and attenuates white matter increases, disrupting changes that are critical to healthy adolescent development.4 Preclinical studies have also showed that adolescents who use cocaine display reduced hippocampal cell proliferation and survival. Cognitive effects associated with this type of damage include deficits to attention, information processing, memory, and executive function.2 These atypical structural alterations are especially detrimental to the developing brain.
However, there is potential to restore a healthy neurological state in adolescents with substance abuse problems, considering the developing brain’s high neural plasticity.4 One review focused on exercise as a treatment mechanism, with specific benefits for adolescents. Exercise effectively promotes neuronal health and aids brain regions that have been damaged by excessive substance use.4 Additionally, exercise activates neurotransmitters that are also triggered by drug use, such as dopamine, norepinephrine, and beta-endorphins – therefore providing a healthier alternative to obtain rewards. Glutamatergic systems which are damaged during substance withdrawal can also be normalized by exercise.4 Therefore, exercise provides several advantages for adolescents recovering from substance abuse through neural restoration, reward activation, and reduced withdrawal severity.
Other treatment alternatives include “Working Memory Training”, which alters biases that addicted individuals develop toward substances.5 Manipulating stimulus selection processes also effectively reduces drug dependency. In other words, delaying the behavioural response to a specific drug cue enforces greater cognitive control during decision making that is often limited during adolescence. This attenuates the automatic inclination to use drugs that is prevalent in adolescents who have a substance use disorder.
Overall, several neurological changes occur during adolescence which leaves individuals particularly vulnerable to substance abuse. With underdeveloped control systems and matured reward systems, teenagers have an increased proclivity to use substances and a greater likelihood of dependency.2 This can be explained by the reward model, a powerful framework which describes how activation of reward systems and negative affective states during drug-abstinence perpetuates the cycle of substance abuse.1,2 Adolescents with substance use disorders are highly susceptible to neural damage as they undergo important developmental changes, causing various cognitive deficits. However, neural plasticity increases the possibility of successful recovery when combined with effective treatment.4 Interventions such as exercise, working memory training, and redirecting selection processes are especially beneficial in mitigating drug dependency. Other psychological changes that occur throughout adolescence can additionally mediate the relationship to drug addiction. Teenagers are highly susceptible to the influence of their peers and have an increased likelihood of risk-taking behaviours when surrounded by groups with a greater propensity for sensation-seeking.3 Thus, in the future, more studies should look toward the interactions between neurological and sociological changes that occur throughout adolescence, to understand the full extent of their risks for drug dependency. Furthermore, accounting for different sociological contexts will help to elucidate how treatment can be realistically applied and how certain individuals might be impacted differently by addiction.
- Koob, G. F., Sanna, P.P., & Bloom, F. E. (1998). Neuroscience of addiction. The Scripps research institute, 21, 467-476.
- Hammond, C. J., Mayes, L. C., & Potenza, M. N. (2014). Neurobiology of adolescent substance use and addictive behaviors: Prevention and treatment implications. Adolescent medicine: State of the art reviews, 25(1), 15-32.
- Arnett, J. (1992). Reckless behaviour in adolescence: A developmental perspective. Developmental review, 12(4), 339-373.
- Nock, N. L., Minnes, S., & Alberts, J. L. (2017). Neurobiology of substance use in adolescence and potential therapeutic effects of exercise for prevention and treatment of substance use disorders. Birth defects research, 109(20), 1811-1729.
- Gladwin, T. E., Figner, B., Crone, E. A., & Wiers, R. W. (2011). Addiction, adolescence, and the integration of control and motivation. Developmental cognitive neuroscience, 1(4), 364-376.