Biological imperative demands that all animals venture from the nest in order to propagate and reproduce. In the wild this means encountering dangerous situations where survival will be dependent on an ability to demonstrate things such as strength that will put the organism in conflict with other animals or the environment itself. These experiences as Kelley et al. (2004) explain it provide the adolescent with the experience and skills necessary to survive away from the protection of the nest. This often is adaptive since experiences to trivial and novel experience help with developing the strategy and problem solving skills that are mandatory for survival.
Increased impulsivity in adolescence can be attributed to developing risk/reward pathways with still developing prefrontal cortices. In rat models, adolescence is characterized by increasing amygdalo-prefrontal innervation (Kelley et al. 2004). This growing connection is a hallmark feature of the teenage brain and distinguishes it from the child’s brain with it’s lack of innervation of the connecting fibers and adult brain with established networks (Kelley et al. 2004). The nucleus accumbens is another area going through developmental changes at this stage, receiving amygdala and PFC inputs and is highly in targeted by dopamine pathways (Kelley et al. 2004). Indeed Andersen & Teicher (2009) note that a consequence of exposure to childhood adversity (e.g. direct child abuse) is a flooding of dopamine to the NAc resulting in baseline anhedonia (inability or blunted affect to experience pleasure). Evidence presented by Moonat & Pandey (2012) that histone deacetylases in the NAc can result in stress-related dysphoria concurs with evidence put forth by Andersen & Teicher (2009) that increased dopamine in the NAc can produce dysphoria through CREB transcription. Taken together, this provides a framework for understanding why the teenage brain is especially susceptible to addiction. With highly activated dopamine systems, the brain is going to process the “high” feeling as very pleasurable and reinforcing. However in stress exposed individuals experiencing anhedonic and dysphoria related cognitive deficits, the pleasurable and reinforcing effect of the the drug will be so great that they become especially vulnerable to addiction.
Two types of stressors commonly referred to in the adolescent-stress-addiction literature are social defeat stress and maternal separation. These two evolutionarily linked drives are critical in the exploration and growth of the organism across species. Aforementioned risk taking to acquire survival skills critically depends on the animal’s ability to navigate social demands and having a secure base from which to begin exploration. In summarizing multiple other studies, Moonat & Pandey (2012) found that BDNF underexpression occurred in the hippocampus in depression related to social defeat stress. Andersen & Teicher (2009) address this as an association between social isolation and reduced gray matter and synaptic density in the prefrontal cortex (similar brain changes were found in child victims of sexual assault). Additionally Andersen & Teicher (2009) create the distinction that early life stress will present as hippocampal dysregulation resulting in enhanced cue-dependent addiction learning whereas stress occurring in adolescence will show as dysregulation in the PFC and often not until later in development. Taken together these arguments demonstrate that the teenage brain, especially when exposed to stress, are highly attuned to motivational and rewarding salient cues and these drug-sensitized cues become vastly more emphasized than flexible behavior typical mediated by the PFC in healthy controls.
Glutamate production also plays a critical role in the risk taking and decision making of teens. Citing Seamans & Yang (2004), Andersen & Teicher (2009) note that GABA activity in the functional brain modulates behavioral flexibility mediated by the PFC as atypical GABA function will attune to all sources of information properly. In addiction conditions, however, D1 receptors become overexpressed on glutamatergic neurons projecting to the NAc, resulting in the aforementioned cue-seeking. In monkey models mentioned by Kelley et al. (2004) considerable synaptic pruning and dopaminergic input alterations occur in the PFC during adolescence. In stress exposure and childhood adversity, molecular changes include structural alterations of GABA-benzodiazepine and high affinity GABA-A receptors in the hippocampus and amygdala (Andersen & Teicher, 2009). These fundamental alterations cause dampened affect in the hippocampus (novelty-context) and amygdala (emotion-affect), and leaving it especially susceptible to addiction due to the overexcitation of glutamate and underexpressed GABA. Thus the brain is signalling fast and without brakes.
In conclusion, adolescence is a time in all species to explore and take risks. This leaves human teenagers especially susceptible to drug initiation since the pleasurable effect will be enhanced in a systematically changing reward pathway. Developing reward pathways and seeking of novelty is beneficial in normative development as it provides the animals with incentive to explore their world away from their parents and learn survival skills. In vulnerable populations – victims of abuse, exposure to constantly stressful environments, social isolation, and maternal separation (i.e. rat models) – these risk taking behaviors are susceptible to becoming addictive behaviors. This is in part due to fundamental changes in brain chemistry which, without proper nourishment, become dependent on exogenous substances to compensate for suboptimal neurotransmitter functioning.
Kelley, A.E., Schochet, T., Landry, C.F. (2004) Risk taking and novelty seeking in
adolescence. Annals of the New York Academy of Sciences 1021:27-32.
Moonat, S., Pandey, S.C. (2012) Stress, epigenetics and alcoholism. Alcohol Research and Health, 34, 495-505.
Andersen, S.L., Teicher, M.H. (2009) Desperately driven and no brakes: Developmental stress exposure and subsequent risk for substance abuse. Neuroscience and Biobehavioral Reviews 33, 516-524.