Prefrontal cortex

Do you have an addictive personality?

You’ll have to bear with me if this is a bit of a self-indulgent post, but I have some exciting news, Brain Study-ers: I’ve officially submitted my dissertation for a PhD in psychology!

In light of this – the culmination of three years of blood, sweat, tears and an exorbitant amount of caffeine – I thought I’d write this week on part of my thesis work (I promise to do my best to keep the jargon out of it!)

One of the biggest questions in addiction research is why do some people become dependent on drugs, while others are able to use in moderation? Certainly some of the risk lies in the addictive potential of the substances themselves, but still the vast majority of individuals who have used drugs never become dependent on them. This then leads to the question, is there really such a thing as an “addictive personality”, and what puts someone at a greater risk for addiction if they do choose to try drugs?

If I can't remember it, it didn't happen: A susceptibility for alcohol-induced blackouts

As anyone who's ever taken an Alcohol Edu course (or been 21 in the last decade) knows, consuming too much alcohol can cause memory loss, colloquially known as a "blackout". This anterograde amnesia stems from an inability of the brain to form new long-term memories and is caused by a disruption in the GABA and NMDA receptors in the prefrontal cortex (PFC) and medial temporal lobes when drinking.

First, for those of you who skipped (or drank) your way through your alcohol education, a brief reminder on the effects of alcohol on the brain. GABA is a primary inhibitory neurotransmitter, acting to decrease the likelihood of a cell's firing. Alcohol acts as a GABA agonist, elevating levels throughout the brain and therefore diminishing the rates of firing in normal cellular processes. At high levels, alcohol also acts upon glutamate NMDA receptors, one of the main excitatory neurotransmitter systems. Alcohol works as an NMDA antagonist, blocking the NMDA receptors and preventing glutamatergic activation, further inhibiting neuronal functioning. This inhibition particularly occurs in the PFC, medial temporal cortex and the parietal lobe, primary targets of alcohol in the brain. In the hippocampus in particular, an area in the medial temporal cortex crucial to memory formation, this inhibition can result in a disruption of long-term potentiation, a cellular process involved in the consolidation of short-term to long-term memories.

Impaired adolescent decision-making

I am pleased to announce that my first first-author publication has recently been released online by the journal Developmental Psychology. The article, on decision-making in children and adolescents, looks at the developmental trajectory of affective decision-making abilities using the Iowa Gambling Task (IGT) in children between the ages of 8 and 17. It compares this type of "hot" executive function with more typical "colder" cognitive abilities, such as impulse control and working memory. Contrary to the accepted belief that children improve universally on cognitive tasks as they age, we discovered that early adolescents (ages 11-13) are actually more impaired on this task than some of the younger participants, making riskier decisions and failing to learn from their mistakes.

The IGT requires participants to choose between four decks of cards that give out varying amounts of wins and losses. Two of the decks issue low wins but also low losses, resulting in an overall net gain, whereas the other two decks are riskier options, giving high payoffs but also higher losses, making them ultimately disadvantageous. A net score is calculated by subtracting the total number of disadvantageous choices from the total advantageous decisions. Early adolescents had significantly lower mean net scores on the task than older participants, but did not differ from the younger children in their ability. However, the total trajectory of mean scores across all ages resulted in a significant J-shaped curve, signifying a dip in ability in early adolescence.

We speculate that this curvilinear trajectory is due to the varying developmental schedules of different regions of the brain, particularly the striatum (involved in reward processing) and the prefrontal cortex, which is responsible for more inhibitory control. Structures in the basal ganglia typically develop earlier in adolescence,  whereas the prefrontal cortex is not fully matured until the early 20s. This earlier development of the striatum could lead adolescents to place undue emphasis on the initially high reward, but ultimately disadvantageous options in the IGT. Coupled with the delayed development of the prefrontal cortex, this group could also lack the necessary inhibitory control to offset this reward-driven urge. Supporting this theory, other imaging studies investigating developing cognitive ability have shown adolescents to disproportionately recruit from subcortical regions, particularly the basal ganglia, on tasks involving monetary rewards.

Conversely, younger children performed neither overtly advantageously nor disadvantageously on the task, choosing between the decks more randomly. This could be due to an earlier neurodevelopmental stage, before the striatum and other limbic regions had fully developed, making them less sensitive to the risky high reward options. Also supporting this J-shape trajectory theory, older adolescents performed the most advantageously on the task, improving their performance and successfully inhibiting the urge to make impulsive choices. This improvement presumably correlates with the continued maturation of their prefrontal cortices, as these inhibitory abilities come on-line.

Notably, all other cognitive tasks administered during the course of testing improved linearly across age, demonstrating that affective decision-making is a unique process that taps into the limbic regions, rather than just relying on the cortical cognitive network.

Importantly, these results are not implying that all adolescents are impulsive risk-seekers doomed to make lasting poor decisions. We all go through these stages of neurodevelopment and the vast majority of us emerge from adolescence relatively unscathed. Also, as this was not an imaging study the neural correlates of the abnormal decision-making development is speculative. However, this study does provide an interesting glimpse into how we develop in our affective decision-making tendencies and how they change as we mature.