Throughout
adolescence, neurodevelopment of the prefrontal cortex is crucial to future
behavior in reward processing and decision making. Consuming alcohol during
this time could have extremely negative consequences on future behavior, as the
cortico-striatal circuitry is maturing. Long-term effects such as
neurodegeneration and depletion of neurogenesis created by disruptions to
development of the prefrontal cortex can emerge as well. As people tend to
start drinking at a young age, it creates an impulsivity that continues into
adulthood, with repercussions such as disrupted cortical processing.
In
the article, “Consequences of Adolescent Ethanol Consumption on Risk Preference
and Orbitofrontal Cortex Encoding of Reward,” the effect of alcohol consumption
on cortical encoding for different sized rewards and probabilities was
examined. The orbitofrontal segment of the prefrontal cortex (OFC) functions
highly in decision making. With consumption of alcohol in young adults, perturbations
of the OFC effect reward expectations. During his talk, Jamie Donahey Roitman
explained the focus of the study was to show an association between a greater
change in activity of OFC from reward responses in situations with risk and a
greater inclination for the option of risk. This study was performed by
categorizing rats into three different consumption groups; Control, EtOH-low,
and EtOH-high. Those in the EtOH-high group had attained blood ethanol levels (BELs)
at the level of binge drinking, while EtOH-low was notably lower. Behavioral
testing was conducted once the animals reached adulthood to record risk
preference. Electrophysiological recordings of activity in the OFC were taken in
neural spike data to mark the units of time of trial events. The results showed
large risky rewards had a greater preference than small but certain rewards. Therefore,
it was concluded that changes in cortical function from consumption of alcohol
in adolescents showed increase in risk preference though adulthood.
The
review article, “The Burden of Binge and Heavy Drinking on the Brain: Effects
on Adolescent and Young Adult Neural Structure and Function,” by Anita
Cservenka, examined the effects of large consumption of alcohol through
adolescence on neural development and function. Using functional magnetic resonance
imaging (fMRI), they examined the brain structures of adolescents who were
heavy drinkers. Thickness and volume of structures such as gray and white
matter as well as cortex and cerebellar regions were evaluated. They used fMRI’s
to look at response inhibition, working memory, verbal learning and memory,
decision making and reward processing, alcohol cue reactivity, and
socio-cognitive/socio-emotional processing. The results showed a thinning in
the thickness of the prefrontal cortex, cerebellar regions, and the development
of white matter. Altered structures of the brain result from binge drinking during
adolescence as well as an increased risk of alcohol use disorder in adulthood.
Both
studies examined the effects of alcohol consumption on neurodevelopment in
adolescents, and showed similar results of altered neural structure and cortical
function. Dr. Roitman looked more at the OFC and risk preference of EtOH-high
adolescents through adulthood by using electrophysiological recordings. Dr.
Cservenka examined the overall brain structure and function from heavy drinking
using fMRI’s. Dr. Cservenka had mixed findings while looking at risky decision
making, but claimed it could be due to variation in the study. Importantly,
both concluded with showing the negative affects alcohol has on maturing
prefrontal cortexes during adolescence.
Citations
Mcmurray,
Matthew Stephen, et al. “Consequences of Adolescent Ethanol Consumption on Risk
Preference and Orbitofrontal Cortex Encoding of Reward.” Neuropsychopharmacology, vol. 41, no. 5, 2015, pp. 1366-1375.,
doi:10.1038/npp.2015.288.
Cservenka
A and Brumback T (2017) The Burden of Binge and Heavy Drinking on the Brain:
Effects on Adolescent and Young Adult Neural Structure and Function. Front.
Psychol. 8:1111. doi: 10.3389/fpsyg.2017.01111
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