The Impact of Prenatal Nicotine Exposure on Impulsivity and Neural Firing in the Medial Prefrontal Cortex
The Impact of Prenatal Nicotine Exposure on Impulsivity and Neural Firing in the Medial Prefrontal Cortex
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Date
2014
Authors
Barnett, Brian
Cohen, Valerie
Hearn, Taylor
Jones, Emily
Kariyil, Reshma
Kunin, Alice
Kwak, Sen
Lee, Jessica
Lubinski, Brooke
Rao, Gautam
Advisor
Roesch, Matthew R.
Citation
DRUM DOI
Abstract
Prenatal nicotine exposure (PNE) is linked to a large number of psychiatric disorders,
including attention deficit hyperactivity disorder (ADHD). Current literature suggests that
core deficits observed in ADHD reflect abnormal inhibitory control governed by the
prefrontal cortex (PFC) of the brain. The PFC is structurally altered by PNE, but it is still
unclear how neural firing is affected during tasks that test behavioral inhibition, such as
the stop-signal task, or if neural correlates related to inhibitory control are affected after
PNE in awake behaving animals. To address these questions, we recorded from single
medial PFC (mPFC) neurons in control rats and PNE rats as they performed our stopsignal
task. We found that PNE rats were faster for all trial types and were less likely to
inhibit the behavioral response on STOP trials. Neurons in mPFC fired more strongly on
STOP trials and were correlated with accuracy and reaction time. Although the number of
neurons exhibiting significant modulation during task performance did not differ between
groups, overall activity in PNE was reduced. We conclude that PNE makes rats impulsive
and reduces firing in mPFC neurons that carry signals related to response inhibition.