# The effects of adolescent alcohol exposure on cognition and corresponding neurophysiology in adolescence and adulthood

> **NIH NIH F32** · OREGON HEALTH & SCIENCE UNIVERSITY · 2020 · $67,446

## Abstract

Project Summary
Deficits in response inhibition are observed in alcohol dependence and are proposed as an endophenotype of
the disorder. It is unclear whether deficits in response inhibition increase vulnerability to alcohol dependence of
whether impaired response inhibition is a consequence of alcohol use. Importantly, these questions can most
conclusively be investigated using a longitudinal approach. However, studies investigating the neural
mechanisms of response inhibition have primarily focused on adult models. Experimentation with alcohol
during adolescence is consistently reported to alter brain structure and function. This is because of the
numerous on-going developmental processes during maturation, which makes adolescence a critical time in
development marked by increased susceptibility to environmental insults. To date, there are few studies which
attempt to understand how adolescent alcohol exposure alters cognition during both adolescence and
adulthood. This is due in part to the short window of adolescence which poses a technical challenge because it
precludes the use of well characterized decision-making behavioral paradigms. Our laboratory has recently
developed a Cued Response Inhibition Task (CRIT) paradigm that assesses response inhibition, stimulus-
response relationships, attentional processes and behavioral flexibility in adolescents or adults. Using this
paradigm, we propose to measure single unit and local field potential activity in male and female adolescent
and adult rats with adolescent alcohol or sucrose drinking histories. By performing simultaneous recordings in
the orbitofrontal cortex (OFC) and dorsal striatum (DS), two regions heavily implicated in reward-seeking
behaviors and hypothesized to mediate behavioral inhibition, these experiments will determine how adolescent
alcohol exposure alters neural activity in adolescence (Aim 1), how adolescent alcohol exposure alters neural
activity in adulthood (Aim 2) and how age influences neural circuitry necessary for response inhibition (Aims 1
and 2). We hypothesize that adolescent alcohol drinking will weaken coordination of neurons in the OFC,
which in turn will reduce OFC-DM connectivity. Reduced functional connectivity between these regions will be
associated with deficits in response inhibition, complementing work in human imaging where impaired frontal
striatal connectivity during response inhibition is associated with increased severity of alcohol dependence.

## Key facts

- **NIH application ID:** 9988134
- **Project number:** 1F32AA027935-01A1
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** Aqilah Maryam McCane
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $67,446
- **Award type:** 1
- **Project period:** 2020-09-28 → 2021-09-27

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9988134

## Citation

> US National Institutes of Health, RePORTER application 9988134, The effects of adolescent alcohol exposure on cognition and corresponding neurophysiology in adolescence and adulthood (1F32AA027935-01A1). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9988134. Licensed CC0.

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