# Prenatal alcohol exposure, GABAergic interneuron circuitry, early motor behavior, and the developing striatum

> **NIH NIH F30** · DARTMOUTH COLLEGE · 2021 · $51,036

## Abstract

Project Summary
 Fetal Alcohol Spectrum Disorders (FASD) are the most common cause of non-genetic neurodevelopmental
disability worldwide. Clinical symptoms of FASD can vary, but include facial dysmorphology, cognitive deficits
and behavioral abnormalities. The variable clinical presentation of FASD makes diagnosis a challenge. Delayed
diagnosis is associated with negative clinical outcomes, while early intervention can improve patients’ quality of
life.
 Deficits in gross and fine motor development are some of the earliest identifiable clinical signs of FASD in
patients. However, the mechanism by which prenatal alcohol exposure contributes to deficits in early motor skills
is not yet known. Functional maturation of neurons within the striatum, the input nucleus of the basal ganglia, is
closely associated with onset of complex movements in neonatal mice. The experiments outlined in this F30
proposal will investigate how aberrant development of GABAergic interneuron circuitry within the striatum may
relate to developmental motor delays after prenatal alcohol exposure. My preliminary data suggest that prenatal
alcohol exposure results in deficient formation of synaptic connections to striatal GABAergic interneurons during
the first two postnatal weeks. Specific Aim 1 will leverage whole cell patch clamp electrophysiology, optogenetic
and trans-synaptic viral approaches to identify the source of deficits in the formation of functional synaptic
afferents to striatal GABAergic interneurons. Specific Aim 2 will establish how observed prenatal alcohol
exposure-induced deficits in striatal GABAergic interneuron signaling may relate to altered morphological and
functional maturation of striatal projection neurons, and neonatal motor development as measured by a series
of brief behavioral tasks assessing the onset of gross, fine, and complex motor abilities during the first two
postnatal weeks.
 This F30 proposal will allow me to fulfill my long-term objective of contributing to a better understanding of
the physiological changes underlying the earliest clinical symptoms of FASD in order to improve efforts to identify
FASD patients and provide targeted treatment. My goals in completing the proposed work are to develop the
intellectual foundations and technical skills necessary to conduct research as physician scientist in the FASD
field, with a focus on how prenatal alcohol exposure can affect the development of neural circuits and result in
changes in early behaviors.

## Key facts

- **NIH application ID:** 10312275
- **Project number:** 1F30AA029261-01A1
- **Recipient organization:** DARTMOUTH COLLEGE
- **Principal Investigator:** Adelaide R Tousley
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $51,036
- **Award type:** 1
- **Project period:** 2021-05-25 → 2026-05-24

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10312275

## Citation

> US National Institutes of Health, RePORTER application 10312275, Prenatal alcohol exposure, GABAergic interneuron circuitry, early motor behavior, and the developing striatum (1F30AA029261-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10312275. Licensed CC0.

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