# Neural Basis of Spatial Memory Deficits After Prenatal Alcohol Exposure

> **NIH NIH R01** · UNIVERSITY OF NEW MEXICO · 2024 · $315,145

## Abstract

PROJECT SUMMARY/ABSTRACT
Fetal Alcohol Spectrum Disorders are a set of major morphological, neurobiological, and cognitive
abnormalities in offspring exposed to alcohol in utero. A common cognitive manifestation of alcohol exposure
during neural development in humans, and in animal models of prenatal alcohol exposure (PAE), are deficits
in spatial learning and memory. In moderate PAE, which accounts for the most common and underestimated
form of PAE, spatial deficits are marked by an inability to accurately discriminate between spatial locations or
recall previously learned spatial relationships. Systems-level monitoring of neural populations in the
hippocampal formation has unraveled a critical role for this circuit in the generation of spatial memories and
their subsequent recall. The well-characterized spatial and oscillatory organization of hippocampal spiking is
thought to play a critical role in these processes. The long-term goal of our research program is to identify the
neurobiological mechanisms of spatial learning and memory impairments after moderate PAE. While the
behavioral phenotype of altered spatial behavior after moderate PAE is well established, there is still a critical
need to identify the systems-level mechanisms including the neural circuitry and brain dynamics involved in
such deficits. A multi-level understanding framework for the study of spatial impairments is essential in
developing a complete understanding of the impact of PAE on nervous system function and toward the
development of targeted interventions. The overall objective of this proposal is to identify these systems-level
alterations by monitoring large ensembles of hippocampal neurons and their oscillatory dynamics during both
spatial learning and memory and in “offline periods” of rest and sleep. In two aims, we will test our central
hypothesis that PAE induced perturbations to spatial learning and memory are a consequence of a loss in
the expression of distinct hippocampal ensemble codes for place and their synchronization and organization
within hippocampal oscillations during rest and sleep. The aims of this R01 represent a critical step towards
our long-term goal of identifying the neurobiological mechanisms of spatial learning and memory deficits after
moderate PAE but will also provide critical insight into the systems-level impact of moderate PAE on
hippocampal population activity. The relationship between hippocampal population activity and spatial
learning and memory is well established in a wide range of species including humans. Thus, this proposal
has the potential to provide a novel scientific framework whereby new strategies for interventions can be
developed and tested in preclinical models but can also be developed for human patient populations.

## Key facts

- **NIH application ID:** 10773088
- **Project number:** 5R01AA029700-03
- **Recipient organization:** UNIVERSITY OF NEW MEXICO
- **Principal Investigator:** Benjamin J Clark
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $315,145
- **Award type:** 5
- **Project period:** 2022-02-22 → 2027-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10773088

## Citation

> US National Institutes of Health, RePORTER application 10773088, Neural Basis of Spatial Memory Deficits After Prenatal Alcohol Exposure (5R01AA029700-03). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10773088. Licensed CC0.

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