# Impact of Prenatal Ethanol on BLA Synaptic Plasticity

> **NIH NIH R21** · STATE UNIVERSITY OF NY,BINGHAMTON · 2020 · $219,133

## Abstract

Abstract
The incidence of alcohol drinking and alcohol abuse during pregnancy is strikingly high which can lead to a
spectrum of deficits in offspring termed Fetal Alcohol Spectrum Disorders. One of the most common
consequences of prenatal alcohol exposure (PAE) is the emergence of anxiety disorders in adolescence,
which are surprisingly observed following exposure to moderate levels of ethanol – a common pattern of
alcohol consumption in pregnancy. Despite these compelling epidemiological data, the neurobiological
mechanisms underlying moderate PAE-induced anxiety are not well understood. Synaptic activity and plasticity
within the basolateral amygdala (BLA) is driven, in part, through inputs from the medial prefrontal cortex
(mPFC), and are associated with regulation and expression of anxiety-like behaviors. Additionally, BLA
synaptic activity and plasticity is modulated by the dynorphin/kappa opioid receptor (DYN/KOR) system that is
also associated with alterations in anxiety-like behaviors. Although studies have shown that PAE can alter
mPFC function, increase BLA plasticity, and reduce amygdala KOR levels (an effect opposite of what is seen
following exposure to ethanol in adulthood), whether moderate PAE at levels more likely seen in pregnant
women affects these targets and the interaction(s) between these alterations during the highly vulnerable
developmental period of adolescence are unknown. We have recently characterized a model of moderate PAE
using a single exposure to vaporized ethanol on gestational day (G) 12, a developmental epoch during which
the amygdala begins to appear, that produces increased social anxiety-like behaviors in adolescent offspring.
Based on this, we hypothesize that moderate G12 PAE increases anxiety-like behavior in adolescence through
enhanced mPFCBLA synaptic plasticity and reduced DYN/KOR function. To test our hypothesis, Aim 1 will
examine the impact of moderate G12 PAE on alterations in mPFCBLA synaptic plasticity using in vitro
optogenetic and electrophysiological tools. Aim 2 will test the effect of moderate G12 PAE on KOR modulation
of mPFCBLA synaptic plasticity using a combination of molecular, electrophysiological and in vivo
optogenetics coupled with behavioral pharmacology. These innovative studies will test novel and unique
hypotheses surrounding the long-term effects of moderate PAE and describe neural mechanisms specific to
deficits in anxiety-like behaviors.

## Key facts

- **NIH application ID:** 9979507
- **Project number:** 1R21AA027873-01A1
- **Recipient organization:** STATE UNIVERSITY OF NY,BINGHAMTON
- **Principal Investigator:** Marvin Rafael Diaz
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $219,133
- **Award type:** 1
- **Project period:** 2020-04-10 → 2022-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9979507

## Citation

> US National Institutes of Health, RePORTER application 9979507, Impact of Prenatal Ethanol on BLA Synaptic Plasticity (1R21AA027873-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9979507. Licensed CC0.

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