# Molecular alterations in primate amygdala following prenatal immune challenge

> **NIH NIH R21** · UNIVERSITY OF CALIFORNIA AT DAVIS · 2020 · $196,100

## Abstract

The amygdala has been implicated in nearly every neurodevelopmental and neuropsychiatric
disorder, from autism to depression to schizophrenia, and likely contributes to socioemotional
deficits that characterize these disorders. Although the causal mechanisms of these disorders
remain unknown, a growing body of evidence suggests that maternal factors in utero may
influence disease susceptibility. Indeed, children who were prenatally exposed to maternal
infection have an increased risk for developing autism, schizophrenia or other
neurodevelopmental disorders. Because the genetic, ecological, and behavioral diversity of
humans is so remarkably heterogeneous, animal models are essential for testing causality,
identifying molecular mechanisms, and developing new diagnostic tools and therapeutics.
Maternal immune activation (MIA) models in rodents have demonstrated a causal relationship
between maternal response to infection and neuropathological and behavioral abnormalities
consistent with a range of neurodevelopmental and psychiatric disorders. However, it was not
known if prenatal immune challenge in primates would lead to similar outcomes. To address this
major gap, we created a nonhuman primate MIA model of rhesus macaques prenatally exposed
to immune challenge. This unprecedented nonhuman primate cohort has undergone extensive
behavioral, immune, and neuroimaging studies, and is now being used to evaluate genomic and
cellular alterations. We have found that MIA-exposed nonhuman primate offspring show biological
and behavioral changes that mimic human psychiatric disease, including amygdala-relevant
alterations in socioemotional development. In this proposal, we will utilize the archived brain tissue
from this cohort and to evaluate, for the first time, how cellular and molecular mechanisms are
altered in the amygdala following prenatal immune challenge. The first step in this pilot proposal
is to ask: Is the molecular signature of the amygdala altered in nonhuman primate offspring
prenatally exposed to a maternal immune system challenge? To address this question, we will
utilize next generation sequencing methods (RNA-seq) to measure genome-wide transcriptome
changes as well as weighted-genome co-expression network analysis (WGCNA), a powerful
unsupervised systems-biology framework, to identify co-expression modules within and across
amygdala nuclei in MIA-exposed animals relative to controls. These modules will be integrated
with behavioral, immunologic, and neuroimaging results from the same cohort to identity putative
molecular drivers of observed phenotypic alterations following MIA exposure.

## Key facts

- **NIH application ID:** 9933116
- **Project number:** 5R21MH119650-02
- **Recipient organization:** UNIVERSITY OF CALIFORNIA AT DAVIS
- **Principal Investigator:** Melissa Dawn Bauman
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $196,100
- **Award type:** 5
- **Project period:** 2019-06-01 → 2022-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9933116

## Citation

> US National Institutes of Health, RePORTER application 9933116, Molecular alterations in primate amygdala following prenatal immune challenge (5R21MH119650-02). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/9933116. Licensed CC0.

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