About

Marissa A. Ehringer is a Professor and Chair of the Department of Integrative Physiology at the University of Colorado Boulder. Her research focuses on identifying genetic mechanisms that contribute to alcohol, tobacco, and substance use, utilizing genomics and bioinformatics to study behavior genetics. She is involved with the Genetics of Substance Use Disorders Laboratory and maintains a profile at the Institute for Behavioral Genetics. Ehringer completed her B.S. in Biology and B.A. in French at Indiana University Bloomington, followed by a Ph.D. in Human Medical Genetics from the University of Colorado Health Sciences Center. Her professional experience includes postdoctoral and research associate roles at the Institute for Behavioral Genetics, and faculty positions at the University of Colorado Boulder, where she has served as Assistant Professor, Associate Professor, and now as Professor and Chair. She has also held the position of Interim Chair of the department. Her contributions extend to leadership roles such as serving on the board of the Research Society on Alcoholism and as President-elect, President, and Past-President of the International Behavioral and Neural Genetics Society. Ehringer's work emphasizes the genetic and neurobiological underpinnings of substance use behaviors, contributing to the understanding of complex traits through her research and leadership in the field.

Research topics

• Genetics
• Biology
• Medicine
• Psychology
• Computational biology
• Internal medicine
• Computer Science
• Neuroscience
• Pharmacology
• Bioinformatics
• Evolutionary biology
• Anesthesia
• Environmental health

Selected publications

• Transcriptome Analysis of Hippocampus After Weekly Binge Alcohol Exposure and Voluntary Exercise in Rats

  OSF Preprints (OSF Preprints) · 2026-04-05

  other
  Publisher

• Oxycodone self-administration and genetic background exert community-specific effects in the gut microbiome

  Scientific Reports · 2026-04-02

  articleOpen accessSenior author

  The gut microbiome and genetic factors contribute to several opioid-related phenotypes in humans and animal models. Here, we examined the effects of genetic background and oxycodone self-administration on the gut microbiome in two genetically divergent rat strains. ACI/EurMcwi and M520/N rats were trained to self-administer oxycodone or saline. Males and females from both strains acquired and escalated oxycodone self-administration, with M520/N rats administering more oxycodone than ACI/EurMcwi rats. Saline self-administration was influenced by a strain-sex interaction, with M520/N females consuming more than any other saline-administering animals. Following the self-administration period, fecal and cecal samples were collected to examine the effects of genetic background, sex, and oxycodone on the gut microbiome. Measures of alpha diversity in the fecal and cecal microbiomes were influenced by strain and sex, but not oxycodone. Beta diversity analyses demonstrated that strain and oxycodone alter the structure of the fecal and cecal microbiomes, while sex had more limited effects. Both oxycodone and strain exerted community-specific effects on gut microbiome composition, with 15 taxa differing between self-administration groups and 51 taxa differing between strains. These findings demonstrate that genetic background influences self-administration phenotypes, and both host genetics and oxycodone influence the diversity and composition of the gut microbiome.

  PublisherOA PDFDOI

• <scp>AKT2</scp> Modulates Astrocytic Nicotine Responses In Vivo

  Glia · 2025-07-15 · 1 citations

  articleOpen access

  A greater understanding of the neurobiology of nicotine is needed to reduce or prevent chronic addiction, ameliorate detrimental nicotine withdrawal effects, and improve cessation rates. Nicotine binds and activates two astrocyte-expressed nicotinic acetylcholine receptors (nAChRs), α4β2 and α7. Protein kinase B-β (Pkb-β or Akt2) expression is restricted to astrocytes in mice and humans and is activated by nicotine. To determine if AKT2 plays a role in astrocytic nicotinic responses, we generated astrocyte-specific Akt2 conditional knockout (cKO) and full Akt2 KO mice. For in/ex vivo studies, we examined mice exposed to chronic nicotine for 2 weeks in drinking water (200 μg/mL) or following acute nicotine challenge (0.09, 0.2 mg/kg) after 24 h. Our in vitro studies used cultured mouse astrocytes to measure nicotine-dependent astrocytic responses. Sholl analysis was used to measure glial fibrillary acidic protein responses in astrocytes. Our data show wild-type (WT) mice exhibit increased astrocyte morphological complexity during acute nicotine exposure, with decreasing complexity during chronic nicotine use, whereas Akt2 cKO mice showed enhanced acute responses and reduced area following chronic exposure. In culture, we found 100 μM nicotine sufficient for morphological changes and blocking α7 or α4β2 nAChRs prevented observed morphological changes. We performed conditioned place preference (CPP) in Akt2 cKO mice, which revealed reduced nicotine preference in cKO mice compared to controls. Finally, we performed RNASeq comparing nicotine- and LPS-mediated gene expression, identifying robust differences between these two astrocytic stimuli. These findings show the importance of nAChRs and AKT2 signaling in the astrocytic response to nicotine.

  PublisherOA PDFDOI

• Genetic background and sex influence somatosensory sensitivity and oxycodone analgesia in the Hybrid Rat Diversity Panel

  Genes Brain & Behavior · 2024 · 4 citations

  • Anesthesia
  • Medicine
  • Pharmacology

  = 0.10-0.15). These data demonstrate that genetic background confers differences in mechanical sensitivity, thermal sensitivity, and oxycodone-induced analgesia.

  PublisherOA PDFDOI

• Sex and genetic background influence intravenous oxycodone self-administration in the Hybrid Rat Diversity Panel

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-10-03

  preprintOpen access

  Opioid Use Disorder (OUD) is an ongoing worldwide public health concern. Genetic factors contribute to multiple OUD-related phenotypes, such as opioid-induced analgesia, initiation of opioid use, and opioid dependence. Here, we present findings from a behavioral phenotyping protocol using male and female rats from 15 genetically diverse inbred strains from the Hybrid Rat Diversity Panel (HRDP). We used a self-administration paradigm to measure the acquisition of oxycodone intake during ten 2-hour sessions and escalation of oxycodone use during ten 12-hour sessions. During both the acquisition and escalation phases of self-administration, we observed that genetic background and sex influence oxycodone intake. The heritability of oxycodone intake phenotypes ranged between 0.26 to 0.54, indicating that genetic background plays a major role in the variability of oxycodone consumption. Genetic background and sex also influenced additional phenotypes recorded during oxycodone self-administration including lever discrimination and timeout responding. The genetic contribution to these traits was slightly more moderate, with heritability estimates ranging between 0.25 to 0.42. Measures of oxycodone intake were highly positively correlated between acquisition and escalation phases. Interestingly, the efficacy of oxycodone analgesia was positively correlated with oxycodone intake during the escalation phase, indicating that the initial behavioral responses to oxycodone may predict self-administration phenotypes. Together, these data demonstrate that sex and genetic background are major contributors to oxycodone self-administration phenotypes.

  PublisherOA PDFDOI

• Loci on chromosome 20 interact with rs16969968 to influence cigarettes per day in European ancestry individuals

  Drug and Alcohol Dependence · 2024-02-15

  reviewOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Sex and genetic background influence intravenous oxycodone self-administration in the hybrid rat diversity panel

  Frontiers in Psychiatry · 2024-12-20 · 4 citations

  articleOpen access

  Opioid Use Disorder (OUD) is an ongoing worldwide public health concern. Genetic factors contribute to multiple OUD-related phenotypes, such as opioid-induced analgesia, initiation of opioid use, and opioid dependence. Here, we present findings from a behavioral phenotyping protocol using male and female rats from 15 genetically diverse inbred strains from the Hybrid Rat Diversity Panel (HRDP). We used a self-administration paradigm to measure the acquisition of oxycodone intake during ten 2-hour sessions and escalation of oxycodone use during ten 12-hour sessions. During both the acquisition and escalation phases of self-administration, we observed that genetic background and sex influence oxycodone intake. The heritability of oxycodone intake phenotypes ranged between 0.26 to 0.54, indicating that genetic background plays a major role in the variability of oxycodone consumption. Genetic background and sex also influenced additional phenotypes recorded during oxycodone self-administration including lever discrimination and timeout responding. The genetic contribution to these traits was slightly more moderate, with heritability estimates ranging between 0.25 to 0.42. Measures of oxycodone intake were highly positively correlated between acquisition and escalation phases. Interestingly, the efficacy of oxycodone analgesia was positively correlated with oxycodone intake during the escalation phase, indicating that the initial behavioral responses to oxycodone may predict self-administration phenotypes. Together, these data demonstrate that sex and genetic background are major contributors to oxycodone self-administration phenotypes.

  PublisherOA PDFDOI

• Maternal Smoking During Pregnancy Interacts With Genetic Factors to Increase Risk for Low Birth Weight but Not Harmful Offspring Smoking Behaviors in Europeans

  Nicotine & Tobacco Research · 2024-12-26

  articleOpen access

  INTRODUCTION: Pregnant individuals who smoke face increased health risks because smoking harms both the mother and their developing offspring. AIMS AND METHODS: Using 307 417 Europeans from the UK Biobank, we examined whether exposure to maternal smoking during pregnancy (MSP) interacts with genetic risk to predict offspring birth weight (BW) and smoking behaviors. We investigated interactions between MSP and genetic risk at multiple levels: single variant, gene level, and polygenic score. We examined self-reported BW, smoking initiation status (SI), age of smoking initiation, cigarettes per day, and smoking cessation status. RESULTS: One locus tagged by single-nucleotide polymorphism rs72689499 on chromosome 14 reached significance for interaction with MSP on the multiplicative (log10) scale for BW (p = 5.13 × 10-9). In gene-level testing, three genes on chromosome 1 and one gene on chromosome 14 reached significance for interaction with MSP on both the additive and multiplicative scale for BW. These genes include PTCH2, EIF2B3, PLK3, and TSHR. Single-nucleotide polymorphism and gene-level results were insignificant for all offspring smoking behaviors. We also detected an interaction between polygenic risk for smoking and MSP on SI on both the additive (p = 4.4 × 10-5) and multiplicative (p = 1.0 × 10-5) scale. We found evidence of gene-environment correlation in the polygenic risk analysis using a post hoc t test which showed that MSP-exposed offspring had a higher SI polygenic risk scores than those unexposed to MSP (p = 5.9 × 10-623). CONCLUSIONS: Our results support the main effect of MSP on BW and show a genetic interaction between MSP and genetic factors influencing BW. IMPLICATIONS: We detected interactions between maternal smoking and genetic factors to influence birth weight; these interactions were detectable at both the single-nucleotide polymorphism and gene levels. Many of the genes detected to interact with maternal smoking to influence birth weight have other reported associations with height or smoking-related traits. For smoking initiation, we detected a negative interaction between maternal smoking and polygenic risk, as well as evidence of gene-environment correlation.

  PublisherOA PDFDOI

• Diazepam effects on anxiety-related defensive behavior of male and female high and low open‐field activity inbred mouse strains

  Physiology & Behavior · 2023-09-09 · 17 citations

  articleOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Characterization of the gut microbiome and oxycodone use disorder phenotypes in select rat strains of the Hybrid Rat Diversity Panel

  Brain Behavior and Immunity · 2023-11-01

  articleSenior author
  PublisherDOI

Recent grants

• Identification of genes and genetic networks contributing to opioid use disorder traits in the Hybrid Rat Diversity Panel

  NIH · $2.3M · 2020–2026

• NIH Grant R21DA026901

  NIH · $872k · 2013

• NIH Grant R01AA017889

  NIH · $2.6M · 2016

Frequent coauthors

• John K. Hewitt

  51 shared

• Christian J. Hopfer

  37 shared

• Luke M. Evans

  Northern Arizona University

  35 shared

• Michael C. Stallings

  University of Colorado System

  29 shared

• Matthew B. McQueen

  Mitre (United States)

  26 shared

• Charles A. Hoeffer

  University of Colorado Boulder

  26 shared

• James M. Sikela

  University of Colorado Anschutz Medical Campus

  26 shared

• Robin P. Corley

  26 shared

Labs

• Genetics of Substance Use Disorders LaboratoryPI

Education

• B.S., Biology

  Indiana University, Bloomington, IN

  1995

• B.A., French

  Indiana University, Bloomington, IN

  1995

• Ph.D., Human Medical Genetics

  University of Colorado Health Sciences Center, Denver, CO

  2001

Awards & honors

• Graduate Student Training Fellowship, National Institute of…
• Postdoctoral Training Fellowship, National Institute of Drug…