Assistant Professor, Department of Human Physiology
Ph.D. Oregon Health and Science University
Elinor Sullivan’s teaching focus is in the areas of nutrition, endocrinology, and neurobiology.
Dr. Sullivan’s research focuses on examining the influence of maternal metabolic state and dietary environment on offspring behavioral regulation, with an emphasis on behaviors that relate to mental health and behavioral disorders including autism spectrum disorders, attention deficit hyperactivity disorder, anxiety, and depression.
Her areas of expertise include behavioral neuroscience, with training and expertise in human and nonhuman primate behavior, brain development, developmental programming, maternal nutrition, and neurodevelopmental disorders.
Dr. Sullivan received her Ph.D. in Physiology from Oregon Health and Science University. She received her postdoctoral training at the University of California San Francisco and Oregon Health and Science University. Prior to coming to the University of Oregon, Dr. Sullivan was an Assistant Professor in the Biology Department at the University of Portland. Dr. Sullivan is currently an Assistant Professor in the Divisions of Neuroscience and Cardiometabolic health at the Oregon National Primate Research Center. She joined the UO Department of Human Physiology in 2017.
Dr. Sullivan has received research grants from the National Institute of Health, the Bill and Melinda Gates Foundation, the Murdock Charitable Trust, and the Obesity Society.
Maternal High-Fat Diet Effects on Adaptations to Metabolic Challenges in Male and Female Juvenile Nonhuman Primates.
Obesity (Silver Spring). 2018 09;26(9):1430-1438
Authors: True C, Dean T, Takahashi D, Sullivan E, Kievit P
OBJECTIVE: This study aimed to determine whether maternal high-fat diet (HFD) consumption in nonhuman primates alters the ability of offspring to adapt metabolically to nutrient and caloric challenges.
METHODS: Offspring from Japanese macaque dams fed either a control (CTR) diet or HFD were weaned onto a CTR diet creating two groups: maternal HFD (mHFD, n = 18) and maternal CTR (mCTR) diet (n = 12). Male and female offspring were exposed to a 5-day 30% calorie restriction and to a 35-day HFD challenge (HFDC), at 16 and 24 months of age, respectively. Caloric intake, body weight, and energy expenditure were measured.
RESULTS: Offspring from both groups showed similar body weight, food intake, and metabolic adaptations to a 5-day calorie restriction. mHFD offspring demonstrated increased food intake and early weight gain in response to a 35-day HFDC; however, group differences in weight dissipated during the challenge. Unlike mCTR animals, the mHFD group had a significant increase in fasting insulin after acute HFD exposure.
CONCLUSIONS: The current findings indicate that offspring exposed to an mHFD show metabolic adaptations to calorie restriction that are largely similar to those of offspring exposed to a mCTR diet but show delayed adaptation upon exposure to an acute HFDC.
PMID: 30226008 [PubMed - indexed for MEDLINE]
Delineating the Macroscale Areal Organization of the Macaque Cortex In Vivo.
Cell Rep. 2018 Apr 10;23(2):429-441
Authors: Xu T, Falchier A, Sullivan EL, Linn G, Ramirez JSB, Ross D, Feczko E, Opitz A, Bagley J, Sturgeon D, Earl E, Miranda-Domínguez O, Perrone A, Craddock RC, Schroeder CE, Colcombe S, Fair DA, Milham MP
Complementing long-standing traditions centered on histology, fMRI approaches are rapidly maturing in delineating brain areal organization at the macroscale. The non-human primate (NHP) provides the opportunity to overcome critical barriers in translational research. Here, we establish the data requirements for achieving reproducible and internally valid parcellations in individuals. We demonstrate that functional boundaries serve as a functional fingerprint of the individual animals and can be achieved under anesthesia or awake conditions (rest, naturalistic viewing), though differences between awake and anesthetized states precluded the detection of individual differences across states. Comparison of awake and anesthetized states suggested a more nuanced picture of changes in connectivity for higher-order association areas, as well as visual and motor cortex. These results establish feasibility and data requirements for the generation of reproducible individual-specific parcellations in NHPs, provide insights into the impact of scan state, and motivate efforts toward harmonizing protocols.
PMID: 29642002 [PubMed - indexed for MEDLINE]
Maternal prenatal depression predicts infant negative affect via maternal inflammatory cytokine levels.
Brain Behav Immun. 2018 10;73:470-481
Authors: Gustafsson HC, Sullivan EL, Nousen EK, Sullivan CA, Huang E, Rincon M, Nigg JT, Loftis JM
Maternal depressive symptoms during pregnancy are associated with risk for offspring emotional and behavioral problems, but the mechanisms by which this association occurs are not known. Infant elevated negative affect (increased crying, irritability, fearfulness, etc.) is a key risk factor for future psychopathology, so understanding its determinants has prevention and early intervention potential. An understudied yet promising hypothesis is that maternal mood affects infant mood via maternal prenatal inflammatory mechanisms, but this has not been prospectively examined in humans. Using data from a pilot study of women followed from the second trimester of pregnancy through six months postpartum (N = 68) our goal was to initiate a prospective study as to whether maternal inflammatory cytokines mediate the association between maternal depressive symptoms and infant offspring negative affect. The study sample was designed to examine a broad range of likely self-regulation and mood-regulation problems in offspring; to that end we over-selected women with a family history or their own history of elevated symptoms of attention-deficit/hyperactivity disorder. Results supported the hypothesis: maternal pro-inflammatory cytokines during the third trimester (indexed using a latent variable that included plasma interleukin-6, tumor necrosis factor-alpha and monocyte chemoattractant protein-1 concentrations as indicators) mediated the effect, such that higher maternal depressive symptoms were associated with higher maternal inflammation, and this mediated the effect on maternal report of infant negative affect (controlling for maternal affect during the infant period). This is the first human study to demonstrate that maternal inflammatory cytokines mediate the association between prenatal depression and infant outcomes, and the first to demonstrate a biological mechanism through which depressive symptoms impact infant temperament.
PMID: 29920327 [PubMed - indexed for MEDLINE]
An Open Resource for Non-human Primate Imaging.
Neuron. 2018 10 10;100(1):61-74.e2
Authors: Milham MP, Ai L, Koo B, Xu T, Amiez C, Balezeau F, Baxter MG, Blezer ELA, Brochier T, Chen A, Croxson PL, Damatac CG, Dehaene S, Everling S, Fair DA, Fleysher L, Freiwald W, Froudist-Walsh S, Griffiths TD, Guedj C, Hadj-Bouziane F, Ben Hamed S, Harel N, Hiba B, Jarraya B, Jung B, Kastner S, Klink PC, Kwok SC, Laland KN, Leopold DA, Lindenfors P, Mars RB, Menon RS, Messinger A, Meunier M, Mok K, Morrison JH, Nacef J, Nagy J, Rios MO, Petkov CI, Pinsk M, Poirier C, Procyk E, Rajimehr R, Reader SM, Roelfsema PR, Rudko DA, Rushworth MFS, Russ BE, Sallet J, Schmid MC, Schwiedrzik CM, Seidlitz J, Sein J, Shmuel A, Sullivan EL, Ungerleider L, Thiele A, Todorov OS, Tsao D, Wang Z, Wilson CRE, Yacoub E, Ye FQ, Zarco W, Zhou YD, Margulies DS, Schroeder CE
Non-human primate neuroimaging is a rapidly growing area of research that promises to transform and scale translational and cross-species comparative neuroscience. Unfortunately, the technological and methodological advances of the past two decades have outpaced the accrual of data, which is particularly challenging given the relatively few centers that have the necessary facilities and capabilities. The PRIMatE Data Exchange (PRIME-DE) addresses this challenge by aggregating independently acquired non-human primate magnetic resonance imaging (MRI) datasets and openly sharing them via the International Neuroimaging Data-sharing Initiative (INDI). Here, we present the rationale, design, and procedures for the PRIME-DE consortium, as well as the initial release, consisting of 25 independent data collections aggregated across 22 sites (total = 217 non-human primates). We also outline the unique pitfalls and challenges that should be considered in the analysis of non-human primate MRI datasets, including providing automated quality assessment of the contributed datasets.
PMID: 30269990 [PubMed - indexed for MEDLINE]