of Neuroscience, Cell Biology, & Anatomy
Research Building 17 Room 5.212B Route: 0620| Tel: (409)772-0135 |
Education and Training
BS in Biophysical Chemistry, Summa cum laude, University of Arkansas, Fayetteville, AR
PhD in Neuroscience, Baylor College of Medicine, Houston, TX
Post-Doctoral in Neuroscience, Memory and Brain Research Center, Baylor College of Medicine, Houston, TX
Our lab studies mammalian social behavior and cognitive function in the context of the holobiont, considering both host intrinsic mechanisms as well as the contribution of the microbiome. To this end, we use a multidisciplinary approach, combining
mouse genetics, behavior, molecular biology, immunology, electrophysiology, and RNAseq with metagenomic sequencing and anaerobic bacteriology to address two primary questions: (1) What are the basic neuronal mechanisms underlying social behavior?
and (2) How do host-microbe interactions shape host brain development, function, and behavior?
To address these questions, we study the oxytocinergic-to-mesolimbic dopaminergic reward circuit and behavior in mouse models of environmentally-induced
behavioral disorders. Specifically, we focus on the long-term effects of maternal health factors on offspring neurodevelopment and behavior. We model environmental factors caused by socioeconomic circumstances, such as limited access to affordable
nutritious food, as well as those associated with climate change, including increased incidence of mosquito-borne infectious diseases. We are particularly interested in the transgenerational influence of maternal environmental factors on the offspring
gut microbiome and its relationship with neurodevelopment and behavior given that maternal environmental factors, such as metabolic status and infection during pregnancy, influence the risk of neurodevelopmental disorders in offspring. The maternal-fetal/infant
connection is the ideal system in which to study how gut microbiota affect brain function and behavior given that gestation, infancy, and the transition to early childhood represent concurrent developmental critical periods in each system.
We have found that changes in maternal diet and metabolic status can lead to persistent, functional changes in the offspring gut microbiome that are causally related to changes in synaptic potentiation and related behavioral impairments
as well as metabolic dysfunction. By understanding the mechanisms by which gut microbiota impact brain function and behavior–from the regulation of protein synthesis to circuit function–we hope that the knowledge gained in our studies
will lead to new, innovative treatments for disorders of social dysfunction.
Buffington SA*, Dooling SD*, Sgritta M, Noecker C, Murillo OD, Felice DF, Turnbaugh PJ, Costa-Mattioli M (2021) Dissecting the contribution of host genetics and the microbiome in complex behaviors. Cell. PMID: 33705688 *Equal Contribution
Di Gesù CM, Matz LM,
Buffington SA (2021) Diet-induced dysbiosis of the maternal gut microbiome in early life programming of neurodevelopmental disorders. Neurosci Res. PMID: 33992660
Johnson JL, Stoica L, Liu Y, Zhu PJ, Bhattacharya A, Buffington SA
, Huq R, Eissa T, Larsson O, Porse BT, Domingo D, Nawaz U, Carroll LJ, Scerri TS, Kim YG, Brignell A, Coleman MJ, Braden R, Kini U, Jackson V, Baxter A, Bahlo M, Scheffer IE, Amor DJ, Hildebrand MS, Bonnen PE, Beeton C, Gecz J, Morgan AT,
Costa-Mattioli M (2019) Inhibition of Upf2-dependent nonsense-mediated decay leads to behavioral and neurophysiological abnormalities by activating the immune response. Neuron
. PMID: 31585809
Sgritta M, Dooling SD, Buffington SA, Momin EN, Francis MB, Britton RA, Costa-Mattioli M (2019) Mechanisms underlying microbial-mediated changes in social behavior in mouse models of autism spectrum disorder. Neuron.
Buffington SA, Viana Di Prisco G, Auchtung TA, Ajami NJ, Petrosino JF, Costa-Mattioli M (2016) Microbial reconstitution reverses maternal diet-induced synaptic and social deficits in offspring. Cell.
Viana Di Prisco* G, Huang* W, Buffington* SA, Hsu, C-C Bonnen, P, Placzek A, Sidrauski C, Krnjević K, Kaufman R, Walter P, Costa-Mattioli M (2014) Translational control of mGluR-dependent long-term
depression and object-place learning by eIF2a. Nat Neurosci. PMID: 24974795 *Equal contribution.
Kaphzan H, Buffington SA, Lingrel JB, Rasband MN, Santini E, Klann E (2013) Genetic reduction of the a1 subunit of the Na/K-ATPase corrects multiple hippocampal phenotypes in Angelman syndrome. Cell Reports.
4(3):405-12. PMID: 23911285
Buffington SA, Rasband, MN (2013) Na+ channel-dependent targeting of Navb4 to axon initial segments and nodes of Ranvier. J Neurosci. 33(14):6191-202. PMID: 23554500
Kaphzan H, Buffington SA, Jung JI, Rasband MN, Klann E (2011) Alterations in intrinsic membrane properties and the axon initial segment in a mouse model of Angelman syndrome. J Neurosci, 31(48):17637-48. PMID: 22131424
Link to PubMed Publications
Link to Google Scholar Page
In the Press
The New York Times (2019) Germs in Your Gut are Talking to Your Brain. Scientists Want to Know What They’re Saying. Carl Zimmer.
Spectrum News (2019) Gut microbes may treat social difficulties in autism mice. Nicholette Zeliadt.
The Economist (2018) Gut bacteria may offer a treatment for autism, treating autism.
Spectrum News (2016) Single microbe may restore social behaviors in mice. Ann Griswold.
The Economist (2016) Gut feelings, microbes and autism.