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School of Medicine Columbia

Faculty and Staff

Fiona Hollis, Ph.D.

Title: Assistant Professor
Department: Pharmacology, Physiology & Neuroscience
School of Medicine Columbia
Phone: 803-216-3514
Fax: 803-216-3538
Office: Building 1, Room D14 (lab)
Building 1, Room D15 (office)
picture of Fiona Hollis


Brain Mind Institute, EPFL, Switzerland
Department of Fundamental Neurosciences, UNIL, Switzerland
Florida State University College of Medicine

Florida State University


Our laboratory aims to fully delineate the role of brain metabolism in neurodevelopmental and psychiatric diseases. We use rodent and human models to identify and characterize the role of brain energy metabolism in neurological disorders at both the behavioral, cellular, and molecular level. To this end, our research employs a wide range of techniques, including animal behavior, high resolution respirometry, pharmacology, and molecular biology.

What is the mechanism underlying mitochondrial influence on behavior?
Mitochondria have long been hailed as the energetic powerhouses of the cell; however, the precise role of brain mitochondrial function on behavior and overall health has been largely overlooked. As the brain utilizes a disproportionate amount of the body’s energy compared to its size, it is clear that the functioning of its mitochondria should be critical to the overall health and well-being of the organism. We have previously identified a role for mitochondrial function in the Nucleus Accumbens in social dominance behavior. However, the precise mechanisms by which mitochondrial function exert control over social behavior is unknown. Here, using rodent models, we explore this question through mechanistic studies focused on potential links between mitochondrial networks, mitochondrial function in local synapses, and behavior.
Can mitochondrial function in the brain be programmed from environmental experiences?
Environmental enrichment, stress, and nutrition have all been known to induce neural transcriptional programming via epigenetic and/or circuit modulation. We have recently demonstrated how even a short-term nutritional intervention can modulate brain mitochondrial function, and subsequent behavior. Additionally, literature suggests the potential for peripheral metabolic programming via nutritional deprivation or enrichment. Using models of stress, enrichment, and/or nutritional interventions, we explore the potential for “neural metabolic programming” across various developmental time points, the subsequent behavioral consequences for the organism, and the underlying mechanism.
What is the role of mitochondrial function in neuropsychiatric disease?
Mitochondrial function has already been implicated in neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease, yet their role in mental health is still unclear. Furthermore, several neuropsychiatric diseases, such as depression and anxiety have systems-wide repercussions, suggesting that mitochondrial health could underlie their development. Using rodent models and cells from human patients, we examine how mitochondrial function in various brain regions and the periphery contributes and interacts with the environment in adulthood and during critical periods of development (e.g. the postpartum period in women), to potentially lead to the development of such diseases. We are also interested in investigating susceptibility to disease, and whether there are inherent differences in mitochondrial function that render one more or less prone to develop such pathologies as depression or anxiety disorders.


  • Guillot de Suduiraut I., Zanoletti O, Grosse J, Sandi C, and Hollis, F. 2020. Astrocytic release of ATP through type 2 inositol 1,4,5-triphosphate receptor calcium signaling and social dominance behavior in mice. Eur J Neurosci; 53: 2973– 2985.
  • Zalachoras I., Hollis F., Ramos E., Trovo L., Sonnay S., Geiser E., Preitner N., Steiner P., Sandi C., and Morato L. 2020. Therapeutic potential of glutathione-enhancers in stress-related psychopathologies. Neurosci Biobehav Rev; Jul;114:134-155. doi: 10.1016/j.neubiorev.2020.03.015.
  • Papilloud A., Weger M., Bacq A., Zalachoras I., Hollis F., Larrieu T., Battivelli D., Grosse J., Zanoletti O., Parnaudeau S., Tronche F., and Sandi C. 2020. The Glucocorticoid Receptor in the Nucleus Accumbens Plays a Crucial Role in Social Rank Attainment in Rodents. Psychoneuroendocrinology. 112, 104538 Feb 220. Doi: 10.1016/jpsyneuen.2019.104538
  • Rosina E., Battan B., Siracusano M., Di Criscio L., Hollis F., Pacini L., Curatolo P., Bagni C. 2019. Disruption of mTOR and MAPK Pathways Correlates with Severity in Idiopathic Autism. Trans Psychiatry. 9(1), 50.
  • Hollis F., Mitchell ES., Canto C., Wang D., and Sandi C. 2018. Medium chain triglyceride diet reduces anxiety-like behaviors and enhances social competitiveness in rats. Neuropharmacology. Aug;138:245-256.
  • van der Kooij MA*., Hollis F*., Lozano L., Zalachoras I, Abad S#, Zanoletti O, Grosse J, Guillot de Suduiraut I, Canto C. and Sandi C. 2018. Diazepam actions in the VTA enhance social dominance by activation of dopamine D1 receptors and mitochondrial function in the nucleus accumbens. Mol Psychiatry. 2018 Mar;23(3):569-578.
  • Hollis F*., Kanellopoulos AK*., and Bagni C. 2017. Mitochondrial dysfunction in Autism Spectrum Disorder: clinical features and perspectives. Curr Opin Neurobiol. 2017 Aug;45:178-187
  • Bendahan S., Goette L., Thoresen J., Loued-Khenissi L., Hollis F., and Sandi C. 2016. Acute stress alters individual risk taking in a time-dependent manner and leads to anti-social risk. Eur J Neurosci. Apr;45(7):877-885.
  • Hollis F*., van der Kooij MA*., Zanoletti O., Lozano L., Canto, C., and Sandi C. 2015. Mitochondrial function in the brain links anxiety with social subordination. PNAS, Dec 15, 112(50):15486-91. Featured on F1000Prime as exceptional breaking research.
  • Goette L., Bendahan S., Thoresen J., Hollis F., and Sandi C. 2015. Stress pulls us apart: anxiety leads to differences in competitive confidence under stress. Psychoneuroendocrinology 54;115-123.
  • Hollis F., and Kabbaj M. 2014. Social defeat as an animal model for depression. ILAR, 55(2): 221 32.

Find Dr. Hollis on Research Gate


Challenge the conventional. Create the exceptional. No Limits.