Academic Appointments

  • Basic Life Research Scientist, Biology

Professional Education

  • Doctor, University Paris XI, Neuroscience (2016)

Community and International Work

  • Volunteer Reviewer

    Partnering Organization(s)

    Ukrainian Global Univeristy

    Ongoing Project


    Opportunities for Student Involvement


All Publications

  • Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer's Disease. Genes Tan, N. A., Carpio, A. M., Heller, H. C., Pittaras, E. C. 2023; 15 (1)


    Alzheimer's disease (AD) is a neurodegenerative disorder that currently affects as many as 50 million people worldwide. It is neurochemically characterized by an aggregation of beta-amyloid plaques and tau neurofibrillary tangles that result in neuronal dysfunction, cognitive decline, and a progressive loss of brain function. TgSwDI is a well-studied transgenic mouse model of AD, but no longitudinal studies have been performed to characterize cognitive deficits or beta-amyloid plaque accumulation for use as a baseline reference in future research. Thus, we use behavioral tests (T-Maze, Novel Object Recognition (NOR), Novel Object Location (NOL)) to study long-term and working memory, and immunostaining to study beta-amyloid plaque deposits, as well as brain size, in hippocampal, cerebellum, and cortical slices in TgSwDI and wild-type (WT) mice at 3, 5, 8, and 12 months old. The behavioral results show that TgSwDI mice exhibit deficits in their long-term spatial memory starting at 8 months old and in long-term recognition memory at all ages, but no deficits in their working memory. Immunohistochemistry showed an exponential increase in beta-amyloid plaque in the hippocampus and cortex of TgSwDI mice over time, whereas there was no significant accumulation of plaque in WT mice at any age. Staining showed a smaller hippocampus and cerebellum starting at 8 months old for the TgSwDI compared to WT mice. Our data show how TgSwDI mice differ from WT mice in their baseline levels of cognitive function and beta-amyloid plaque load throughout their lives.

    View details for DOI 10.3390/genes15010047

    View details for PubMedID 38254938

  • Enhancing sleep after training improves memory in down syndrome model mice. Sleep Pittaras, E., Colas, D., Chuluun, B., Allocca, G., Heller, C. 2022; 45 (4)


    Down syndrome (DS) is a genetic disorder caused by the presence of all or part of the third copy of chromosome 21. DS is associated with cognitive disabilities, for which there are no drug therapies. In spite of significant behavioral and pharmacological efforts to treat cognitive disabilities, new and continued efforts are still necessary. Over 60% of children with DS are reported to have sleep apnea that disrupt normal sleep. Normal and adequate sleep is necessary to maintain optimal cognitive functions. Therefore, we asked whether improved quality and/or quantity of sleep could improve cognitive capacities of people with DS. To investigate this possibility, we used the Ts65Dn mouse model of DS and applied two methods for enhancing their sleep following training on mouse memory tasks. A behavioral method was to impose sleep deprivation prior to training resulting in sleep rebound following the training. A pharmacologic method, hypocretin receptor 2 antagonist, was used immediately after the training to enhance subsequent sleep knowing that hypocretin is involved in the maintenance of wake. Our behavioral method resulted in a sleep reorganization that decreased wake and increased rapid eye movement sleep following the training associated with an improvement of recognition memory and spatial memory in the DS model mice. Our pharmacologic approach decreased wake and increased non-rapid eye movement sleep and was associated with improvement only in the spatial memory task. These results show that enhancing sleep after the training in a memory task improves memory consolidation in a mouse model of DS.

    View details for DOI 10.1093/sleep/zsab247

    View details for PubMedID 35934511

  • Handling, task complexity, time-of-day, and sleep deprivation as dynamic modulators of recognition memory in mice. Physiology & behavior Gessner, N., Shinbashi, M., Chuluun, B., Heller, C., Pittaras, E. 2022: 113803


    Sleep is essential for optimal cognitive functioning. Although we lack a complete understanding of the role of sleep in memory consolidation, we know that various factors that disturb sleep or sleep quality have consequences for cognitive performance. Such factors can be unintended components of behavioral experiments on rodents and other experimental animals that generate differing results from different labs. These experimental variables include habituation to handling, intended or unintended sleep deprivation, task complexity, time of testing, and environmental features. We have examined how these variables impact recognition memory in C57BL/6 mice. Handled mice outperformed their non-handled counterparts across different combinations of delay phase duration and lighting conditions. Results also suggest that simple task recall is more resistant to diurnal variation and the impairing effects of sleep deprivation than is complex task recall. This study underscores the role of protocol and environmental factors in recognition memory and in conflicting results from different laboratories.

    View details for DOI 10.1016/j.physbeh.2022.113803

    View details for PubMedID 35398333

  • Inter-Individual Differences in Cognitive Tasks: Focusing on the Shaping of Decision-Making Strategies. Frontiers in behavioral neuroscience Pittaras, E., Hamelin, H., Granon, S. 2022; 16: 818746


    In this paper, we review recent (published and novel) data showing inter-individual variation in decision-making strategies established by mice in a gambling task (MGT for Mouse Gambling Task). It may look intriguing, at first, that congenic animals develop divergent behaviors. However, using large groups of mice, we show that individualities emerge in the MGT, with about 30% of healthy mice displaying risk-averse choices while about 20-25% of mice make risk-prone choices. These strategies are accompanied by different brain network mobilization and individual levels of regional -prefrontal and striatal- monoamines. We further illustrate three ecological ways that influence drastically cognitive strategies in healthy adult mice: sleep deprivation, sucrose or artificial sweetener exposure, and regular exposure to stimulating environments. Questioning how to unmask individual strategies, what are their neural/neurochemical bases and whether we can shape or reshape them with different environmental manipulations is of great value, first to understand how the brain may build flexible decisions, and second to study behavioral plasticity, in healthy adult, as well as in developing brains. The latter may open new avenues for the identification of vulnerability traits to adverse events, before the emergence of mental pathologies.

    View details for DOI 10.3389/fnbeh.2022.818746

    View details for PubMedID 35431831

  • Enhancing sleep after training improves memory in Down syndrome model mice. Sleep Pittaras, E., Colas, D., Chuluun, B., Allocca, G., Heller, C. 2021
  • Prolonged Consumption of Sweetened Beverages Lastingly Deteriorates Cognitive Functions and Reward Processing in Mice. . 00: 1–14. Cerebral Cortex Hamelin, H., Poizat, G., Florian, C., Bartosz Kursa, M., Pittaras, E., Callebert , J., Rampon , C., Taouis , M., Hamed, A., Granon, S. 2021

    View details for DOI 10.1093/cercor/bhab274

  • The Mouse Gambling Task: Assessing Individual Decision-making Strategies in Mice BIO-PROTOCOL Pittaras, E., Rabat, A., Granon, S. 2020; 10 (1)
  • Suprachiasmatic lesions restore object recognition in down syndrome model mice. Neurobiology of sleep and circadian rhythms Chuluun, B. n., Pittaras, E. n., Hong, H. n., Fisher, N. n., Colas, D. n., Ruby, N. F., Heller, H. C. 2020; 8: 100049


    The Ts65Dn mouse is a well-studied model of trisomy 21, Down syndrome. This mouse strain has severe learning disability as measured by several rodent learning tests that depend on hippocampal spatial memory function. Hippocampal long-term potentiation (LTP) is deficient in these mice. Short-term daily treatment with low-dose GABA receptor antagonists rescue spatial learning and LTP in Ts65Dn mice leading to the hypothesis that the learning disability is due to GABAergic over-inhibition of hippocampal circuits. The fact that the GABA receptor antagonists were only effective if delivered during the daily light phase suggested that the source of the excess GABA was controlled directly or indirectly by the circadian system. The central circadian pacemaker of mammals is the suprachiasmatic nucleus (SCN), which is largely a GABAergic nucleus. In this study we investigated whether elimination of the SCN in Ts65Dn mice would restore their ability to form recognition memories as tested by the novel object recognition (NOR) task. Full, but not partial lesions of the SCN of Ts65Dn mice normalized their ability to perform on the NOR test. These results suggest that the circadian system modulates neuroplasticity over the time frame involved in the process of consolidation of recognition memories.

    View details for DOI 10.1016/j.nbscr.2020.100049

    View details for PubMedID 32195448

    View details for PubMedCentralID PMC7075983

  • One week of chronic sleep debt does not affect decision-making processes in a mouse version of the Iowa Gambling Task. BioRxiv Pittaras, E., Granon , S., Rabat, A. 2019
  • Mouse Gambling Task reveals differential effects of acute sleep debt on decision-making and associated neurochemical changes. Sleep Pittaras, E., Callebert, J., Dorey, R., Chennaoui, M., Granon, S., Rabat, A. 2018


    Sleep loss is associated with sleepiness, sustained attention, and memory deficits. However, vulnerability of higher cognitive processes (i.e. decision making) to sleep debt is less understood. Therefore, a major challenge is to understand why and how higher cognitive processes are affected by sleep debt. We had established in mice correlations between individual decision-making strategies, prefrontal activity, and regional monoaminergic levels. Now, we show that acute sleep debt (ASD) disturbs decision-making processes and provokes brain regional modifications of serotonin and dopamine that could explain why ASD promotes inflexible and more risk-prone behaviors. Finally, we highlight, for the first time, that in a large group of healthy inbred mice some of them are more sensitive to ASD by showing inflexible behavior and decision-making deficits. We were also able to predict mice that would be the most vulnerable to ASD depending of their behavior before ASD exposure.

    View details for PubMedID 30304537

  • Dissociated features of social cognition altered in mice schizophrenia models: focus on social dominance and acoustic communication Neuropharm Faure, A., Nosjean, A., Pittaras, E., Duchene, A., Andrieux, A., Gaury-Faure, S., Charveriat, M., Granon, S. 2018; 159 (107334)
  • War pediatrics: epidemiologic characteristics of admissions on the critical care unit of the medical and surgical French hospital in Kabul. Anesthésie & Réanimation Salvadori, A., Pittaras, E., Pasquier, P., Merrat, S. 2017; 3(5):426-432
  • Nicotinic receptors are crucial for tuning of E/I balance in prelimbic cortex and for gambling performance in mouse. Frontiers in Psychiatry Pittaras, E., Faure, A., Leray, X., Moraitopoulou, E., Cressant, A., Rabat, A., Meunier, C., Fossier, P., Granon, S. 2016: 7:17.
  • Social behaviors and acoustic social communication in different strains of mice Behavioral Brain Research Faure, A., Pittaras, E., Nosjean, A., Chabout, J., Cressant, A., Granon, S. 2016; 320:383-390
  • Individual behavioral and neurochemical markers of unadapted decision-making processes in healthy inbred mice. Brain Struct Funct. Pittaras, E., Callebert, J., Chennaoui, M., Rabat, A., Granon, S. 2016; 221(9):4615-4629.
  • Mice gamble for food: individual differences in risky choices and prefrontal cortex serotonin . J Addict Res Ther. Pittaras, E., Cressant, A., Serreau, P., Bruijel, J., Dellu-Hagedorn, F., Callebert, J., Rabat, A., Granon, S. 2013; S4:011