Team
REMEMBeR
Team leaders: Rampon Claire & Verret Laure
Presentation
Our team is interested in brain plasticity phenomena related to spatial and episodic memory in healthy mice or in models of pathology associated with memory dysfunctions. The aim of our research is to identify the plasticity processes induced by learning by studying them at different levels of brain function, ranging from the activity of neuronal networks (brain oscillations, synaptic plasticity, inhibitory functions) to cellular analysis (neurogenesis, neuronal morphology, neuron-glial cell interactions), biochemical (protein expression, neurotransmitter release, role of mitochondria) and molecular (epigenetic regulation, role of transcription factors). We are also studying these brain mechanisms in the context of Alzheimer’s disease, mood disorders and post-traumatic stress. Using mouse models of these diseases, we are also conducting projects aimed at assessing the therapeutic value of pharmacological or behavioral strategies.
Project 1
Alzheimer’s disease (AD) is the most common form of dementia in the elderly and is characterized by an inexorable loss of memory as well as other cognitive functions. Our team focuses on the mechanisms responsible for memory loss in AD. Using transgenic mouse models of AD, we study how the pathology affects hippocampal plasticity, from the network level down to the cellular level, with particular attention to forms of plasticity that are preserved despite the disease. We are also testing new behavioral and pharmacological approaches aimed at improving memory functions in AD-affected mice.
Our current projects are more specifically focused on:
– The mechanisms underlying physical activity-mediated attenuation of cognitive decline in Alzheimer’s disease (Claire Rampon, Fanny Rayssiguier, Sébastien Gauzin, Camille Lejards, collaboration with Cécile Malnou – Infinity Toulouse)
– The neural substrates of cognitive reserve (Laure Verret, Fanny Tixier)
– The involvement of mitochondrial dysfunction in adult born-neurons in cognitive impairment in Alzheimer’s disease. (Claire Rampon, Zahra Ghasemi-Abyazani, Sébastien Gauzin, Camille Lejards collaboration avec Pascale Belenguer et Laetitia Arnauné-Pelloquin, Minding Team CRCA).
– The mechanisms of recognition and social memory deficits in Alzheimer’s disease (Laure Verret, Claire Rampon, Lola Fauré, Sébastien Gauzin, Camille Lejards)
– Network dysfunctions in mouse models of Alzheimer’s disease (Laure Verret)
– Epilepsy and associated memory deficits in Alzheimer’s disease (Lionel Dahan, Cécile Merveillie, collaboration with Emmanuel Barbeau and Lionel Nowak – CerCo, Toulouse and Jonathan Curot and Luc Valton – CHU, Toulouse).
Project 2
Current theories of learning and memory suggest that they rely on Long-Term Potentiation (LTP), a mechanism that strengthens synaptic connections based on experience, occurring in the hippocampus. However, these theories do not explain why only certain events are remembered. Our recent work shows that dopamine neurons in the ventral tegmental area (VTA) trigger LTP in the hippocampus and enhance contextual learning. This supports the idea that dopamine acts as a “learning signal,” informing the hippocampus of which experiences should be remembered. We combine optogenetic, in vivo electrophysiology, dopaminergic transmission imaging, and behavioral approaches to address 3 questions:
1. What cellular and molecular mechanisms underlie dopamine-induced LTP? (Lionel Dahan, collaboration with Paula Pousinha, IPMC-Nice and Peter Vanhoutte, IBPS-Paris)
2. What types of events trigger dopamine release in the hippocampus and learning? (Lionel Dahan, collaboration with Yaroslav Sych INCI, Strasbourg)
3. Does dopamine contribute to learning-induced LTP? (Lionel Dahan)
Project 3
Long-term synaptic plasticity and memory formation depend on de novo gene transcription. Epigenetic modifications (via HDAC activity) and chromatin remodeling are key molecular mechanisms that regulate gene expression and memory consolidation in the hippocampus. Furthermore, our recent findings have shown that SIN3A, a scaffolding protein that can recruit different transcription factors, acts as an enhancer of long-term memory. In this project, we propose to understand how regulators of gene expression such as REST, SIN3A or HDAC, act during memory consolidation and age-related memory disorders. Our aim is to provide new insights into the role of epigenetic mechanisms in memory storage and to propose potential new targets for treating memory deficits. (Cédrick Florian, Camille Lejards, Sébastien Gauzin)
Team members
– Andraini T, Fauré LM, Mouledous L, Gauzin S, Ghasemi Z, Lejards C, Florian C, Belenguer P, Miquel MC, Rampon C. Targeting adult-born neurons to correct early deficits in pattern separation in the Tg2576 mouse model of Alzheimer’s disease. Neurobiol Dis. 2025 Oct 30;217:107158. doi: 10.1016/j.nbd.2025.107158. Epub ahead of print. PMID: 41175989.
– Bouisset G, Tixier FJ, Dupak T, Lejards C, Verret L. Enriched environment requires the remodeling of hippocampal perineuronal nets to trigger memory improvement in Alzheimer’s mouse model. iScience. 2025 Aug 12;28(9):113344. doi: 10.1016/j.isci.2025.113344. PMID: 40917885; PMCID: PMC12410357.
– Fauré LMP, Gauzin S, Lejards C, Rampon C, Verret L. Fine social discrimination of siblings in mice: Implications for early detection of Alzheimer’s disease. Neurobiol Dis. 2025 Mar;206:106799. doi: 10.1016/j.nbd.2025.106799. Epub 2025 Jan 13. PMID: 39814270.
– Bak C, Boutin A, Gauzin S, Lejards C, Rampon C, Florian C. Age-associated alteration of innate defensive response to a looming stimulus and brain functional connectivity pattern in mice. Sci Rep. 2024 Oct 25;14(1):25323. doi: 10.1038/s41598-024-76884-y. PMID: 39455881; PMCID: PMC11511918.
– B Szabo A, Sayegh F, Gauzin S, Lejards C, Guiard B, Valton L, Verret L, Rampon C, Dahan L. No major effect of dopamine receptor 1/5 antagonist SCH-23390 on epileptic activity in the Tg2576 mouse model of amyloidosis. Eur J Neurosci. 2024 Apr;59(7):1558-1566. doi: 10.1111/ejn.16268. Epub 2024 Feb 3. PMID: 38308520.
– Sayegh, F, Mouledous L, Macri C, Pi Macedo J, Lejards C, Rampon C, Verret L & Dahan L. Ventral tegmental area dopamine projections to the hippocampus trigger long-term potentiation and contextual learning. Nature Com, May 21;15(1):4100. doi: 10.1038/s41467-024-47481-4.
– Andraini T, Moulédous L, Petsophonsakul P, Florian C, Gauzin S, Botella-Daloyau M, Arrázola M, Nikolla K, Philip A, Leydier A, Marque M, Arnauné-Pelloquin L, Belenguer P, Rampon C, Miquel MC. Mitochondrial OPA1 Deficiency Is Associated to Reversible Defects in Spatial Memory Related to Adult Neurogenesis in Mice eNeuro. 2023 Nov 20;10(11):ENEURO.0073-23.2023 2023 Nov
– Coutens B, Lejards C, Bouisset G, Verret L, Rampon C, Guiard BP. Enriched environmental exposure reduces the onset of action of the serotonin norepinephrin reuptake inhibitor venlafaxine through its effect on parvalbumin interneurons plasticity in mice Transl Psychiatry. 2023 Jun 26;13(1):227. doi: 10.1038/s41398-023-02519-x 2023 Jun
– B Szabo A, Cattaud V, Bezzina C, Dard RF, Sayegh F, Gauzin S, Lejards C, Valton L, Rampon C, Verret L, Dahan L. Neuronal hyperexcitability in the Tg2576 mouse model of Alzheimer’s disease – the influence of sleep and noradrenergic transmission Neurobiol Aging. 2023 Mar;123:35-48. doi: 10.1016/j.neurobiolaging.2022.11.017 2023 Mar
– Rey CC, Robert V, Bouisset G, Loisy M, Lopez S, Cattaud V, Lejards C, Piskorowski RA, Rampon C, Chevaleyre V, Verret L. iScience. 2022 Feb Altered inhibitory function in hippocampal CA2 contributes in social memory deficits in Alzheimer’s mouse model. 9;25(3):103895. doi: 10.1016/j.isci.2022.103895.
Affiliation
