Memory formation is a key brain feature in which our human nature relies. It is now clear that memories evolve over time. Upon learning, memories are initially labile and become stabilized by consolidation. Interestingly, reactivation of previous consolidated memories renders them in an active, unstable state and therefore susceptible to perturbation. If memory acquisition leads to the reactivation of a previously acquired memory, it is possible that different temporal events can re-enforce or interfere with each other. Recently, it was shown that novelty exposure, prior or after, weak training in a spatial recognition task, can lead to the formation of a long-term memory of the spatial recognition. This suggests a cooperative interaction in memory acquisition but leaves innumerous open questions. How are memory cooperation and competition orchestrated and what are the rules that determine whether a particular memory is re-enforced or lost by a new learning event? We are interested in understanding how memories evolve and the rules underlying this constant updating.
Cellular models of plasticity share similar features to memory acquisition. We found that long-lasting forms of plasticity, such as LTP and LTD, display synaptic cooperation and competition. Synaptic cooperation and competition rely on the distribution of plasticity-related proteins within activated synapses, similarly to memory cooperation. Our studies show that modulation of the actin cytoskeleton is involved in the capture of proteins in activated synapses necessary for the maintenance of LTP and LTD. We have also found that activation of CB1 endocannabinoid receptors can restrict the time window of synaptic cooperation in amygdala synapses. We are currently addressing the molecular mechanisms involved in synaptic cooperation and competition by using super-resolution imaging of actin and CaMKII in neurons. We are also addressing whether such cellular mechanism is involved in discriminative learning using amygdala-dependent behavioral tasks aiming to mirror synaptic rules into memory acquisition.
- First prize on Audio Slides from Elsevier - Endocannabinoid signaling and memory dynamics: A synaptic perspective.
2017-2020 Role: PI, “Synaptic competition and cooperation in reward learning: the role of hippocampal and prefrontal inputs to the nucleus accumbens” Bial Foundation
2017-2019 Role: PI, “Fear not to remember: Impact of acute stress in amygdala synaptic cooperation, NARSAD Young Investigator Grant, Brain and Behavior Research Foundation.
2016-2019 Role: PI, Rules of memory allocation: the role of actin dynamics in synaptic cooperation and competition, Fundação para a Ciência e Tecnologia (FCT – Portuguese Research Council).
2015-2018 Role: PI, The synaptic tag: a structural hypothesis, Fundação para a Ciência e Tecnologia.
- J Pinho, C Marcut, R Fonseca. Actin remodeling, the synaptic tag and the maintenance of synaptic plasticity. IUBMB life. 2020. 72 (4), 577-589.
- N Madeira, A Drumond, R Fonseca. Temporal Gating of Synaptic Competition in the Amygdala by Cannabinoid Receptor Activation. Cerebral Cortex. 2020. 30 (7), 4064-4075.
- Szabo, E., Manguinhas, R., Fonseca, R., (2016) “The interplay between neuronal activity and actin dynamics mimic the setting of an LTD synaptic tag” Scientific Reports
- Rosalina Fonseca (2016), “The aging memory: modulating epigenetic modifications to improve cognitive function” Review, Neurobiology of Learning and Memory, 133, pages 182-184.
- Drumond, A., Madeira, N., Fonseca, R., (2016), “Endocannabinoid signaling and memory dynamics: A synaptic perspective” Neurobiology of Learning and Memory", 2016
- Rosalina Fonseca (2015), "Synaptic cooperation and competition: two sides of the same coin? Chapter in book ”Synaptic Tagging and Capture. From Synapses to Behavior” Edited by Sajikumar, Sreedharan (Ed.).
- Rosalina Fonseca (2013) “Asymmetrical synaptic cooperation between cortical and thalamic inputs to the amygdala”, Neuropsychopharmacology, 38: 2675-2687;
- Rosalina Fonseca (2012) “Activity-dependent actin dynamics are required for the maintenance of long-term plasticity and for synaptic capture” EJN, 35:195–206.
- Becker N1, Wierenga CJ, Fonseca R, Bonhoeffer T, Nägerl UV (2008) “LTD induction causes morphological changes of presynaptic boutons and reduces their contacts with spines.”, Neuron, 60(4):590-7. doi: 10.1016/j.neuron.2008.09.018.
- Rosalina Fonseca, Ramunas M Vabulas, Tobias Bonhoeffer, U Valentin Nägerl (2006) “A balance of protein synthesis and proteasome-dependent degradation determines the maintenance of LTP” Neuron, 52: 239-245.
- Rosalina Fonseca, U Valentin Nägerl, and Tobias Bonhoeffer (2006) “Neuronal activity determines the proteins synthesis-dependence of late-phase LTP”, Nat Neuroscience, 9:478-480.
- Rosalina Fonseca, U Valentin Nägerl, Richard G.M. Morris and Tobias Bonhoeffer (2004) “Competing for memory: hippocampal LTP under regimes of reduced protein synthesis”, Neuron, 44: 1011-1020.
• Dr. U. Valentin Nägerl, Morphological aspects of synaptic plasticity, Synaptic Plasticity and Super-resolution Microscopy, Université de Bordeaux, France.
• Dr. Gal Richter-Levin, Cellular plasticity in a model of post-traumatic stress disorder, Haifa University, Israel.
• Dr. Stephen Martin, Division of Neuroscience, University of Dundee.
- FCT PhD Fellowship
Two projects proposals suitable for an application to a FCT PhD fellowship, under the supervision of Rosalina Fonseca from the Cellular and Systems Neurobiology Group, CEDOC, NMS. We aim to address the rules of memory dynamics, using electrophysiology, behaviour and optogenetic approaches. Learn more about these two positions here and here.
For additional information, please contact Rosalina Fonseca (rosalina.fonseca(at)nms.unl.pt)
- Motivated students (Undergraduate, Master and PhD) are encouraged to apply. Interested candidates, please send your CV, a letter explaining your interests and the name/contact information for 1-3 references to rosalina.fonseca(at)nms.unl.pt.