Neuroscience and Disease

Neuronal Circuits and Behavior

Autism Spectrum Disorder


Models of disease




João Peça


Research lines

Synaptic plasticity and autism

Early life stress and brain wiring

ProTeAN: Brain Organoids

Microglia and Neurodevelopment


Weighing an average of 1.3 kilograms, the human brain is a marvel of nature. Our brain has evolved to provide us with amazing sensory, emotional, memory and cognitive abilities. From an evolutionary perspective, it has even been argued that the most critical changes imposed on the human brain are directly linked to refinements in the “social brain”. Mammals use several brain regions to fully process and respond to social environments – from the senses, to memory of others and emotional centers, many regions are needed for the expression of social behaviors. As a consequence of this complexity, neuropsychiatric and neurodevelopmental disorders share impairments in social behaviors.

Our research aims to understand at the molecular, cellular and circuit levels, how genetics, environment and gene-environment interactions control neuronal circuit function in health and disease, with a specific focus on neurodevelopmental disorders and social behaviors. To achieve this goal, we use a combination of molecular genetics, behavior, electrophysiology and optogenetics techniques. Specifically, we develop both mouse and human cell-based models of disease to understand both the genetic and environmental components of neurodevelopmental diseases, with a special focus on the mechanisms that underlie behaviors reminiscent of these conditions.


Show less

Information about journal articles, updated at 28-11-2021, from platform CIÊNCIAVITAE.

The old guard: Age-related changes in microglia and their consequences

Jéssica Costa; Solange Martins; Pedro A. Ferreira; Ana M.S. Cardoso; Joana R. Guedes; João Peça; Ana L. Cardoso, 2021. Mechanisms of Ageing and Development. 111512 - 111512. 197. 2021. . 10.1016/j.mad.2021.111512 . Mechanisms of Ageing and Development

Regeneration of pulp-dentin complex using human stem cells of the apical papilla: in vivo interaction with two bioactive materials

Sequeira, Diana B.; Oliveira, Ana Rafaela; Seabra, Catarina M.; Palma, Paulo J.; Ramos, Carlos; Figueiredo, Maria H.; Santos, Ana C.; et al, 2021. Clinical Oral Investigations. 2021. . 10.1007/s00784-021-03840-9 . Clinical Oral Investigations

Ligand-independent activity of the ghrelin receptor modulates AMPA receptor trafficking and supports memory formation

Ribeiro, Luís F.; Catarino, Tatiana; Carvalho, Mário; Cortes, Luísa; Santos, Sandra D.; Opazo, Patricio O.; Ribeiro, Lyn Rosenbrier; et al, 2021. Science Signaling. 670. 14. 2021. . 10.1126/scisignal.abb1953 . Science Signaling

Galectin-3 in the Gut-liver axis Regulates Autistic-like Behaviors by Mechanism Associated with Cerebral Shank-3+ cell Niches in BALB/c Mice

Lemos, Filipe; Prins, Caio; Carpi-Santos, Raul; Waclawiak, Ingrid; Sofia, Santos; Bernardes, Emerson; Peça, João; et al, 2021. Preprint. 2021. submitted Preprint

Social subordination induced by early life adversity rewires inhibitory control of the prefrontal cortex via enhanced Npy1r signaling

Franco, Lara O.; Carvalho, Mário J.; Costa, Jéssica; Ferreira, Pedro A.; Guedes, Joana R.; Sousa, Renato; Edfawy, Mohamed; et al, 2020. Neuropsychopharmacology. 1438 - 1447. 9. 45. 2020. . 10.1038/s41386-020-0727-7 . Neuropsychopharmacology

Distinct subnetworks of the thalamic reticular nucleus

Li, Yinqing; Lopez-Huerta, Violeta G.; Adiconis, Xian; Levandowski, Kirsten; Choi, Soonwook; Simmons, Sean K.; Arias-Garcia, Mario A.; et al, 2020. Nature. 819 - 824. 7818. 583. 2020. . 10.1038/s41586-020-2504-5 . Nature

Social subordination induced by early life adversity rewires inhibitory control of the prefrontal cortex via enhanced Npy1r signaling

Franco, Lara Oliveira; Carvalho, Mário Jorge da Silva; Costa, Jéssica; Ferreira, Pedro; Sousa, Renato; Guedes, Joana; Edfawy, Mohamed; et al, 2020. Neuropsychopharmacology. 2020. under revision Neuropsychopharmacology

Constitutive ghrelin receptor activity modulates AMPA receptor traffic and supports memory formation

Ribeiro, L.F.; Catarino, Tatiana; Carvalho, Mário Jorge da Silva; Santos, Sandra; Cortes, Luisa; Opazo, P. O.; Ribeiro., L. R.; et al, 2020. bioRxiv . 2020. submitted bioRxiv

miRNA-31 Improves Cognition and Abolishes Amyloid-ß Pathology by Targeting APP and BACE1 in an Animal Model of Alzheimer’s Disease

Barros-Viegas, Ana Teresa; Carmona, Vítor; Ferreiro, Elisabete; Guedes, Joana; Cardoso, Ana Maria; Cunha, Pedro; Pereira de Almeida, Luís; et al, 2020. Molecular Therapy - Nucleic Acids. 1219 - 1236. 19. 2020. . 10.1016/j.omtn.2020.01.010 . Molecular Therapy - Nucleic Acids

New insights on synaptic dysfunction in neuropsychiatric disorders

Lima Caldeira, Gladys; Peça, João; Carvalho, Ana Luísa, 2019. Current Opinion in Neurobiology. 62 - 70. 57. 2019. . 10.1016/j.conb.2019.01.004 . Current Opinion in Neurobiology

Abnormal mGluR-mediated synaptic plasticity and autism-like behaviours in Gprasp2 mutant mice

Edfawy, Mohamed; Guedes, Joana R.; Pereira, Marta I.; Laranjo, Mariana; Carvalho, Mário J.; Gao, Xian; Ferreira, Pedro A.; et al, 2019. Nature Communications. 1. 10. 2019. . 10.1038/s41467-019-09382-9 . Nature Communications

Effects of a New Bioceramic Material on Human Apical Papilla Cells

Sequeira, Diana; Seabra, Catarina; Palma, Paulo; Cardoso, Ana; Peça, João; Santos, João, 2018. Journal of Functional Biomaterials. 4. 9. 2018. . 10.3390/jfb9040074 . Journal of Functional Biomaterials

Blue light potentiates neurogenesis induced by retinoic acid-loaded responsive nanoparticles

Santos, Tiago; Ferreira, Raquel; Quartin, Emanuel; Boto, Carlos; Saraiva, Cláudia; Bragança, José; Peça, João; et al, 2017. Acta Biomaterialia. 293 - 302. 59. 2017. . 10.1016/j.actbio.2017.06.044 . published Acta Biomaterialia

Functional Consequences of Mutations in Postsynaptic Scaffolding Proteins and Relevance to Psychiatric Disorders

Ting, Jonathan T.*; Peça, João*; Feng, Guoping, 2012. Annual Review of Neuroscience. 49 - 71. 1. 35. 2012. . 10.1146/annurev-neuro-062111-150442 . Annual Review of Neuroscience

Cellular and synaptic network defects in autism

Peça, J.; Feng, G., 2012. Current Opinion in Neurobiology. 866 - 872. 5. 22. 2012. . 10.1016/j.conb.2012.02.015 . Current Opinion in Neurobiology

Shank3 mutant mice display autistic-like behaviours and striatal dysfunction

Peça, J.; Feliciano, C.; Ting, J.T.; Wang, W.; Wells, M.F.; Venkatraman, T.N.; Lascola, C.D.; Fu, Z.; Feng, G., 2011. Nature. 437 - 442. 7344. 472. 2011. . 10.1038/nature09965 . Nature

Neuroscience: When lights take the circuits out

Peça, J.; Feng, G., 2011. Nature. 165 - 166. 7363. 477. 2011. . 10.1038/477165a . Nature

SnapShot: Autism and the synapse

Peça, J.; Ting, J.; Feng, G., 2011. Cell. 3. 147. 2011. . 10.1016/j.cell.2011.10.015 . Cell

Using Light to Reinstate Respiratory Plasticity

Arenkiel, Benjamin R.; Peça, João, 2009. Journal of Neurophysiology. 1695 - 1698. 4. 101. 2009. . 10.1152/jn.00009.2009 . Journal of Neurophysiology

Cortico-striatal synaptic defects and OCD-like behaviours in Sapap3-mutant mice

Welch, Jeffrey M.; Lu, Jing; Rodriguiz, Ramona M.; Trotta, Nicholas C.; Peca, Joao; Ding, Jin-Dong; Feliciano, Catia; et al, 2007. Nature. 894 - 900. 7156. 448. 2007. . 10.1038/nature06104 . Nature

In Vivo Light-Induced Activation of Neural Circuitry in Transgenic Mice Expressing Channelrhodopsin-2

Arenkiel, Benjamin R.; Peca, Joao; Davison, Ian G.; Feliciano, Catia; Deisseroth, Karl; Augustine, George J.; Ehlers, Michael D.; Feng, Guoping, 2007. Neuron. 205 - 218. 2. 54. 2007. . 10.1016/j.neuron.2007.03.005 . published Neuron

High-speed mapping of synaptic connectivity using photostimulation in Channelrhodopsin-2 transgenic mice

Wang, H.*; Peca, J.*; Matsuzaki, M.*; Matsuzaki, K.; Noguchi, J.; Qiu, L.; Wang, D.; et al, 2007. Proceedings of the National Academy of Sciences. 8143 - 8148. 19. 104. 2007. . 10.1073/pnas.0700384104 . Proceedings of the National Academy of Sciences



Pfizer Prize - Basic Science

We use cookies to improve your visit to our website.