João Peça

Prof. Dr. João Peça

University of Coimbra, Coimbra, Portugal
+1
orcid

Research Focus & Metrics

Academic Career Length

20Years (2007-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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20 March 2011 in Nature
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Journal Article
Open access
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João PeçaJoão Peça
João Peça
CFCátia Feliciano
Cátia Feliciano
JTJonathan T. Ting
Jonathan T. Ting
WWWenting Wang
Wenting Wang
MWMichael F. Wells
Michael F. Wells
GFGuoping Feng
Guoping Feng
Autism spectrum disorders (ASDs) comprise a range of disorders that share a core of neurobehavioural deficits characterized by widespread abnormalities in social interactions, deficits in communication as well as restricted interests and repetitive behaviours. The neurological basis and circuitry mechanisms underlying these abnormal behaviours are poorly understood. SHANK3 is a postsynaptic protein, whose disruption at the genetic level is thought to be responsible for the development of 22q13 deletion syndrome (Phelan–McDermid syndrome) and other non-syndromic ASDs. Here we show that mice with Shank3 gene deletions exhibit self-injurious repetitive grooming and deficits in social interaction. Cellular, electrophysiological and biochemical analyses uncovered defects at striatal synapses and cortico-striatal circuits in Shank3 mutant mice. Our findings demonstrate a critical role for SHANK3 in the normal development of neuronal connectivity and establish causality between a disruption in the Shank3 gene and the genesis of autistic-like behaviours in mice.

23 August 2007 in Nature
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Journal Article
Closed access
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JWJeffrey M. Welch
Jeffrey M. Welch
JLJing Lu
Jing Lu
RRRamona M. Rodriguiz
Ramona M. Rodriguiz
NTNicholas C. Trotta
Nicholas C. Trotta
João PeçaJoão Peça
João Peça
GFGuoping Feng
Guoping Feng

1 April 2007 in Neuron
Verified
Journal Article
Closed access
BABenjamin Arenkiel
Benjamin Arenkiel
João PeçaJoão Peça
João Peça
IDIan G. Davison
Ian G. Davison
CFCatia Feliciano
Catia Feliciano
KDKarl Deisseroth
Karl Deisseroth
GFGuoping Feng
Guoping Feng

8 May 2007 in Proceedings of the National Academy of Sciences
Verified
Journal Article
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HWH. Wang
H. Wang
João PeçaJoão Peça
João Peça
MMM. Matsuzaki
M. Matsuzaki
KMK. Matsuzaki
K. Matsuzaki
JNJ. Noguchi
J. Noguchi
GAG. J. Augustine
G. J. Augustine
To permit rapid optical control of brain activity, we have engineered multiple lines of transgenic mice that express the light-activated cation channel Channelrhodopsin-2 (ChR2) in subsets of neurons. Illumination of ChR2-positive neurons in brain slices produced photocurrents that generated action potentials within milliseconds and with precisely timed latencies. The number of light-evoked action potentials could be controlled by varying either the amplitude or duration of illumination. Furthermore, the frequency of light-evoked action potentials could be precisely controlled up to 30 Hz. Photostimulation also could evoke synaptic transmission between neurons, and, by scanning with a small laser light spot, we were able to map the spatial distribution of synaptic circuits connecting neurons within living cerebral cortex. We conclude that ChR2 is a genetically based photostimulation technology that permits analysis of neural circuits with high spatial and temporal resolution in transgenic mammals.

22 July 2020 in Nature
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Journal Article
Closed access
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YLYinqing Li
Yinqing Li
VLVioleta G. Lopez-Huerta
Violeta G. Lopez-Huerta
XAXian Adiconis
Xian Adiconis
KLKirsten Levandowski
Kirsten Levandowski
SCSoonwook Choi
Soonwook Choi
GFGuoping Feng
Guoping Feng

1 October 2012 in Current Opinion in Neurobiology
Verified
Journal Article
Open access
João PeçaJoão Peça
João Peça
GFGuoping Feng
Guoping Feng
Many candidate genes are now thought to confer susceptibility to autism spectrum disorders (ASDs). Here we review four interrelated complexes, each composed of multiple families of genes that functionally coalesce on common cellular pathways. We illustrate a common thread in the organization of glutamatergic synapses and suggest a link between genes involved in Tuberous Sclerosis Complex, Fragile X syndrome, Angelman syndrome and several synaptic ASD candidate genes. When viewed in this context, progress in deciphering the molecular architecture of cellular protein-protein interactions together with the unraveling of synaptic dysfunction in neural networks may prove pivotal to advancing our understanding of ASDs.