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Neurodevelopmental Disorders
 
March 14 - 18
Carlos B. Duarte (cbduarte@ci.uc.pt)

João Peça (jpeca@cnc.uc.pt)
PD in Experimental Biology and Biomedicine (PDBEB)
CNC - Center for Neuroscience and Cell Biology, University of Coimbra

Neurodevelopmental Disorders
Course 2016

March 14-18, 2016

Location CNC Auditorium (except on the 18th – to be determined)

Coordinators:
Carlos B. Duarte (cbduarte@ci.uc.pt)
João Peça (jpeca@cnc.uc.pt)

Lecturers:
Carlos B. Duarte, CNC and Dep Life Sciences, UC
João Peça, CNC and III, UC
Guiomar Oliveira, HP-CHUC, FMUC, UC
Ana Luísa Cardoso, CNC, UC
Catarina Gomes, IBILI, UC
Joana Guedes, CNC, UC
Gladys Caldeira, CNC, UC
Mohamed Edfawi, CNC, UC
Miranda Mele, CNC, UC
Ramiro Almeida, CNC, UC
Patrícia Monteiro, ICVS, Braga

March  14 PDBEB + MBCM
9.15h-9.30h: Structure of the course; Introduction of students and lecturers
9.30h-10.30h: Autism Spectrum Disorders – João Peça
11.00h-12.00h: Autism Spectrum Disorders – João Peça
14.00h-15.00h: Autism – Clinical Perspective – Guiomar Oliveira


March 15 PDBEB + MBCM
9.30h-10.30h: Epilepsy – Carlos Duarte
11.00h-12.00h: Epilepsy – Carlos Duarte
14.00h-15.00h: Animal models of Neurodevelopmental Disorders – João Peça


March 16 PDBEB
9.30h - 10.15h: Schizophrenia and TARPs – Gladys Caldeira
10.45h - 11.30h: Autism and mGluRs – Mohamed Edfawi
14:15h - 15:00h: Dysfunction of GABAergic synapses in status epilepticus:  changes in GABAA receptor dynamics - Miranda Mele

March  17 PDBEB
9.15h-10.00h: Microglia: the guardians of the brain – Ana Cardoso
10.30h-11.30h: Microglia main functions in protection and neuroinflammation – Ana Cardoso
12.00h-13.00h: Microglia in health, development and adulthood – Joana Guedes

14:15h-15:00h: ATP regulation of microglia activity during development in health and disease – Catarina Gomes
15:15- 16:00h: Neurodevelopment disorders: what’s the role of microglia? – Catarina Gomes


March  18 PDBEB
9.00h-10.00h: Development of the neuromuscular synapse – Ramiro Almeida
10.30h-11.30h: Motor neuron diseases – Ramiro Almeida

14.00h-15.15h: Synaptic and circuitry mechanisms of the basal ganglia– Patricia Monteiro
15:30h-16:30h: Adult restoration of Shank3 expression rescues selective autistic-like phenotypes Patricia Monteiro CNC Seminar


Student Assignment:
The students will individually write a grant proposal based on the results presented in an original paper. The grant proposal is 3 pages long and should include the following sections: a) State of the art; b) Objectives of proposal; 3) Proposed tasks and methodology. The students will meet with tutors throughout the week to discuss their ideas and approaches for the proposal.
Friday, April 1st, – Written grant proposal delivery.


Background Reading:

Lai, M.-C., Lombardo, M. V & Baron-Cohen, S. Autism. Lancet 383, 896–910 (2014).
Bourgeron, T., From the genetic architecture to synaptic plasticity in autism spectrum disorder.
Nat Rev Neurosci, 2015. 16(9): p. 551-63.

Peça, J., Feliciano, C., Ting, J. T., Wang, W., Wells, M. F., Venkatraman, T. N., … Feng, G. (2011). Shank3 mutant mice display autistic-like behaviours and striatal dysfunction. Nature, 472(7344), 437–42. doi:10.1038/nature09965

Mei, Y., Monteiro, P., Zhou, Y., Kim, J.-A., Gao, X., Fu, Z., & Feng, G. (2016). Adult restoration of Shank3 expression rescues selective autistic-like phenotypes. Nature, advance on. doi:10.1038/nature16971

Tabuchi, K. et al. A Neuroligin-3 Mutation Implicated in Autism Increases Inhibitory Synaptic Transmission in Mice. Science (80-. ). 318, 71–76 (2007).

Rothwell, P. E. et al. Autism-associated neuroligin-3 mutations commonly impair striatal circuits to boost repetitive behaviors. Cell 158, 198–212 (2014).

Yin, D. M. et al. Reversal of behavioral deficits and synaptic dysfunction in mice overexpressing neuregulin 1. Neuron 78, 644–657 (2013).

Devlin, A.-C. et al. Human iPSC-derived motoneurons harbouring TARDBP or C9ORF72 ALS mutations are dysfunctional despite maintaining viability. Nat. Commun. 6, 1–12 (1AD).

Gu, B. et al. A Peptide Uncoupling BDNF Receptor TrkB from Phospholipase C[gamma]1 Prevents Epilepsy Induced by Status Epilepticus. Neuron 88, 484–491 (2015).

Parkhurst, C. N. et al. Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor. Cell 155, 1596–1609 (2013).

Sekar, A. et al. Schizophrenia risk from complex variation of complement component 4. Nature 1–17 (2016). doi:10.1038/nature16549

Kreisel, T. et al. Dynamic microglial alterations underlie stress-induced depressive-like behavior and suppressed neurogenesis. Mol. Psychiatry 19, 699–709 (2014).

For Grant Proposal:
Marcos Gomes (marcosargomes@gmail.com)
Sekar, A. et al. Schizophrenia risk from complex variation of complement component 4. Nature 1–17 (2016). doi:10.1038/nature16549

Luís Martins (luisfmxiv@hotmail.com)
Mei, Y., Monteiro, P., Zhou, Y., Kim, J.-A., Gao, X., Fu, Z., & Feng, G. (2016). Adult restoration of Shank3 expression rescues selective autistic-like phenotypes. Nature, advance on. doi:10.1038/nature16971

João Amorim (jfilipe.aamorim@gmail.com)
Yin, D. M. et al. Reversal of behavioral deficits and synaptic dysfunction in mice overexpressing neuregulin 1. Neuron 78, 644–657 (2013).

M.ª Inês Martins (ines.martins@outlook.com)
Gu, B. et al. A Peptide Uncoupling BDNF Receptor TrkB from Phospholipase C[gamma]1 Prevents Epilepsy Induced by Status Epilepticus. Neuron 88, 484–491 (2015).
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