• Thursday, September 17th 2020 at 16:00 - 17:00 UK (Other timezones)
  • General participation info   |   Participate online   |   + Phone in United States (Toll Free): 1 877 309 2073 United States: +1 (571) 317-3129 Australia (Toll Free): 1 800 193 385 Australia: +61 2 8355 1020 Austria (Toll Free): 0 800 202148 Belgium (Toll Free): 0 800 78884 Canada (Toll Free): 1 888 455 1389 Denmark (Toll Free): 8090 1924 France (Toll Free): 0 805 541 047 Germany (Toll Free): 0 800 184 4222 Greece (Toll Free): 00 800 4414 3838 Hungary (Toll Free): (06) 80 986 255 Iceland (Toll Free): 800 9869 Ireland (Toll Free): 1 800 946 538 Israel (Toll Free): 1 809 454 830 Italy (Toll Free): 800 793887 Japan (Toll Free): 0 120 663 800 Luxembourg (Toll Free): 800 22104 Netherlands (Toll Free): 0 800 020 0182 New Zealand (Toll Free): 0 800 47 0011 Norway (Toll Free): 800 69 046 Poland (Toll Free): 00 800 1213979 Portugal (Toll Free): 800 819 575 Spain (Toll Free): 800 900 582 Sweden (Toll Free): 0 200 330 905 Switzerland (Toll Free): 0 800 740 393 United Kingdom (Toll Free): 0 800 169 0432 Access Code: 731-636-357

A mechanistic understanding of core cognitive processes, such as working memory, is crucial to addressing psychiatric symptoms in brain disorders. I will present a combined psychophysical, electrophysiological and computational approach to the study of two symptomatologically related diseases, both linked to hypofunctional NMDARs: schizophrenia and autoimmune anti-NMDAR encephalitis. We found shared working memory alterations in a delayed-response task: a markedly reduced influence of previous stimuli on working memory contents, despite preserved memory precision. Electroencephalography measures revealed marked differences in the encoding of task parameters, including weaker memory traces between trials in patients. We then simulated this finding with NMDAR-dependent synaptic alterations in a microcircuit model of prefrontal cortex. Changes in cortical excitation destabilized within-trial memory maintenance and could not account for disrupted serial dependence in working memory. Rather, a quantitative fit between data and simulations supports alterations of an NMDAR-dependent memory mechanism operating on longer timescales, such as short-term potentiation.

 

 

 

 

 

 

 

Albert Compte
Group Leader
Brain Circuits and Behaviour Lab
IDIBAPS (Institute for Biomedical Research “August Pi i Sunyer”)
Barcelona, Spain

Albert Compte – Synaptic basis of reduced serial dependence in anti-NMDAR encephalitis and schizophrenia