Reduced serial dependence suggests deficits in synaptic potentiation in anti-NMDAR encephalitis and schizophrenia

Heike Stein, Joao Barbosa, Mireia Rosa-Justicia, Laia Prades, Alba Morató, Adrià Galan-Gadea, Helena Ariño, Eugenia Martinez-Hernandez, Josefina Castro-Fornieles, Josep Dalmau and Albert Compte ()
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Heike Stein: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Joao Barbosa: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Mireia Rosa-Justicia: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Laia Prades: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Alba Morató: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Adrià Galan-Gadea: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Helena Ariño: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Eugenia Martinez-Hernandez: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Josefina Castro-Fornieles: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Josep Dalmau: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
Albert Compte: Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)

Nature Communications, 2020, vol. 11, issue 1, 1-11

Abstract: Abstract A mechanistic understanding of core cognitive processes, such as working memory, is crucial to addressing psychiatric symptoms in brain disorders. We propose a combined psychophysical and biophysical account of two symptomatologically related diseases, both linked to hypofunctional NMDARs: schizophrenia and autoimmune anti-NMDAR encephalitis. We first quantified shared working memory alterations in a delayed-response task. In both patient groups, we report a markedly reduced influence of previous stimuli on working memory contents, despite preserved memory precision. 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.

Date: 2020
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DOI: 10.1038/s41467-020-18033-3

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