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In working memory (WM) tasks, attractive biases to previous items are evidence for continuous temporal integration of memories. These serial biases have been modeled as a product of synaptic short-term plasticity, allowing WM representations to endure in a synaptic trace and interfere with the next trial even when neural activity returns to baseline values. We hypothesized that the NMDAR, a key component of both short-term potentiation (STP) and stable WM delay activity, would be of central importance to serial biases in a visuospatial WM task. Confirming this hypothesis, we found drastically reduced biases in patients with anti-NMDAR encephalitis and schizophrenia, both diseases that have been related to NMDAR hypofunction. We simulated serial biases in a spiking neural network supported by a Hebbian STP mechanism that builds up during persistent delay-activity. We found a close correspondence between patient and model behavior when gradually lowering levels of STP, suggesting a disruption of short-term plasticity in associative cortices of schizophrenic and anti-NMDAR encephalitis patients. Further, we explored the capability of the model to explain reduced biases in light of the disinhibition theory of schizophrenia.

NMDA-Receptor Dysfunction Disrupts Serial Biases in Spatial Working Memory