Neural signatures of reduced serial dependence in anti-NMDAR encephalitis and schizophrenia

Serial dependence, a behavioral phenomenon where information from previous trials biases current trial reports, is pervasive in working memory tasks. There is growing interest in its mechanisms, and recent work has shown that individuals with schizophrenia and anti-NMDA receptor (NMDAR) encephalitis exhibit reduced serial dependence in simple delayed-response tasks. Modeling and experimental evidence suggest that serial dependence stems from the interplay between persistent neural activity and short-term synaptic plasticity in cortical circuits, with neural reactivations in between trials increasing serial dependence. A computational model that implements this hypothesis showed that a reduction in short-term plasticity, potentially due to NMDAR dysfunction, can replicate the observed reduction of serial dependence in patients with anti-NMDAR encephalitis and schizophrenia, compared with healthy subjects. Yet, its neurophysiological predictions remain untested. Here, we used electroencephalography (EEG) to test if these patient groups have reduced neural reactivations, as the model predicts. Our findings confirm the absence of memory reactivations in schizophrenia and anti-NMDAR encephalitis. We show that this result does not depend on motor-related activity. Further, while memory codes are specifically impaired in these patients, the perceptual component of the code is as robust as in healthy participants. Overall, we report empirical evidence supporting a mechanistic model of serial dependence, which links reduced neural reactivations with diminished serial dependence in neuropsychiatric disorders.