The article "P300 in Schizophrenia: Then and Now" provides a comprehensive review of the P300 component of the event-related potential (ERP) in the context of schizophrenia. The P300, a positive-going wave that peaks around 300 milliseconds, was initially described in 1965 as a measure of cognitive processes, particularly attention and context updating. Early studies found that P300 amplitude was reduced in individuals with schizophrenia compared to healthy controls, suggesting a cognitive deficit. This reduction in P300 amplitude has been replicated over the past 50 years and is considered a robust biomarker of schizophrenia. The article discusses the various subcomponents of P300, including P3b and P3a, and their psychological and neural underpinnings. P3b is elicited by infrequent target stimuli, while P3a is elicited by novel or salient distractor stimuli. Both subcomponents have been shown to be reduced in schizophrenia, with P3b being more consistently affected than P3a. Recent research has explored the role of P300 in predicting clinical outcomes, particularly in individuals at high risk for psychosis (CHR-P). Studies have found that reduced P3b amplitude in CHR-P individuals may predict future psychosis onset, while larger P3b amplitudes may indicate remission from psychosis. Additionally, P300 has been proposed as an endophenotype, linking genetic risk for psychosis to phenotypic expression. The article also examines the influence of stimulus probability and task parameters on P300, noting that P300 is more likely to be elicited when stimuli deviate from expected patterns. It highlights the importance of stimulus context and the ability to update context in individuals with schizophrenia, suggesting that P300 reductions reflect deficits in this process. Furthermore, the article discusses the potential of P300 as a biomarker for psychosis and its role in treatment development. It reviews studies using pharmacological challenges, such as ketamine, to model N-methyl-D-aspartate receptor (NMDAR) hypofunction, which is implicated in schizophrenia. These studies have shown that ketamine administration reduces P300 amplitude, supporting the NMDAR hypofunction model. Finally, the article suggests future directions for research, including the use of time-frequency analysis to better understand P300 dynamics and the exploration of P300 in rodent models to bridge the species gap. The authors emphasize the need for large-scale studies to replicate findings and establish the predictive utility of P300 in clinical settings.The article "P300 in Schizophrenia: Then and Now" provides a comprehensive review of the P300 component of the event-related potential (ERP) in the context of schizophrenia. The P300, a positive-going wave that peaks around 300 milliseconds, was initially described in 1965 as a measure of cognitive processes, particularly attention and context updating. Early studies found that P300 amplitude was reduced in individuals with schizophrenia compared to healthy controls, suggesting a cognitive deficit. This reduction in P300 amplitude has been replicated over the past 50 years and is considered a robust biomarker of schizophrenia. The article discusses the various subcomponents of P300, including P3b and P3a, and their psychological and neural underpinnings. P3b is elicited by infrequent target stimuli, while P3a is elicited by novel or salient distractor stimuli. Both subcomponents have been shown to be reduced in schizophrenia, with P3b being more consistently affected than P3a. Recent research has explored the role of P300 in predicting clinical outcomes, particularly in individuals at high risk for psychosis (CHR-P). Studies have found that reduced P3b amplitude in CHR-P individuals may predict future psychosis onset, while larger P3b amplitudes may indicate remission from psychosis. Additionally, P300 has been proposed as an endophenotype, linking genetic risk for psychosis to phenotypic expression. The article also examines the influence of stimulus probability and task parameters on P300, noting that P300 is more likely to be elicited when stimuli deviate from expected patterns. It highlights the importance of stimulus context and the ability to update context in individuals with schizophrenia, suggesting that P300 reductions reflect deficits in this process. Furthermore, the article discusses the potential of P300 as a biomarker for psychosis and its role in treatment development. It reviews studies using pharmacological challenges, such as ketamine, to model N-methyl-D-aspartate receptor (NMDAR) hypofunction, which is implicated in schizophrenia. These studies have shown that ketamine administration reduces P300 amplitude, supporting the NMDAR hypofunction model. Finally, the article suggests future directions for research, including the use of time-frequency analysis to better understand P300 dynamics and the exploration of P300 in rodent models to bridge the species gap. The authors emphasize the need for large-scale studies to replicate findings and establish the predictive utility of P300 in clinical settings.