Abstract
Acute stress results from sudden short-term events, and individuals need to quickly adjust their physiological and psychological to re-establish balance. Chronic stress, on the other hand, results in long-term physiological and psychological burdens due to the continued existence of stressors, making it difficult for individuals to recover and prone to pathological symptoms. Both types of stress can affect working memory and change cognitive function. In this study, we explored the impact of acute and chronic stress on synaptic modulation using a biologically inspired, data-driven rodent prefrontal neural network model. The model consists of a specific number of excitatory and inhibitory neurons that are connected through AMPA, NMDA, and GABA synapses. The study used a short-term recall to simulate working memory tasks and assess the ability of neuronal populations to maintain information over time. The results showed that acute stress can enhance working memory information retention by enhancing AMPA and NMDA synaptic currents. In contrast, chronic stress reduces dendritic spine density and weakens the regulatory effect of GABA currents on working memory tasks. In addition, this structural damage can be complemented by strong connections between excitatory neurons with the same selectivity. These findings provide a reference scheme for understanding the neural basis of working memory under different stress conditions.