A way to use computers to figure out how chemical pathways affect brain function on a large scale

The study introduces a computational method for brain simulations using mean-field models with biophysical foundations, focusing on membrane conductances and synaptic receptors. It demonstrates that anesthetics targeting GABAA and NMDA receptors can cause brain changes to generalized slow-wave patterns. The study demonstrates that slow-wave states are less sensitive to stimuli and have functional connectivity limited by anatomical connection, providing a robust framework for understanding molecular pharmacological actions on whole-brain dynamics. In order to support our ideas, we show that these slow-wave states are less sensitive to outside stimuli and have functional connectivity that is limited by anatomical connection, which is consistent with observations made in anesthetic states in other animals. Our method offers a strong framework for comprehending how pharmacological actions at the molecular level affect whole-brain dynamics since it is based on mean-field models that take molecular reality into account. The study simulates the molecular actions of general anesthesia, specifically ketamine and propofol, and investigates their effects at mesoscale and whole-brain levels. It focuses on slow-wave activity, reduced responsiveness to stimuli, and increased anatomical-functional correlations in anesthetized states.

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