PI3K/AKT/GSK3β/CRMP-2-mediated neuroplasticity in depression induced by stress.

Early neurodevelopmental dysplasia or disorder is an important stimulus for depression, but early stress can easily damage nerve development and lead to decreased neural plasticity. Because of the characteristics of nerve cell, nerve loop, structure instability and so on, stress can often lead to the occurrence and recurrence of depression. Stress is often associated with the release of inflammatory factors in the central nervous system. Recent studies suggest that neuroinflammatory factors are most likely involved in the occurrence and development of stress-induced depression, attacking neuronal cells through central inflammatory factors. The changes in neural plasticity, such as microtubule system of nerve scaffold, extension of axonal dendrites, regeneration of nerve junctions, disturbance of neurotransmitter synthesis, transmission and release, and abnormal synapses, cause abnormal transmission of information between nerve cells and cause symptoms of depression. The changes in the structure of neural stent microtubules are closely related to the neuroplastic damage of depression induced by stress. Our previous studies and current studies have found that the AKT/GSK3β/CRMP-2 pathway mediates the changes in neural stent microtubule plasticity. There is an interaction between central inflammatory factors and this pathway. Therefore, from the point of view of neuritis injury and the plasticity change of nerve scaffold, it can be concluded that after the activation and release of central inflammatory factor under stress, the possible mechanism of depression is mediated by the AKT/GSK3β/CRMP-2 pathway by changing the normal structure and function of the central nervous cell scaffold microtubule system.