Researchers have identified a protein necessary to maintain behavioral flexibility, which allows us to modify our behaviors to adjust to circumstances that are similar, but not identical, to previous experiences. Their findings, which appear in the journal Cell Reports, may offer new insights into addressing autism and schizophrenia—afflictions marked by impaired behavioral flexibility.
Our stored memories from previous experiences allow us to repeat certain tasks. For instance, after driving to a particular location, we recall the route the next time we make that trip. However, sometimes circumstances change—one road on the route is temporarily closed—and we need to make adjustments to reach our destination. Our behavioral flexibility allows us to make such changes and, then, successfully complete our task. It is driven, in part, by protein synthesis, which produces experience-dependent changes in neural function and behavior.
However, this process is impaired for many, preventing an adjustment in behavior when faced with different circumstances. In the Cell Reports study, the researchers sought to understand how protein synthesis is regulated during behavioral flexibility.
To do so, they focused on the kinase PERK, an enzyme that regulates protein synthesis. PERK is known to modify eIF2α, a factor that is required for proper protein synthesis. Their experiments involved comparing normal lab mice, which possessed the enzyme, with those that lacked it.
In their study, the mice were asked to navigate a water maze, which included elevating themselves onto a platform to get out of the water. Normal mice and those lacking PERK learned to complete this task.
However, in a second step, the researchers tested the mice's behavioral flexibility by moving the maze's platform to another location, thereby requiring them to respond to a change in the terrain. Here, the normal mice located the platform, but those lacking PERK were unable to do so or took significantly more time to complete the task.