Investigators from MIT’s Picower Institute for Learning and Memory believe they have identified a molecular mechanism that might somehow be responsible for fear:
Li-Huei Tsai, Picower Professor of Neuroscience in the Department of Brain and Cognitive Sciences, and colleagues show that inhibiting a kinase (kinases are enzymes that change proteins) called Cdk5 facilitates the extinction of fear learned in a particular context. Conversely, the learned fear persisted when the kinase’s activity was increased in the hippocampus, the brain’s center for storing memories.
Cdk5, paired with the protein p35, helps new brain cells, or neurons, form and migrate to their correct positions during early brain development. In the current work, the MIT researchers looked at how Cdk5 affects the ability to form and eliminate fear-related memories.
“Remarkably, inhibiting Cdk5 facilitated extinction of learned fear in mice. This data points to a promising therapeutic avenue to treat emotional disorders and raises hope for patients suffering from post-traumatic stress disorder or phobia,” Tsai said.
Emotional disorders such as post-traumatic stress and panic attacks stem from the inability of the brain to stop experiencing the fear associated with a specific incident or series of incidents. For some people, upsetting memories of traumatic events do not go away on their own, or may even get worse over time, severely affecting their lives.
Treating these disorders involves methods geared toward making the behavior go away, or become extinct, but the molecular mechanisms underlying the extinction process are not well understood. However, Tsai said, studies have shown that some of the molecular machinery that initially encodes the troubling memories also regulates their extinction.
In the current work, genetically engineered mice received mild foot shocks in a certain environment and were re-exposed to the same environment without the foot shock. Mice with increased levels of Cdk5 activity had more trouble letting go–or extinguishing–the memory of the foot shock and continued to freeze in fear. Conversely, in mice whose Cdk5 activity was inhibited, the bad memory of the shocks disappeared when the mice learned that they no longer needed to fear the environment where the foot shocks had once occurred.
This research was published in the latest Nature Neuroscience.
Press release: MIT IDs mechanism behind fear …
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