When activated, a specific protein in the brain enhances long-term storage of fearful memories and strengthens previously established fearful memories, Yale School of Medicine researchers report this week in Nature Neuroscience.
"This report is the first to demonstrate evidence of enhancements in memory reconsolidation in the brain," said the senior author, Jane Taylor, associate professor in the Department of Psychiatry. "Understanding these molecular mechanisms may provide critical insights into psychiatric disorders."
She said recent data suggest that memories can continue to be changed or eliminated long after they have been formed, or consolidated. Based on findings that suggest memories are susceptible to loss after retrieval, a mechanism that is required to maintain and place back memories into long-term storage has been proposed, Taylor said.
"This 'reconsolidation' process is supported by studies suggesting that disruption of cellular functions known to be required for memory storage after retrieval of a memory can cause a specific loss of that memory," she said.
Taylor and her colleagues found that within the amygdala, a brain region known to be critically involved in the creation and storage of fearful memories, selective activation of protein kinase A (PKA) is sufficient to enhance memory reconsolidation and strengthen a previously established fearful memory. Conversely, inhibiting PKA in the amygdala disrupted memory reconsolidation.