"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.

"These findings show bidirectional behavioral plasticity after memory retrieval," Taylor said. "Moreover, we find that amygdalar PKA activation does not affect other memory processes after retrieval, including extinction of fear memory, further showing that our findings are specific for a reconsolidation process."

She said enhancement of reconsolidation may contribute to the development of maladaptive memories in psychiatric disorders such as post-traumatic stress disorder, depression and drug addiction.

"Additionally, the ability to strengthen memories by retrieval has important implications for psychotherapies," she said.

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