A recently published paper in ‘Science’ magazine explores the way in which our long-term memories can be affected when they are recalled.

Past research has shown that following a fearful learning experience, there is a period of ‘consolidation’, during which the memory for that event can be disrupted by amnestic agents (substances that cause amnesia), or a physical injury such as a severe bang on the head. Previous theory held that following consolidation, a memory is stable and therefore resistant to the effects of amnestic agents.

This study shows; however, that a consolidated memory, when retrieved and reactivated (for example, placing a person back in the context where something frightening happened), can be disrupted again for a limited amount of time. The apparent similarity of this phenomenon to consolidation has led to it being termed ‘reconsolidation’.

In a paper, published this month in ‘Science’ magazine, by Jonathon Lee, Barry Everitt and Kerrie Thomas; the inhibition of the production of specific signalling proteins between cells was used to investigate the molecular basis of consolidation and reconsolidation within neurons of the hippocampus of the brain, a structure long known to be important for memory in animals and humans.

The protein, Brain Derived Neurotrophic Factor (BDNF), was shown to be required specifically for the consolidation, but not reconsolidation, of fear memories, whereas a different protein, Zif268, was only required for the reconsolidation, but not consolidation, of fear memories.

Professor Everitt, outlined the possibilities of these findings, said:

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