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Dr Kerrie Thomas 

Protein in the hippocampus.

Protein in the hippocampus.

Fresh memories need time to stabilise. The process of memory consolidation involves changes protein synthesis in a number of brain regions. These proteins contribute to the enduring synaptic and/or structural modifications that underlie the persistence of the memory trace in the face of an ever-changing brain. However, fully consolidated memories are far from being stable and resistant to disruption. When retrieved and reactivated, memories can be disrupted for a limited time and require reconsolidation to be maintained long term. With repeated recall stable memories can also undergo extinction leading to a decline a learned behavioural response. Like consolidation, reconsolidation and extinction are protein synthesis-dependent memory processes. The brain regions supporting the memory trace can also undergo reorganisation with time.

Using the inhibition of specific signalling proteins in the hippocampus, a structure important for memory in humans and animals, we were the first group to show that the molecular processes underlying long-term fear memory consolidation and reconsolidation are different. In addition, we have recently demonstrated that proteolysis of the pro-form of the neurotrophin BDNF is a key regulator in the consolidation and extinction of memory. This leads us to consider for the first time that the emerging data showing dissociations between molecular events underlying the formation of new memories and the reconsolidation or extinction after recall may be controlled by a single regulatory mechanism.

Heat map of 28 000 genes.

Heat map of 28 000 genes.

Currently our work aims to: -

  • Identify the genes regulated during memory processing using of large throughput profiling using Affymetrix microarray technology and qPCR.
  • Determine the processes that initiate the differential transcriptional programmes of the component memory processes using chromatin immunoprecipitation (ChIP) assays.
  • Investigate the role for several Schizophrenia-susceptibility genes in normal memory formation using a combination of correlational analysis using in situ hybridisation and targeted interference of protein expression with antisense and lentiviral technologies to show a causal link between genes and behaviour.
Amplification plot after qPCR.

Amplification plot after qPCR.



Understanding the molecular processes that support the formation of long-term memories and their maintenance after recall is a first key step in providing therapeutic targets for aberrant memory that can produce pathological behaviour in humans such as drug addiction, post-traumatic stress disorder chronic anxiety and phobias. Potentially novel molecular targets can be identified to provide therapies for these conditions.

Changes in the hippocampus after memory recall.

Changes in the hippocampus after memory recall.

One day we may be able to promote the extinction or to inhibit the reconsolidation of reactivated memories without affecting the acquisition of new memories or other non-recalled memories.


Royal Society Research Grant
“The role of BDNF in memory extinction”(£15 000).

BBSRC Responsive Research Grant, priority area “From Neurone to Behaviour” under the New Investigator Scheme. “The identification of independent molecular processes for the consolidation and reconsolidation of long-term memory in the hippocampus” (£264 000).

MRC Quota Studentship (2006-2009)


Dr Rosalind John, Genetics Group, School of Biosciences, Cardiff University
Prof John Aggleton, School of Psychology, Cardiff University
Dr Jeremy Hall, Department of Psychiatry, University of Edinburgh

Lab members

Dr Philip Barnes
Anne Kirtley