The Memory persistence laboratory
The Memory Persistence Laboratory is based in the School of Psychology at the University of Birmingham, UK, under the direction of Dr Jonathan Lee.
We are interested broadly in the question of how memories are built and maintained in such a way that they are both long-lasting and accurate. We actually investigate these questions in quite simple non-human animal (but also sometimes human) memory settings. Therefore, there is a focus on memories that, while basic and unconscious in nature, have an important impact upon behaviour. These include pavlovian* and instrumental** memories.
There are several reasons why our research is important. First, there is the fundamental importance of understanding memory processes. Second, and perhaps more important from a societal perspective, there is the potential that this greater knowledge of memory processes may lead to progress in the understanding and even treatment of disorders in which abnormally-powerful pavlovian and instrumental memories play an important role. In particular, treatment strategies based upon fundamental memory research have been applied to conditions such as posttraumatic stress disorder (PTSD), phobias and drug addiction. In PTSD and phobias, one aim of treatment is to weaken the memory link either between cues and the event(s) that may have precipitated the condition, or between the cues and the feeling and symptoms of anxiety. In drug addiction, one of the overriding problems for treatment is to prolong abstinence in the face of the potential for relapse induced by drug cues (think about the cravings that smokers used to get in pubs prior to the smoking ban; these were likely induced by exposure to many cues that had been linked to smoking previously in pubs).
Newly-acquired memories are not immediately stably stored in the brain. Rather, they require a period of memory consolidation in order to persist into the long term. However, even once the consolidation process is complete, this does not mean that the resultant memory is "fixed in stone". Memories need to be flexible and modified in order to remain useful and relevant. This is where reconsolidation may come in. The retrieval of a memory sometimes, but not always, renders that memory vulnerable to disruption. It seems that when a memory is retrieved it can become reactivated or destabilised, necessitating a reconsolidation process in order to restabilise it back into an inactive stable form. Therefore, memories can undergo cycles of destabilisation and reconsolidation.
It appears that this cycle of reactivation and reconsolidation may allow memories to be updated. We have shown this for the updating of contextual fear memory strength and content. Given that learning theories seek to explain the amount of learning that is accrued on a given trial, this can also be conceptualised as memory updating. Therefore, it may be possible to integrate our understanding of memory reconsolidation with concepts of learning theory. In particular, we have previously argued that the prediction error signal, which is hypothesised to regulate the magnitude of learning, may be critical for the triggering of memory destabilisation.
Other research focusses on the potential for targeting reconsolidation (and extinction) processes in the treatment of disorders such as phobias, posttraumatic stress disorder and drug addiction. All these disorders feature abnormally strong and persistent memories that might be diminished either by disrupting the reconsolidation of destabilised memories or by exploiting the updating nature of reconsolidation to modify beneficially the previously-maladaptive memory. We have previously demonstrated that cue-induced cocaine seeking can be reduced by interfering with the cue-cocaine memory. Moreover, we have shown that a reactivated light-food memory can be modified with extinction training (in a retrieval-extinction procedure) to reduce cue-induced food seeking. This retrieval-extinction approach is a new area of research and we are currently investigating its underlying mechanisms.
One of the constraints of research into memory reconsolidation is knowing how successfully to reactivate and destabilise a memory. Retrieving a memory is not always sufficient to destabilise it. Our current hypothesis is that there has to be some updating information present at memory retrieval in order to engage the reconsolidation process. Therefore, we are currently very interested in the so-called boundary conditions on memory reconsolidation; that is, when it does and does not take place. Several boundary conditions, such as the strength and age of a memory, have been described by us and others. In particular, we are interested in the apparent competition between reconsolidation and extinction. This question is particularly important as without knowing whether a retrieval session engages reconsolidation or extinction preferentially, attempts to disrupt reconsolidation and diminish a memory may instead impair extinction to preserve the memory. Conversely, interventions aimed at potentiating extinction to diminish a memory might instead enhance reconsolidation and make the memory stronger.
We have also recently focussed on whether instrumental memories undergo reconsolidation. We have shown that instrumental sucrose seeking memories do indeed undergo reconsolidation, and are currently seeking to extend this to models of instrumental drug seeking (e.g. cocaine & nicotine).
Leverhulme Trust Research Grant
"Stimulating the Destabilisation of Fear and Traumatic Memories"
3 yr; Oct 2015 – Sept 2018; £180k
MRC Responsive Mode Research Grant
"The Reconsolidation of Instrumental Cocaine Seeking Memories"
3 yr; July 2015 – June 2018; £605k
BBSRC Responsive Mode Research Grant
"Neural Mechanisms of Memory Updating"
3 yr; Oct 2013 – Sept 2016; £508k
Leverhulme Trust Research Project Grant
"Prediction Error and Memory Reconsolidation"
April 2011 - Mar 2014; £208k
MRC New Investigator Research Grant
"Neural Systems and Neurobiological Pathways Underlying Aversive Memories"
Mar 2009 - Feb 2012; £473k
Royal Society Research Grant
"Molecular Mechanisms of Fear Memory Reconsolidation and Extinction"
Oct 2007 - Sept 2008; £15k