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1.  Rescue of long-term memory after reconsolidation blockade 
Nature Communications  2015;6:7897.
Memory reconsolidation is considered to be the process whereby stored memories become labile on recall, allowing updating. Blocking the restabilization of a memory during reconsolidation is held to result in a permanent amnesia. The targeted knockdown of either Zif268 or Arc levels in the brain, and inhibition of protein synthesis, after a brief recall results in a non-recoverable retrograde amnesia, known as reconsolidation blockade. These experimental manipulations are seen as key proof for the existence of reconsolidation. However, here we demonstrate that despite disrupting the molecular correlates of reconsolidation in the hippocampus, rodents are still able to recover contextual memories. Our results challenge the view that reconsolidation is a separate memory process and instead suggest that the molecular events activated initially at recall act to constrain premature extinction.
Recalled memories enter a labile state and are thought to be restabilized through reconsolidation. Here, the authors challenge the long-held notion that reconsolidation is a distinct memory process and demonstrate that the molecular events initiated at recall act instead to constrain premature extinction.
PMCID: PMC4532853  PMID: 26238574
2.  In the psychiatrist's chair: how neurologists understand conversion disorder 
Brain  2009;132(10):2889-2896.
Conversion disorder (‘hysteria’) was largely considered to be a neurological problem in the 19th century, but without a neuropathological explanation it was commonly assimilated with malingering. The theories of Janet and Freud transformed hysteria into a psychiatric condition, but as such models decline in popularity and a neurobiology of conversion has yet to be found, today's neurologists once again face a disorder without an accepted model. This article explores how today's neurologists understand conversion through in-depth interviews with 22 neurology consultants. The neurologists endorsed psychological models but did not understand their patients in such terms. Rather, they distinguished conversion from other unexplained conditions clinically by its severity and inconsistency. While many did not see this as clearly distinct from feigning, they did not feel that this was their problem to resolve. They saw themselves as ‘agnostic’ regarding non-neuropathological explanations. However, since neurologists are in some ways more expert in conversion than psychiatrists, their continuing support for the deception model is important, and begs an explanation. One reason for the model's persistence may be that it is employed as a diagnostic device, used to differentiate between those unexplained symptoms that could, in principle, have a medical explanation and those that could not.
PMCID: PMC2759333  PMID: 19321463
conversion disorder; hysteria; malingering; deception; factitious disorder
3.  Proteolysis of proBDNF Is a Key Regulator in the Formation of Memory 
PLoS ONE  2008;3(9):e3248.
It is essential to understand the molecular processes underlying long-term memory to provide therapeutic targets of aberrant memory that produce pathological behaviour in humans. Under conditions of recall, fully-consolidated memories can undergo reconsolidation or extinction. These retrieval-mediated memory processes may rely on distinct molecular processes. The cellular mechanisms initiating the signature molecular events are not known. Using infusions of protein synthesis inhibitors, antisense oligonucleotide targeting brain-derived neurotrophic factor (BDNF) mRNA or tPA-STOP (an inhibitor of the proteolysis of BDNF protein) into the hippocampus of the awake rat, we show that acquisition and extinction of contextual fear memory depended on the increased and decreased proteolysis of proBDNF (precursor BDNF) in the hippocampus, respectively. Conditions of retrieval that are known to initiate the reconsolidation of contextual fear memory, a BDNF-independent memory process, were not correlated with altered proBDNF cleavage. Thus, the processing of BDNF was associated with the acquisition of new information and the updating of information about a salient stimulus. Furthermore, the differential requirement for the processing of proBDNF by tPA in distinct memory processes suggest that the molecular events actively engaged to support the storage and/or the successful retrieval of memory depends on the integration of ongoing experience with past learning.
PMCID: PMC2532744  PMID: 18813339

Results 1-5 (5)