35-37 A study by Lee demonstrated that neurons use consolidation mechanisms the first time a memory is acquired. For subsequent modification of the memory, including strengthening of the memory, neurons engage reconsolidation to stabilize the strengthening of the memory.38,39 One implication from this study is that memories rely on reconsolidation mechanisms throughout their lifetime. The brain engages consolidation mechanisms only during Inhibitors,research,lifescience,medical the initial memory storage. Memory impairments induced
by blocking reconsolidation can be relatively memory-specific. Indeed, onlyreactivated memories will be impaired.40 From a therapeutic perspective, this means that when a patient is asked to recall, for example, a traumatic
memory and then given an reconsolidation blockage agent, only that memory and not others will be blocked from being reconsolidated (ie, restabilized). While most of the therapeutic tools at the psychiatrist’s disposal may have wide-ranging effects, the Inhibitors,research,lifescience,medical ability to target one memory at a time should be very good news for the field. Clinical implications of reconsolidation Why should clinicians care about the mechanisms mediating memory stabilization? Inhibitors,research,lifescience,medical As basic TSA HDAC concentration research scientists we need to explain how an understanding of the mechanisms of memory storage may shed light on the processes that maintain several mental disorders. The fact is that memory phases and mechanisms are thought to be common for synapses representing a memory, the dysfunctional synapses that Inhibitors,research,lifescience,medical contribute to many disorders.14 The finding that consolidated memories return to a labile state and have to be restored has significant implications for a number of clinical conditions such as post-traumatic stress disorder (PTSD),
addiction, obsessive-compulsive disorder (OCD), or delusions/hallucinations. Inhibitors,research,lifescience,medical An understanding of the mechanisms mediating reconsolidation could provide the basis for developing new or refining old therapeutic tools to successfully manage, if not cure, some of these conditions. As an example of how this could be applied, imagine a patient with PTSD whose symptoms were resistant to both drugs and psychotherapy. A new way of treating this condition could be to reactivate the patient’s traumatic memory and block its reconsolidation. Theoretically, this should lead Astemizole to a “cure” within a single session. Although finding a cure in the removal of a memory in a single session may sound worthy of fiction, early studies on humans using electroconvulsive therapy (ECT) demonstrates that this possibility may not be incompatible with real life. Franks and colleagues41,42 treated patients suffering from either hallucinations, delusions, major depression, or OCD. In contrast to other studies that administered ECT when the subjects were anesthetized, Rubin and colleagues kept the patients awake and directed them to focus on the objects of their compulsions or hallucinations.