The reconsolidation process results in a reactivated memory trace, which returns to a state of lability and must undergo consolidation once more if it is to remain in long-term storage. This process has enormous clinical

implications ranging from a greater understanding of traumatic remembrance to neural mechanisms affected by psychotherapy. The reconsolidation process involves Inhibitors,research,lifescience,medical NMDA receptors, β-adrenergic receptors, and requires cyclic AMP response element binding protein (CREB) induction.130 NM’DA receptor antagonists and β-receptor antagonists impair reconsolidation.127,131 The effect of the β-receptor antagonist, propranolol, Inhibitors,research,lifescience,medical is greater after memory reactivation than when administered

immediately after initial training. These results suggest that reactivation of memory initiates a cascade of intracellular events that involve both NMDA receptor and β-receptor activation in a fashion similar to postacquisition consolidation. This remarkable lability of a memory trace, which permits a reorganization of an existing memory in a retrieval environment, provides a theoretical basis for both psychotherapeutic and pharmatherapeutic intervention for Akt inhibitor anxiety disorders Inhibitors,research,lifescience,medical exacerbated by traumatic stress exposure. Administration of β-receptor and NM.DA receptor antagonists shortly after the initial trauma exposure as well as after reactivation of memory associated with the event may reduce the strength of the original traumatic memory. The effects of efficacious psychothcrapics on memory reconsolidation Inhibitors,research,lifescience,medical should be investigated. Extinction Extinction is a process defined

by Inhibitors,research,lifescience,medical a reduction in the conditioned fear responses. It forms the basis for exposurebased psychotherapies for the treatment of a variety of anxiety disorders, particularly those characterized by phobic behaviors. Individuals who show an ability to quickly attenuate learned fear through a powerful and efficient extinction processes may be less vulnerable to the development of anxiety disorders. They may also be less susceptible Adenylyl cyclase to the effects of intermittent exposure to fear stimuli, which can reinstate fear-conditioned learning. Considerable advancement has been made in our understanding of the neural circuitry mediating extinction. It has been established that the mPFC plays an important role in extinction. For example, destruction of the mPFC blocks recall of fear extinction,132,133 indicating that the mPFC might, store long-term extinction memory An inadequate level of activation of the mPFC after extinction might, lead to persistent fear responses.134 Individuals with the capacity to function well following states of high fear may be characterized by potent mPFC inhibition of amygdala responsiveness.