Abstract
Memories are fragile and easily forgotten at first, but after a consolidation period of hours to weeks, are inscribed in our brains as stable traces, no longer vulnerable to conventional amnesic treatments. Retrieval of a memory renders it labile, akin to the early stages of consolidation. This phenomenon has been explored as memory reactivation, in the sense that the memory is temporarily ‘deconsolidated’, allowing a short time window for amnesic intervention. This window closes again after reconsolidation, which restores the stability of the memory. In contrast to this ‘transient deconsolidation’ and the short-spanned amnesic effects of consolidation blockers, some specific treatments can disrupt even consolidated memory, leading to apparent amnesia. We propose the term ‘amnesic deconsolidation’ to describe such processes that lead to disruption of consolidated memory and/or consolidated memory traces. We review studies of these ‘amnesic deconsolidation’ treatments that enhance memory extinction, alleviate relapse, and reverse learning-induced plasticity. The transient deconsolidation that memory retrieval induces and the amnesic deconsolidation that these regimes induce both seem to dislodge a component that stabilizes consolidated memory. Characterizing this component, at both molecular and network levels, will provide a key to developing clinical treatments for memory-related disorders and to defining the consolidated memory trace.
©2011 by Walter de Gruyter Berlin New York
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Articles in the same Issue
- Imaging spatial learning in the brain using immediate early genes: insights, opportunities and limitations
- Silencing of CDK5 as potential therapy for Alzheimer’s disease
- The role of CREB signaling in Alzheimer’s disease and other cognitive disorders
- The positive impact of physical activity on cognition during adulthood: a review of underlying mechanisms, evidence and recommendations
- Representation of temporal sound features in the human auditory cortex
- Modulation of fear memory by retrieval and extinction: a clue for memory deconsolidation
- Adenosine 2A receptor: a crucial neuromodulator with bidirectional effect in neuroinflammation and brain injury
- Errata
- Anatomical reference frame versus planar analysis: implications for the kinematics of the rat hindlimb during locomotion
- Estradiol acts through nuclear- and membrane-initiated mechanisms to maintain a balance between GABAergic and glutamatergic signaling in the brain: implications for hormone replacement therapy