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Review
. 2013 Jun;36(6):343-52.
doi: 10.1016/j.tins.2013.03.004. Epub 2013 Apr 18.

How to erase memory traces of pain and fear

Jürgen Sandkühler  1 , Jonathan Lee
Affiliations
Review

How to erase memory traces of pain and fear

Jürgen Sandkühler et al. Trends Neurosci. 2013 Jun.

Abstract

Pain and fear are both aversive experiences that strongly impact on behaviour and well being. They are considered protective when they lead to meaningful, adaptive behaviour such as the avoidance of situations that are potentially dangerous to the integrity of tissue (pain) or the individual (fear). Pain and fear may, however, become maladaptive if expressed under inappropriate conditions or at excessive intensities for extended durations. Currently emerging concepts of maladaptive pain and fear suggest that basic neuronal mechanisms of memory formation are relevant for the development of pathological forms of pain and fear. Thus, the processes of erasing memory traces of pain and fear may constitute promising targets for future therapies.

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Figures

Figure 1
Figure 1
Signalling pathways of long-term potentiation (LTP) consolidation and LTP reversal at C-fibre synapses. The schemes summarise elements of signalling pathways that are required for the maintenance of LTP at spinal C-fibre synapses. Thus, when any of these elements is blocked, established LTP diminishes or disappears (required elements for LTP consolidation, A). (B) summarises elements that, when activated, reverse established LTP. These sufficient elements for the reversal of LTP are underlined. Elements that are not underlined are required for the reversal of LTP. When blocked, these elements prevent the reversal of LTP by at least one of the sufficient elements. Blockers and activators of the respective elements were usually applied topically to the spinal cord. Many of the known signalling elements are expressed at more than one cellular site, as shown in the figure. The cellular sites of action are thus unknown in most cases. Suggested signalling pathways are indicated by arrows. Modified from .
Figure 2
Figure 2
Phases of fear memory and their modulation to reduce fear expression. Blue arrows/text represent normal memory processes; red arrows/text represent interventions to reduce fear expression. (A) Phases of fear memory. Consolidation of a memory after its acquisition (Acq) stabilises the long-term memory (LTM) and thereby increases memory expression. Mechanisms of memory maintenance enable the consolidated memory to persist. Reactivation of a LTM can lead to its destabilisation, necessitating a process of reconsolidation to restabilise the memory again into a persistent long-term form (post-reactivation LTM, PR-LTM). Exposure to fear stimuli in the absence of the aversive outcome results in extinction that suppresses memory expression. (B) Impairment of consolidation to erase fear memories. Interference with the cellular mechanisms that are required to consolidate a newly acquired memory can prevent the formation of LTM; the memory trace instead decays, leading to reduced memory expression. (C) Impairment of memory maintenance to erase fear memories. Interference with the cellular mechanisms of memory maintenance leads to rapid erasure of the memory and hence decay of memory expression. (D) Impairment of reconsolidation to erase fear memories. Interference with the cellular mechanisms of memory reconsolidation prevents a destabilised memory from being successfully restabilised; the destabilised memory instead decays, leading to reduced memory expression. (E) Enhancement of extinction as a compensatory mechanism to reduce fear. An extinguished memory normally recovers easily. However, pharmacological enhancement of extinction results in a persistent reduction in fear memory expression that appears not to recover.
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