Month: June 2018

Om Reconsolidation:EMDR Therapy Mechanisms Explained by the Theory of Neural Cognition

EMDR/Mekanisme/Reconsolidation/ 2017 a

Stephanie Khalfa and Touzet CF

Eye Movement Desensitization and Reprocessing (EMDR) is a therapy of choice for post-traumatic stress disorder (PTSD). The mechanism of EMDR therapy is still unknown but it is hypothesized to favor memory reconsolidation. A new learning occurs relieved from the emotional load. Based on the Theory of neural Cognition (TnC), we propose an explanation of this phenomenon that implicates hebbian synaptic plasticity, i.e., long-term potentiation (LTP) and long-term depression (LTD). The new learning is mediated by the bilateral alternating stimulations (BAS) that are essential to the EMDR therapy. These repeated BAS modify the neural traces of a traumatic memory through the incorporation of newly activated cortical columns. These activated columns form a sparse coding representation of the situation called the global state of activation (GSA). Some of these added cortical activities will eventually crystallize in a column’s activation that is able to join the current GSA, making a new GSA, i.e., a stable network of activity. This process (trauma recall and BAS) is repeated several times, and each time, the activity of new columns is being added to the current GSA, until a GSAn totally cleared of its emotional content is obtained. Each GSA is a stable network of activity which gets reinforced thanks to LTP. Each time, a lessened traumatic memory is experienced. These modifications end up with a shift from the amygdalae’s involvement in the traumatic memory towards a more cognitive representation of the traumatic event, exempt from the previously associated strong negative feeling.

Memory Reconsolidation and Extinction Have Distinct Temporal and Biochemical Signatures

Mappe: Boundaties/2004 a

Akinobu Suzuki, 1 Sheena A. Josselyn, 3,4Paul W. Frankland,3,4 Shoichi Masushige,1,2 Alcino J. Silva, 4 and Satoshi Kid

Resummen:

Reonsolidation and extinction, two opposing processes triggered by memory retrieval, have distinct biochemical signatures: cannabinoid receptor 1 or L-type voltage-gated calcium channels blocks extinction but not reconsolidation. These studies demonstrate the dynamic nature of memory processing after retrieval and represent a first step toward a molecular dissection of underlying

Experimental extinction does not reflect forgetting of the original memory trace but rather reflects new learning.

Memory retrieval may initiate two potentially dissociable but opposite processes: reconsolidation and extinction. Re-consolidation acts to stabilize, whereas extinction tends to weaken, the expression of the original memory. The duration of a reminder event may be an important determinant of subsequent memory processing: brief reminders lead to reconsolidation, whereas longer reminders result in memory extinction (Debiec et al., 2002; Eisenberg et al., 2003; Pedreira and Maldonado, 2003).

There has been renewed interest in memory processing after retrieval: brief exposure to the CS seems to trigger a second wave of memory consolidation (reconsolidation), whereas prolonged exposure to the CS leads to the formation of a new memory that competes with the original memory (extinction)

We provided a systematic demonstration of how reexposure duration, the age of the memory, and the strength of the memory interact to influence behavior in tasks that model declarative memory.

The results presented here reveal three distinct timedependent phases of memory processing after memory retrieval. 

During the first phase, the retrieved memory is in a state that precedes both the reconsolidation and extinction processes. Further extending reexposure, however, initiates the protein synthesis-dependent reconsolidation processes required for the stability of the memory trace. Hence, blocking protein synthesis during this second phase compromises the long-term stability of the trace. Finally, prolonged reexposures to the CS in the absence of the US trigger the formation of a new memory trace that encodes the dissociation between the CS and the US (CS–no US; extinction memory), therefore competing with the original memory (CS–US). Inhibition of protein synthesis at this stage blocks the formation of this new extinction memory, leaving expression of the original memory unchanged. It is important to note that our results also indicate that there is an interaction between the extinction and reconsolidation processes: although blocking protein synthesis during short reexposures (reconsolidation) disrupts the original memory, blocking protein synthesis during prolonged reexposure, conditions in which both reconsolidation and extinction would be expected to be initiated, leaves the original memory unaffected.