Zap the Evil PTSD memory

Some years ago Your servant twisted his brain and came up with a scheme to lessen the strength of associative clues to PTSD provoking memory traces. This complex procedure consisted of collecting specific knowledge about the patients PTSD problem, checking out stress levels induced by different associative links by using HRV and GSR measurements and then switching to ERP measurements of specific visual (or auditive) stimuli to find when (and where using Loreta) the sources of the culprit networks would be. The general idea was that when one evokes memories (images, feelings) these memory traces are recalled from their stores and temporarily vulnerable to interfering interventions (fi rTMS) on the re encoding phase of the recall process. Literature in nature Neurosciences had shown this sequence to happen in order of 100-200 msec. Timed by the ERP sources a fast neuronavigated rTMS could zap it at that stage erasing it or probably lessen the associative strenght wich could the be measured (we do EBM over here) by reasseessing the HRV and GSR to cues again. Nice and elegant ? Although the idea looked worth pursuing (in the eye of the beholder) as it would allow specific personalized therapy it was also clear that this would be complex, involving lots of time and resources and would probably be way to costly to be used on a large base. When it became clear that propanolol also weakens the re encoding it the plan became again put on the drawing table. However the solution these authors came up with (in mice) is much better and way more elegant !! A very readable description of the whole strategy whereby CREB expressing neurons (learning neurons) are selectively botoxed out is found in this blog: NEUROTOPIA . A must read. Science 13 March 2009: Vol. 323. no. 5920, pp. 1492 - 1496 DOI: 10.1126/science.1164139 Reports Selective Erasure of a Fear Memory Jin-Hee Han,1,2,3 Steven A. Kushner,1,4 Adelaide P. Yiu,1,2 Hwa-Lin (Liz) Hsiang,1,2 Thorsten Buch,5 Ari Waisman,6 Bruno Bontempi,7 Rachael L. Neve,8 Paul W. Frankland,1,2,3 Sheena A. Josselyn1,2,3* Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased cyclic adenosine monophosphate response element–binding protein (CREB) are preferentially activated by fear memory expression, which suggests that they are selectively recruited into the memory trace. We used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning blocked expression of that fear memory. The resulting memory loss was robust and persistent, which suggests that the memory was permanently erased. These results establish a causal link between a specific neuronal subpopulation and memory expression, thereby identifying critical neurons within the memory trace.