Science has moved away from considering memories to be simply long-term structural changes in the brain to seeing memories as the products of “continuous enzymatic activity” (Sacktor, 2007). Enzyme activity ceases after death, which could lead to memory destruction.
For instance, in a slightly unnerving study, Sacktor and colleagues taught mice to avoid the taste of saccharin before injecting them with a PKMzeta-blocking drug called ZIP into the insular cortex. PKM, an enzyme, has been associated with increasing receptors between synapses that fire together during memory recollection. Within hours, the mice forgot that saccharin made them nauseous and began guzzling it again. It seems blocking the activity of PKM destroys memories. Since PKM activity (like all enzyme activity) also happens to be blocked following death, a possible extension of this research is that the brain automatically “forgets” everything after death, so a simulation of your brain after death would not be very similar to you.
Accessing long term memory appears to be a reconstructive process, which additionally results in accessed memories becoming fragile again; this is what I believe is occurring here. The learned aversion is reconstructed and as then susceptible to damage much more than other non-recently accessed LTM. Consider that the drug didn’t destroy ALL of the mice’s (fear?) memories, only that which was most recently accessed.
simply long-term structural changes in the brain to seeing memories as the products of “continuous enzymatic activity”
Long-term structural maintenance requires continuous enzymatic activity. For example, the average AMPA receptor lasts only around one day: http://www.ncbi.nlm.nih.gov/pubmed/18320299. The actin cytoskeleton, made up of molecules which largely specify the structure of synapses, also requires continuous remodeling. If a structure is visibly the same after vitrification (not trivial), that means the molecules specifying it are likely to not have changed much.
Science has moved away from considering memories to be simply long-term structural changes in the brain to seeing memories as the products of “continuous enzymatic activity” (Sacktor, 2007). Enzyme activity ceases after death, which could lead to memory destruction.
For instance, in a slightly unnerving study, Sacktor and colleagues taught mice to avoid the taste of saccharin before injecting them with a PKMzeta-blocking drug called ZIP into the insular cortex. PKM, an enzyme, has been associated with increasing receptors between synapses that fire together during memory recollection. Within hours, the mice forgot that saccharin made them nauseous and began guzzling it again. It seems blocking the activity of PKM destroys memories. Since PKM activity (like all enzyme activity) also happens to be blocked following death, a possible extension of this research is that the brain automatically “forgets” everything after death, so a simulation of your brain after death would not be very similar to you.
http://www.nimh.nih.gov/science-news/2007/memory-sustaining-enzyme-may-help-treat-ptsd-cognitive-decline.shtml
Accessing long term memory appears to be a reconstructive process, which additionally results in accessed memories becoming fragile again; this is what I believe is occurring here. The learned aversion is reconstructed and as then susceptible to damage much more than other non-recently accessed LTM. Consider that the drug didn’t destroy ALL of the mice’s (fear?) memories, only that which was most recently accessed.
So no worries to cryonics!
Long-term structural maintenance requires continuous enzymatic activity. For example, the average AMPA receptor lasts only around one day: http://www.ncbi.nlm.nih.gov/pubmed/18320299. The actin cytoskeleton, made up of molecules which largely specify the structure of synapses, also requires continuous remodeling. If a structure is visibly the same after vitrification (not trivial), that means the molecules specifying it are likely to not have changed much.