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brain-plasticity-cognifit

Many people believe in the materialistic explanation of consciousness, which demands that all functions of our mind take place into our brain. And even more people believe that the very basic problem of memory is one of the first that have been “solved”.

Right? Wrong.

Scientists do not know where exactly is memory located. To be exact, the more they look into the problem the more the tend to the conclusion that memory is not located somewhere in specific, but it is more something like “diffused” all over the brain. I have already mentioned in a previous article (Mind, Morphogenetic fields, Quantum physics…) about experiments conducted during which the scientists removed whole areas of the brain where memory seemed to be created, only to realize that the guinea pigs used still continued to remember what they were taught!

The chain of refutations of the abovementioned belief grew larger this week.

The up to now accepted theory that PKM-ζ plays a major role in the formation of long-term memory in the human brain, was found to be simply wrong.

Long-term potentiation (LTP), a well-characterized form of synaptic plasticity, has long been postulated as a cellular correlate of learning and memory. Although LTP can persist for long periods of time, the mechanisms underlying LTP maintenance, in the midst of ongoing protein turnover and synaptic activity, remain elusive.

Sustained activation of the brain-specific protein kinase C (PKC) isoform protein kinase M-ζ (PKM-ζ) has been reported to be necessary for both LTP maintenance and long-term memory. Inhibiting PKM-ζ activity using a synthetic zeta inhibitory peptide (ZIP) based on the PKC-ζ pseudosubstrate sequence reverses established LTP in vitro and in vivo. More notably, infusion of ZIP eliminates memories for a growing list of experience-dependent behaviours, including active place avoidance4, conditioned taste aversion, fear conditioning and spatial learning.

However, most of the evidence supporting a role for PKM-ζ in LTP and memory relies heavily on pharmacological inhibition of PKM-ζ by ZIP and conclusions that a “mechanism for memory” has been found were rather hasty. To further investigate the involvement of PKM-ζ in the maintenance of LTP and memory, scientists generated transgenic mice lacking PKC-ζ and PKM-ζ. They were suprised to found that both conventional and conditional PKC-ζ/PKM-ζ knockout mice showed NORMAL synaptic transmission and LTP at Schaffer collateral-CA1 synapses, and have no deficits in several hippocampal-dependent learning and memory tasks. (source: Nature 1, Nature 2)

May this be a constant reminder that finding a correlation between two elements does not mean nothing more that… there is a correlation between these two things. Jumping to conclusions like “A produced B” should be made with caution.

Memory which is not located anywhere specific and which remains functional even when we deactivate elements which seem actively related to it, can only mean one thing: the brain is just a receiver or a filter with access (better: limited access) to an immaterial field of information…

It sounds “crazy”.
So it must be true…

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