Artificial Consciousness/Neural Correlates/Synaptic Models/link between Synaptic Function and Fibril Growth

The Link Between Synaptic Function and Fibril Growth
If, as Kandel and his contemporaries are correct, there is a link between synaptic function and Fibril Growth, that turns a volatile memory, into a long-term memory. If Sisson is right, there may be many intermediate stages of memory each with its own parallel molecular trace. At first this seems to counter the first statement, until you realize, that the only way the signal can be recieved by the neuron, is if it first passes through the synapse, before the molecular traces actually start work.

The extension of the memory, in all the molecular traces therefore must depend on the function of the synapse. However since we can't trace everything that is going on in any neuron let alone the complex mammalian neurons found in the human brain, we must accept that the memory traces we can find, are those that are triggered as a result, of discrete events that we can dissociate from each other.

Kandel's work depends on the traces found in the hippocampus neurons that have NMDA synapses. Some other researchers are working on Cerebral Cortex neurons where NMDA synapses are much rarer, but where S type synapses may be found. Some scientists have shown evidence that S synapses also share both calcium ion channel activity, and cAMP secondary messenger activity, suggesting that they may also have the same type of chemical cascade reaction as the NMDA synapses produce.

If so, the trigger for the various different molecular traces, may have a common origin, in the operation of one or the other of these two synapses. Here we get into trouble, in that, the nature of the interfaces between the various different traces is hard to map. Just as in modern technology we often use the same button, to trigger multiple different functions, it seems that the same synapse triggers multiple different memory functions. Which we get, depends on how the button is pushed. Figuring out how to translate complex patterns of synapse activation, is as yet beyond us, however separating the molecular traces is getting easier with the advent of bio-molecular tools like the knock-out gene, and our current level of sophistication in blocking traces so that we can dissociate them.

The primary task we must accomplish in order to convert a synaptic weight into a longer term memory, is simply, to detect the presence of an active synapse at a sensitive point in a molecular trace. The only tool we have discovered so far, for doing so, is the sequestering of protein tags, and the most important tags for this purpose are the survivable tags.

So we might expect, that the first stage in the chemical cascade reaction would be the release of more protein tag material for synapses to sequester. It is my belief that this step is common to most other types of memory we will find.

Once we have tagged the synapse, then we can use that tag as a trigger for other chemical reactions. at this point, I suspect the traces split, and each goes on to do its own thing. Two such traces might be a trace that does synaptogenesis, and a trace that does fibril growth. Each of these would require completely different DNA, and would require complex proteins to be built, and would take different time periods to complete, but there might be simularities such as each going through a cycle where first unused elements are absorbed, and then the tags are used to find which synapses are active, and steer development towards the most productive areas. Then new elements are created, and steered during their development to keep the relative cost of connection down. As a result, by the end of the various trace cycles, new connections would form between cells that at least marginally echoed the connections made at the synapse level, but with physical rather than ion channel based reinforcements. This fusion of Kandel, and Sisson's work, suggests how both of them could be correct, how there could be parallel traces, and yet how the end result would be the conversion of synaptic weights into physical connections based on a dialogue between the synapse and the genes. It should be easily testable that blocking the sequestering of survivable tags, blocks most traces and thus long-term memory. Any traces not blocked by this means can be thought not to be connected to long-term memory and may therefore be dissociated from it.