|MadSci Network: Neuroscience|
Hello Ray, You have asked a very important question, one that many in the field of psychology and neuroscience are asking. In fact, we've been asking this question for many years, and unfortunately, we don't have ONE all encompassing answer. From a neural network perspective, certain attributes of memories are brought to the level of consciousness and then the brain acts to fill in with greater detail. For instance, when asked to remember details about the kitchen of our youth, we may first recall Mom giving us a cookie then slowly fill in other information such as the arrangement of appliances, the pattern of tiles on the floor, and perhaps what pictures were hanging on the fridge. The brain has a marvelous ability to take a limited amount of input and use it to re-create a whole experience. In this manner, the memories, or memory traces, are stored in the neuronal circuitry or connectivity. Activating part of the circuit turns on other parts of the circuit until the (mostly) complete memory is recalled. So just how does this happen on a molecular/cellular/chemical level? One of the leading hypotheses today is that memory storage is the result of strengthening of the communication between two neurons. This has been termed "Long-Term Potentiation" or LTP. In a nutshell, LTP of synaptic transmission occurs when there is sufficient release of the transmitter glutamate that the post-synaptic neuron is excited to a threshold level that a critical receptor, the NMDA receptor, is activated and opens an ion channel. The NMDA receptor/ion channel complex is very permeable to calcium ions, and results in high intracellular concentration of calcium in the post-synaptic neuron. The calcium then signals several enzymes, such as protein kinase A (PKA) and protein kinase C (PKC), to become active. Calcium-calmodulin dependent protein kinase II (CaMKII) also plays an important role in establishing LTP. The critical function of these kinase enzymes is to attatch phosphate molecules (a process called phosphorylation) to cellular proteins that are involved in synaptic trasmission. The end result being an enhanced efficiency of synaptic transmission. Of course this is a very simplified version of the cellular processes of learning and memory. In fact, only recently, was enhanced synaptic transmission first shown to actually occur in a learning process. Also, I have left out very debatable influences of so-called "retrograde messengers" such as nitric oxidie (NO) and carbon monoxide (CO) that are reported to be released from the post-synaptic neuron and travel back to the presynaptic neuron to affect the transmitter release machinery. Also, there are influences of other transmitter systems, such as acetylcholine, serotonin and dopamine, which certainly play a role. Notably, disruption of acetylcholine transmission is at the heart of the neuropathology underlying Alzheimer's disease.
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