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Thursday, September 27, 2007

How does short-term memory work in relation to long-term memory?


Interesting question in relation to Electroconvulsive therapy (ECT). Retrograde amnesia and anterograde amnesia can occur during an ECT course. The memory of some recent events can be lost due to ECT, some patients complain of forgetting recent events. This retrograde amnesia extends from shortly before ECT to events that occured during the illness episode.
That is why this is an interesting question. How is it possible that some memories are not consolidated. It takes time for a short-term memory to become long-term memory. The passage of time allows it to become resistant to interference from competing stimuli or disrupting factors such as a ECT treatment. Consolidation is the time-dependent process of stabilization, whereby our experiences achieve a permanent record in our memory.
This consolidation is explained on ask the expert from ScientificAmerican.com

Just a tip of veil:

Memory consolidation can occur at many organizational levels in the brain. Cellular and molecular changes typically take place within the first minutes or hours of learning and result in structural and functional changes to neurons (nerve cells) or sets of neurons. Systems-level consolidation, involving the reorganization of brain networks that handle the processing of individual memories, may then happen, but on a much slower time frame that can take several days or years.


More in dept information about changes on a molecular and neuron level can be found on the site of Chemical and Engineering News.

Forgetting is also discussed. Where did you park your car? Were are your keys?
BUT WHAT happens to memories that last for a while but aren't permanently retained?

Understanding of the process of forgetting is murky, and the proposed mechanisms are controversial. Some researchers believe certain parts of the brain employ "long-term depression" to clean the slate, so to speak. In the hippocampus, for example, long-term depression weakens connections between synapses that are only rarely stimulated. Under these conditions, glutamate binding to NMDA receptors on the postsynaptic membrane brings only a small number of calcium ions into the neuron. This small amount of calcium activates enzymes that dephosphorylate the receptors, making them less responsive to glutamate.

Long-term depression also reduces the number of AMPA receptors in the postsynaptic membrane. It also might alter the structure of synaptic connections between the neurons. The net result of these steps is to return the neuron to a state in which it's ready to receive new information.



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