The neurons in your brain work through sensory coding. That is, indormation is contained in the firing of neurons, representing what we percieve. Specific things, (ie: the faces, smells, buildings, movie) are represented in the IT cortex. These things are recognized in your brain by the neurons firing in a specific pattern for each specific stimulus. In other words, the recognition and memory of the waiter's face is done by your neurons firing in a specific pattern (say if the neurons were colored, the waiter is remembered when 4 blue, 3 yellow and one red neuron fire). When you think of the movie, another pattern of neurons fires(say, 3 blue, 3 yellow, and 2 red). These firing neurons are retrieving information from your LTM in the cerebral cortex. Hope that helps.
2007-03-03 06:33:48
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answer #1
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answered by Cait 2
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Wiki says:
Classification
There are several ways to classify memories, based on duration, nature and retrieval of information. From an information processing perspective there are three main stages in the formation and retrieval of memory:
Encoding or registration (processing and combining of received information)
Storage (creation of a permanent record of the encoded information)
Retrieval or recall (calling back the stored information in response to some cue for use in a process or activity)
[edit] Classification by duration
A basic and generally accepted classification of memory is based on the duration of memory retention, and identifies three distinct types of memory: sensory memory, short term memory and long term memory.
[edit] Sensory
Sensory memory corresponds approximately to the initial 200 - 500 ms after an item is perceived. The ability to look at an item, and remember what it looked like with just a second of observation, or memorization, is an example of sensory memory. With very short presentations, participants often report that they seem to "see" more than they can actually report. The first experiments exploring this form of sensory memory were conducted by George Sperling using the "partial report paradigm." Subjects were presented with a grid of 12 letters, arranged into three rows of 4. After a brief presentation, subjects were then played either a high, medium or low tone, cuing them which of the rows to report. Based on these partial report experiments, Sperling was able to show that the capacity of sensory memory was approximately 12 items, but that it degraded very quickly (within a few hundred milliseconds). Because this form of memory degrades so quickly, participants would see the display, but be unable to report all of the items (12 in the "whole report" procedure) before they decayed. This type of memory cannot be prolonged via rehearsal.
[edit] Short-term
Some of the information in sensory memory is then transferred to short-term memory. Short-term memory allows one to recall something from several seconds to as long as a minute without rehearsal. Its capacity is also very limited: George A. Miller, when working at Bell Laboratories, conducted experiments showing that the store of short term memory was 7±2 items (the title of his famous paper, "The magic number 7±2"). Modern estimates of the capacity of short-term memory are lower, typically on the order of 4-5 items, and we know that memory capacity can be increased through a process called chunking. For example, if presented with the string:
2007-03-03 14:31:37
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answer #2
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answered by Giggly Giraffe 7
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look up alan baddeley (spelling?) 'working memory model'. as far as i recall thats the most accepted model of how memory works. too detailed to go thru here (plus i can barely remember!!)
x
2007-03-03 14:27:49
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answer #3
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answered by third space 4
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There are numerous materials and theories regarding Human Memory. It ranges from the Molecular Biological Theory to Cognitive Theory .This is the Human Gene Theory which I think is more plausible. and directly answers your question.
National Health of Institute scientists have shown that a common gene variant influences memory for events in humans by altering a growth factor in the brain's memory hub. On average, people with a particular version of the gene that codes for brain derived neurotrophic factor (BDNF) performed worse on tests of episodic memory - tasks like recalling what happened yesterday.
They also showed differences in activation of the hippocampus, a brain area known to mediate memory, and signs of decreased neuronal health and interconnections. These effects are likely traceable to limited movement and secretion of BDNF within cells, according to the study, which reveals how a gene affects the normal range of human memory, and confirms that BDNF affects human hippocampal function much as it does animals'.
Long known to be critical for the growth and survival of neurons, BDNF has also recently been shown to play a key role in memory and hippocampal function in animals. To find out if it works similarly in humans, the researchers explored the consequences of a tiny variance in the human BDNF gene, where its molecular makeup differs slightly across individuals.
People inherit two copies of the BDNF gene -- one from each parent - in either of two versions. Slightly more than a third inherit at least one copy of a version nicknamed "met," which the researchers have now linked to poorer memory. It's called "met" because its chemical sequence contains the amino acid methionine in a location where the more common version, "val," contains valine.
They are finding that this one amino acid substitution exerts a substantial influence on human memory, presumably because of its effects on the biology of the hippocampus.
Despite its negative effect on memory, the "met" version's survival in the human genome suggests that it "may confer some compensatory advantage in other biological processes," note the researchers. Although they found that it does not confer increased susceptibility to schizophrenia, they suggest that the "met" variant might contribute to risk for - or increase functional impairment in -- other disorders involving hippocampal dysfunction, such as Alzheimer's disease or mood disorders.
Unlike other growth factors, hippocampal BDNF is secreted, in part, in response to neuronal activity, making it a likely candidate for a key role in synaptic plasticity, learning and memory. To explore possible mechanisms underlying the observed "met"- related memory impairment, the researchers examined the distribution, processing and secretion of the BDNF proteins expressed by the two different gene variants within hippocampal cells.
When they tagged the gene variants with green fluorescent protein and introduced them into cultured neurons, they discovered that "val" BDNF spreads throughout the cell and into the branch-like dendrites that form synapses, while "met" BDNF mostly clumps inside the cell body without being transported to the synapses. To regulate memory function, BDNF must be secreted near the synapses.
They were surprised to see that 'met' BDNF secretion can't be properly regulated by neural activity,
The observed memory decrements are likely traceable to the failure of "met" BDNF to reach the synapses, as well as its inability to secrete in response to neuronal activity, say the researchers.
Their study provides direct in vivo data that the molecular mechanisms related to activity dependent BDNF secretion and signaling, such as synaptic plasticity, may underlie humans' greatly expanded verbally-mediated memory system, just as it does for more rudimentary forms of memory in animals.
In following-up their leads, the researchers are searching for a possible BDNF connection with the memory problems and hippocampal changes of Alzheimer's disease, depression and normal aging.
2007-03-03 14:35:29
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answer #4
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answered by rosieC 7
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