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Baddeley & Atkinson–Shiffrin Model of Working Memory

  • Thread starter Thread starter DeviationNormal
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DeviationNormal

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I think that processes of memory and structures associated with it are gonna get less and less compartmentalized as research goes on.. for example, a lot of Medial Temporal Lobe/Hippocampal research in last decade has shown its not just External Environment -> Perception -> Memory System [various models], but that structures in MTL are also involved in processing visual representations, not just storing and transferring them.


More specifically, I'd be interested to see how people view these new systems of understanding memory analogous to neurotransmitters and the interaction they may have with psychoactive substances.
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What do you mean exactly?
 
DeviationNormal said:
I am interested in personal feedback regarding these memory models. More specifically, I'd be interested to see how people view these new systems of understanding memory analogous to neurotransmitters and the interaction they may have with psychoactive substances. If this could circulate around the appropriate forums that'd be great.

http://en.wikipedia.org/wiki/Baddeley's_model_of_working_memory

http://en.wikipedia.org/wiki/Atkinson–Shiffrin_memory_model
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I get what you're saying. I could see how free memory on a computer hard drive could be similar to working memory of focus in the brain.
 
More specifically, I'd be interested to see how people view these new systems of understanding memory analogous to neurotransmitters and the interaction they may have with psychoactive substances.
Click to expand...

Not quite sure what you are getting at here? Baddeley and Hitch/Attkinson-Shiffrin models are not by any means "new understandings of memory", in the field of learning and memory I think these are considered as "classical" models :P. They are behavioural models that attempt to explain how memory works on a macro scale. Neurotransmitters and psychoactive substances are things that relate to memory function at the molecular/cellular level.

Long term potentiation (LTP) and long term depression (LTD) between synapses is what we currently think is the cellular correlate to behavioural level memory, although some forms of memory appear to not depend on these two processes. LTP can occur on short-term scale and also on long-term scale. Called early and late LTP. E-LTP can be induced quite simply by the presence of a strong stimulus whereas L-LTP is a bit more complex. How exactly we go from e-LTP (which lasts a few hours) to L-LTP (lasts from days to years) is still unclear. Synaptic tagging and capture model is the best bet we've got at the moment (http://en.wikipedia.org/wiki/Synaptic_tagging is a good place to start, more in depth references can also be found on there!).

As for neurotransmitters, the role NMDA receptors play in hippocampal memory is pretty undisputed. Obviously taking drugs like ketamine which block this type of receptor are going to cause inhibition of memory formatin. Dopamine and noradrenaline have been shown to be required to make the switch from E-LTP to L-LTP in the hippocampus, respectively messing with these systems can cause selective increase or decrease in memory retention... Cannabinoids are also involved in memory, more particularly they probably play a crucial role in forming and deleting emotionally charged memories. (I can probably find the original references for some of these statements if anyones really interested).
 
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