MadSci Network: Neuroscience

Re: Long term memory

Date: Wed Jan 21 10:09:23 1998
Posted By: Brad Keele, Grad student Neuroscience Graduate Program
Area of science: Neuroscience
ID: 884046020.Ns

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 

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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