Re: How do we learn?

	The capacity of the nervous system to undergo change continues 
throughout life.  This capacity is referred to as neural plasticity.  It is 
thought that learning (i.e. the process by which the nervous system 
acquires new information) is mediated by carefully regulated changes in the 
strength of existing synapses.
	Changes in the strength of synaptic transmission between connected 
neurons are widely believed to underlie changes in perceptual and 
behavioral function experienced during development and learning.  Long-term 
potentiation (LTP) of synaptic strength, seen widely in the central nervous 
system, is the dominant experimental model for use-dependent synaptic 
learning. The most well-studied synaptic pathway exhibiting LTP is in the 
hippocampal area CA1.  This pathway has been implicated in the storage of 
declarative perceptual memories( memories that are available to the 
conscious mind as opposed to procedural memory which are not available to 
the conscious mind such as the ability to ride a bicycle) in humans and 
spatial learning in rodents.  The most extensively studied form of LTP 
requires the activation of postsynaptic N-methyl-D-aspartate (NMDA) type 
glutamate receptors.  The influx of Ca2+ ions through NMDA receptors 
triggers a partly understood cascade of enzyme activity which results in a 
long-term strengthening of the synapse. The above is a partial explanation 
of how we can take information and store it, in essence how we learn, at 
the molecular level. Namely a stimulus leads to firing of neurons and 
release of neurotransmitter which can bind to the NMDA-receptor and lead to 
Ca2+ influx and setting of a cascade that leads to LTP. How we retrieve the 
information later on is much more of a mystery at this point.

References
Neuroscience 1997 Edited by Purves et al. Published by Sinauer associates 
inc. Sunderland, MA.