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Origin of LongTerm Memory
28 Mar 15
Long-Term
Potentiation
Published by
The Neuromarketing Business Association
Werner A. Goerlich
How Long Term-Memory is Generated
Introduction to Short and Long-Term Memory
The human brain is capable to store a information for as little as thirty seconds, or a life time in Long-Term Memory.
As an example we could use what happens in the brain while studding - the process of studding leads to an
activation of a series of pathways, and the continuous activation of those pathways is what creates the memory of it.
The Hippocampus
The structure that is associated to long-term
memories is the hippocampus, as seen in the
image aside. It is a horseshoe shaped structure
with a external tip that has a size and shape similar
to a pea.
This horseshoe like structure, is found in both
sides of the brain and is located at the medial
temporal lobe and coordinates the storage and
retrieval of the memories.
Memory processing begins when signals from the
entorhinal cortex enter the hippocampus by a
substructure the Dental Gyrus which then proceed
trough the CA3 and CA1 areas, this is of particular
importance since the synaptic changes to store a
memory occur at that particular spot.
Substructures of the Hippocampus - Dental Gyrus, CA1 and CA3
The stimulus captured and processed and passed
to the hippocampus - via the nerve fibers from the
entorhinal cortex (ento - interior, rhino - nose,
entorhinal - interior to the rhinal sulcus) - is then
passed by the dental gyrus to the CA1 area, and
there on to the CA3. The neuroplasticity that has to occur, in order to
create a long-term memory, is situated at the
synoptical spaces between the CA1 and CA3 area.
Long-Term Potentiation (LTP)
The cellular and chemical underpinning of long
term memory, is contributed to a phenomenon
referred as Long-Term Potentiation (LTP). LTP occurs at the synaptical intersection of the
neurons from the CA3 area, known as the
Schaeffer-Collaterals, and the neurons of the
region located in the CA1 area.
The information/stimulus passes from the
entorhinal cortex, to the dental gyrus, trough the
CA3 region - making its run-through the SchaefferCollaterals - until the CA1 region, after that the
information is passed to the subiculum and then
back to the entorhinal cortex.
LTP has been most commonly been studied at the
CA3 neurons, at the Schaeffer-Collateral axons
and the CA1 pyramidal cells. Low and High Frequency Action Potentials and LTP
On the postsynaptic cells that receives
the stimulus of the Schaeffer-Collaterals
two main receptors, that are localized
together, are associated to the creation
of long term memories. The APMA receptor, that reacts to the
glutamate liberation as a result of a
potential passed trough the SchafferCollaterals, permitting the passing of
sodium ions (Na+) and the NMDA
receptor which is also permeable to
sodium ions, but has high permeability
to calcium (Ca 2+), but at this state is
blocked by magnesium (Mg 2+).
With a High Frequency Action Potential, which is comparable to long times of studying and memorization, the
increased the amount of glutamate liberation permits, not only the passing of sodium ions through the APMA
receptor, but a longer period -and therefor - concentration and depolarization of the synapses. This longer and higher depolarization displaces de magnesium ion that was obstructing the NMDA receptor, by
electromagnetic repulsion, to the synaptic interspace, allowing sodium and calcium enter through its pore.
Actual generation of Long-Term Memory
In the early case, caused by the higher concentration of calcium, the amount of APMA receptor is increased
preparing for a future higher concentration of calcium.
In the late case, the higher levels of calcium, increases the amount of Transcription Factors (CREB), ultimately
resulting in Gene Expression.
Gene Expression
The Transcription Factors increases the production of a variety of
proteins - some include APMA receptors, which are inserted into he
postsynaptic cell membrane at the synapse - others increase the
Growth Factor, involved in the formation of new synapses, which is the
basis of synaptic plasticity, as shown in the illustration.
The Learning and Changing Brain
Concluding, the memorization and learning process, is a grater bond between the CA1 and CA3 neurons. The late
changes can last for twenty-four hours to a life time.
It’s important to remember, that LTP is not a mechanism, but a outcome of the increased activity in two neurons, that
result of a increase of APMA receptors, strengthen the synaptic connection, which allows the low frequent action
potential a greater depolarization potential - This is the foundation of memory, however the hippocampus is not the
only region to act in the creation of memories, other parts including the cerebral cortex.
Activation of the pathways, continuous stimuli are ways to forge memories creating high frequency activation
potentials.
References
Netter MD, F. (2014). Atlas of Human Anatomy, Amsterdam, NX: Elsevier Inc
Royden Jones, J., Srinivasan, J., Allam, G., Baker, R. (2011). Netter’s Neurology, Toronto, ON: Saunders
Purves, D., Cabeza R., Huettel S., LaBar, K., Platt, M., Woldorff, M. (2012). Principles of Cognitive Neuroscience.
Duke, FL: Sinauer Associates, Inc
Rudy, J. W. (2013). The Neurobiology of Learning and Memory. Boulder, FL: Sinauer Associates, Inc
Blumenfeld, H (2011). Neuroanatomy Through Clinical Cases. Sunderland, Sinauer Associates, Inc
Published by The Neuromarketing Business Association
Author: Werner A. Goerlich