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Synaptic Feedback Loop: Long-term Potentiation and Long-term Depression in Synapses

Note: Contained in the following post are notes on what I called the synaptic feedback loop. Any errors are mine. References are at the end of this entry to reduce any risk of misunderstanding. YMMV. SHK: 2010-05-27 09:02 AM

Feedback Loop for Synaptic Nerves

Long-term Potentiation (LTP)

  • long-lasting enhancement in signal transmission between two neurons (neuron pair)
  • results from stimulating neuron pairs synchronously
  • one of many phenomena underlying synaptic plasticity (the ability of chemical synapses to change their strength)
  • Theory: memories are encoded by modifying synaptic strength
  • LTP considered one of fundamental cellular mechanisms behind learning and memory

    hippocampus: learning and memory
  • located in medial temporal lobe (in the centre of the brain behind the temple)
  • enhances synaptic transmission
  • improves communication between presynaptic and postsyanptic neurons
  • predominantly carried out by improving postsynaptic cell's sensitivity to signals received from presynaptic cell

    LTP shares many features with long-term memory(LT memory), which makes it a strong candidate for cellular mechanism of learning i.e. to validate the biological model of learning.

  • Both LTP and LT memory:
    • triggered rapidly
    • dependent on sythesis of new proteins
    • has properties of associativity
    • lasts for many months
    LTP: accounts for many types of learning from realitively simple classical conditioning in animals to higher-level cognition in humans.
  • At cellular level, LTP enhances synaptic transmission
  • improves ability of two neurons (presnaptic and postsynaptic) to communicate with each other across a synapse

    Def. synapse: the junction between two neurons (axon-to-dendrite)

    How LTP is supposed to work: "enhanced communication is predominantly carried out by improving the postsynaptic cell's sensitivity to signals received from the presynaptic cell".

    How LTP probably works: communication is enhanced by a complex balance and change of neurotransmitter levels coupled with calcium and potassium ions as well as the catalytic and metabolic functions requiring iron, magnesium, selenium and other essential metallic ions, as well as chloride ions, all of which various proteins and enzymes need in order to be created, changed and destroyed.

    Signals from a presynaptic cell to its corresponding postsynaptic cell are carried by neurotransmitter molecules to neurotransmitter receptors on the surface of the postsynaptic cell.

    How LTP improves sensitivity of the postsynaptic cell to neurotransmitters is largely done as follows:
  • By increasing activity of existing receptors
  • By increasing number of receptors on postsynaptic cell surface

    Long-term Depression

    NOTE: This term is not related to the psychoneurosis known as depression in adolescence, nor is it associated with the immature paranoid-schizoid behaviors and mental cognition associated with younger children, as per M. Klein's theory of childhood development.

    Long-term depression (LT depression):
  • activity-dependent reduction in efficacy of neuronal synapses lasting hours or longer occurs in many areas of CNS
  • varying mechanisms involved
  • dependent on brain region and developmental progress
  • LT depression in cerebellum and hippocampus
  • best characterized i.e. researched
  • other brain areas also understood in terms of LT depression
  • LTD: found to occur different kinds of neurons which release various neurotransmitters
  • can result:
    1. from synaptic stimulation i.e. in cerebellar Purkinje cells (a class of GABAergic neurons located in the cerebellar cortex)
    2. from persistent weak synaptic stimulation (as in the hippocampus) - this is related to memory and learning
  • LTP opposes LTD
  • LTD results mainly from decreases in postsynaptic receptor density, with decrease in presynaptic neurotransmitter release also playing a role
  • Cerebellar LTD may be related to motor learning, according to the current hypothesis - but may also be related to body memory, i.e. to accurately perform a task without error and with efficiency after months of practice


    However, other plasticity mechanisms may influence motor learning.

    Hippocampal LTD can be important for removing old memory traces - IMHO in the same way computer data is backed up from hard drives, and unused documents files archived on backup tape. Hypothesis: old memory traces may be backed up in the store consciousness but this process is so mysterious, it may become a spiritual truism within Buddhism.

    Hippocampal and cortical LTD can be dependent on NMDA receptors, metabotrophic glutamate receptors (MGluR), or endocannaboids.

    LTD: one of several processes serving to selectively weaken specific synapses to ensure constructive use of synaptic strengthening caused by LTP.

    Why is this necessary? Because, if synapses continue increasing in strength, they would ultimately reach a ceiling level of efficiency, leading to inhibition of encoding of new information.

    IMHO Once synapses become limited in efficiency, memories would never be transfered from short-term memory (wherever they are stored) to long-term memory (in the hippocampus). Fatigue is a good example of when LTP leads to neurons reaching that ceiling level. It also explains why some people lose muscle strength after working for 4 hours or more, whether due to disease or lack of muscle mass.


    Yes, I know the links below don't go anywhere when clicked on. Understanding what I am saying requires effort on the gentle reader's part.


    LTD, LT depression:
    For more information about paranoid-schizoid and depressive positions, which are about psychological development of childhood, please look at
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