Implicit memory uses presynaptic mechanisms and is an older system evolutionarily speaking. Explicit memory is a newer form of memory, using post synaptic mechanisms and is exclusively mammalian. It is exclusively mammalian because it is memory related to facts and events (semantic and episodic memory respectively) and so is a newer memory form, it also includes spatial memory. Implicit memory consists of motor memory and perceptual memory, it is habituation, sensitisation, classical conditioning and operant conditioning. If anyone ever has trouble working out if what you're looking at is implicit or explicit memory ask yourself 2 questions:
1. Is it conscious (explicit) or unconscious (implicit)- learned fear or kicking a ball is implicit. remembering where you left your keys or remembering which way to turn because you recognise the pub on the crossroads is explicit.
2. Which area of the brain is involved? if it is the hippocampus or medial temporal lobe it is explicit (hippocampus only found in newer species like mammals), if it is the cerebellum, reflex pathway (grabbing to stop falling) or the amygdala (fear and recognition (often mainly recognition of friend or foe in older species)) then it is implicit memory.
I am just going to talk about presynaptic plasticity with some images, I will then do another post for post synaptic. You are best off reading the previous post for all the information as these will just dive into the details of certain specifics. The other post will give you a more rounded understanding before reading these.
This image shows the basic action of the synapse, action potential depolarising the neuron opens calcium channels which act to release neurotransmitter from vesicles which diffuse to the post synaptic membrane, interact with receptors on sodium channels causing them to open and depolarise that neuron.
In implicit memory it is the presynaptic membrane that is altered. In the previous post I stated one alteration and explained how that was only short term memory, this would not be enough for implicit memory because it is only short term and I have said that presynaptic modifications are the only thing that cause changes to implicit memory.
This short term mechanism is the increase in vesicle fusion an therefore neurotransmitter release. What occurs is repeated stimulation of the presynaptic neuron depolarises a branch of that neuron enough that it depolarises a serotonergic interneuron. This interneuron has an output connection to the same presynaptic neuron that activated it but the connection terminates at the synapse with the post synaptic neuron (most likely a motor neuron). This interneuron is modulatory because under normal conditions it is not active, but upon repeated stimulation it becomes active and releases serotonin to the presynaptic terminal. The serotonin will bind to 5-HT4, 5-HT6 or 5-HT7 because all of these receptors for serotonin are Gs protein coupled receptors which activate Gs protein. A Gs protein once activated will increase the level of activated adenylate cyclase which catalyses the conversion of ATP to cAMP. cAMP binds to the regulator unit of protein kinase A allowing the catalytic unit to break free thus becoming active. The catalytic unit of PKA phosphorylates calcium channels which causes them to remain open longer thus allowing more calcium in. Calcium binds to synaptotagmin which allows synaptobrevin on the vesicle to bind to SNAP25 on the membrane causing vesicle fusion and so glutamate release. Increasing the level of calcium will cause it to bind to calmodulin, causing calmodulin to bind to Munc13 proteins to increase their interaction with syntaxin, increasing this interaction increases the number of primed vesicles meaning more vesicles ready t have calcium bind to syntaxin. The increased neurotransmitter release strengthens the synapse. However, phosphorylation is transient and all the activation of molecules is reversed over a period of minutes to hours.
Therefore what needs to happen is more high frequency stimulation of the presynaptic neuron to increase the serotonin release from the interneuron. When this happens it increases the level of activated protein kinase A so some of it can diffuse into the nucleus rather than going to phosphorylate calcium channels. Once in the nucleus PKA phosphorylates CREB, allowing it to bind to the promoter region at the cAMP response element site and allows CREB binding protein to bind to CREB. Once this has happened it acetylates the histones that make up the chromatin which loosens their interacting with the DNA making up the genes which makes it easier for RNA polymerase and transcription facotrs other than CREB to bind to the promoter region. This will happen in many genes which will ultimately cause the growth of new presynaptic terminals which strengthens the communication between the two neurons.
The image below shows how extensive this growth of new synapses is between a sensory (A and B) and motor (1 and 2) neuron after a memory has been formed.
This particular memory is the implicit memory type sensitisation. What has happened is in (A) and (1) an aplysia (type of sea snail) is sensing an innocuous touch (not harmful) to its siphon, it is then retracting its gill because of it (gill withdrawal reflex)
In (B) and (2) the siphon has been shocked with electricity (tactile/noxious stimulus) causing the gill to retract much further, then a few minutes later the siphon has had an innocuous touch applied (the gill retacts much further than before the shock) in (B) this process has been done repeatedly for a few days (for example) and this has caused the interneuron to release serotonin and CREB to be activated a lot which has caused the formation of many new synapses between the sensory neuron receiving the innocuous touch and the motor neuron causing the gill to withdraw. so when the siphon is just touched, many of these synapses are activated which repeatedly depolarises the motor neuron causing the gill to withdraw further than before. Therefore, fear has led to an increased response of the gill which has been remembered by having more synapses formed.
As you can see in (2) the motor neuron has increased synapse growth too, to match up to the presynaptic change. So when I said that in implicit memory on the presynaptic changes occur, technically I was lying, well sort of anyway. Because the post synaptic membrane will have small nubs coming off them, not by the active zone but in the areas close to the presynaptic neurons, and the membrane here will have proteins in them called neuroligin which extend out in to the extracellular matrix. When the growth occurs presynaptically the membrane will contain a protein called neurexin which reaches out into the ECM too. These two proteins interact which causes the post synaptic neuron to extend to that area creating a new synapse.
As an extra bit of information. Using an inhibitor of CREB stops all this growth and long term memory completely but the short term process involving PKA is unaffected.
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