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Memory and the brain
How Memory Works
Forgetting and Amnesia

Help Linked Module: A New Functional Role for Cerebellar Long Term Depression

A Microprocessor That Simulates a Synapse

The precise role or roles that LTD plays in the manufacture of memories have yet to be determined. One thing is certain: it does not seem to be only the “opposite” of LTP. It might play a more active role than causing superfluous memories to be forgotten. Thus, we know that too little LTD diminishes certain types of memory.

Linked Module: Forebrain-specific calcineurin knockout selectively impairs bidirectional synaptic plasticity and working/episodic-like memory Researcher Module: Learning and Memory in Genetically Engineered Mice

Long-term depression (LTD) was discovered in the cerebellum in the early 1980s. Therefore, slightly less is known about its workings than about those of the other major mechanism of synaptic plasticity, long-term potentiation (LTP), which was discovered about a decade earlier. Scientists soon discovered, however, that LTD was not limited to the cerebellum and that it also occurred in the synapses of the cortex, the hippocampus, the corpus striatum, and other structures.

If LTD is so common, it is probably because it plays an essential role in memorization. The question is still open, however, as to whether LTD contributes directly to the storage of memories, as LTP does, or whether it simply makes us forget the traces of things we learned long ago so that we can learn new things. Some models of procedural memory, for example, postulate that the neural networks of the cerebellum become more efficient by “depressing” the synapses that have led to errors in learning motor behaviours.

Contrary to LTP, which is triggered by high-frequency stimulation of the synapses, LTD is produced by nerve impulses reaching the synapses at very low frequencies (1 to 5 Hertz). The synapses then undergo the reverse transformation from LTP: instead of becoming more efficient, the synaptic connections are weakened.

The reason for this difference comes from the differing effects that these two activation patterns have on the concentration of calcium ions inside the cell: LTP increases this concentration substantially, but LTD increases it by only a small amount. These differing concentrations of calcium in the cell activate different second messengers. In the case of LTP, the high calcium levels activate kinase proteins, while the small amount of calcium released by LTD activates phosphatases instead. It is these enzymes that modify the synapse to make it more or less efficient at relaying nerve impulses.

Interestingly, the same neurotransmitters (glutamate) and the same receptors (NMDA) are involved in both the large influx of calcium associated with LTP and the small influx associated with LTD. The forgetting generated by LTD is therefore just as active a process as LTP and employs, at least at the start of the cascade of chemical reactions, the same molecules.


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