# Synaptic plasticity / LTP

Synaptic plasticity is the activity-driven change in the strength of connections between your neurons. It is considered the cellular basis of learning and memory. The classic form is long-term potentiation (LTP). Bliss and Lomo first reported it in 1973, in the rabbit hippocampus, after high-frequency stimulation. In the hippocampus, LTP usually depends on the NMDA receptor. Here is the sequence. Strong activity depolarizes the neuron, which removes a magnesium block on NMDA receptors. Calcium then floods in and activates an enzyme (CaMKII). That inserts more AMPA receptors at the synapse, boosting its gain. Other mechanisms add to this: long-term depression, reshaping of dendritic spines, and 'metaplasticity'. NMDA-dependent LTP declines with age in rodents, and amyloid-beta clusters impair it. That links the loss of plasticity directly to Alzheimer's symptoms.

## Sources

- Bliss TV, Lomo T. (1973). Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. Journal of Physiology. https://doi.org/10.1113/jphysiol.1973.sp010273
- Bliss TV, Collingridge GL. (1993). A synaptic model of memory: long-term potentiation in the hippocampus. Nature. https://doi.org/10.1038/361031a0

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