LTPS

Long-Term Potentiation (LTP) is a persistent enhancement of synaptic transmission following specific patterns of activity. First described in the hippocampus by Bliss and Lomo in 1973, LTP is a form of synaptic plasticity considered a cellular mechanism underlying learning and memory. It is typically studied as an increase in synaptic strength between presynaptic and postsynaptic neurons after high-frequency or patterned stimulation.

Induction of LTP commonly requires a large, rapid influx of calcium into the postsynaptic neuron, usually through NMDA-type glutamate receptors. Calcium triggers signaling cascades, including activation of CaMKII and other kinases, leading to the phosphorylation and trafficking of AMPA receptors to the synapse. A distinction is made between early LTP (E-LTP), which lasts minutes to hours and does not require new protein synthesis, and late LTP (L-LTP), which can last days and depends on gene transcription and protein synthesis.

LTP has been observed in various brain regions, notably the hippocampus (CA1, CA3, dentate gyrus) but also in cortex, amygdala, and cerebellum. Different induction protocols can engage NMDA receptor-dependent forms or NMDA receptor-independent variants, underscoring heterogeneity in mechanisms.

Functionally, LTP is viewed as a cellular correlate of learning processes, including spatial navigation and memory formation. It is subject to modulation by neuromodulators and neurotrophins (e.g., BDNF) and can be disrupted by aging, stress, or disease. Some researchers emphasize that LTP is one of several plasticity mechanisms contributing to memory.

Experimentally, LTP is commonly measured as an increased field excitatory postsynaptic potential or slope in electrophysiological recordings following patterned stimulation. Pharmacological blockade of NMDA receptors or genetic manipulations can prevent LTP, illustrating its dependence on specific molecular pathways.