long term potentiation (LTP)
Introduction
LTP is an activity-dependent synapse-specific increase in synaptic efficacy. It is long-lasting, persisting for days to weeks.
LTP is a form of neuronal plasticity that may form the basis for associative learning. It has been demonstrated in 3 major excitatory pathways in the hippocampus:
LTP occurs when a brief high frequency train of stimuli is applied to any of the 3 pathways above. The result is an increase in excitatory postsynaptic potential which may last days to weeks.
LTP has 3 important properties:
- cooperativity (more than 1 fiber must be activated to facilitate LTP)
- associativity* (Hebb's rule: LTP requires depolarization of the postsynaptic neuron coincident with activity of the presynaptic pathway)
- specificity (LTP is specific to the active pathway)
* LTP of the mossy fiber pathway may not be associative
Ca+2 influx through NMDA receptors is critical for induction of LTP; it is also necessary for LTP decay[2]. Phosphorylation/dephosphorylation at GluR1 of AMPA receptors may also play a role.[3]
In contast to LTD, high levels of intracellular Ca+2 are required for LTP.[3]
The voltage-gated K+ channels, K+ A channel & K+ D channel may participate in LTP through inhibition or termination of Ca+ influx.[4]
More general terms
Additional terms
- associative memory/learning (conditioning)
- hippocampal mossy fiber pathway
- learning
- NMDA receptor
- perforant pathway
- Schaeffer collaterals
References
- ↑ Principles of Neural Science, 3rd ed., Kandel, Schwartz & Jessell (eds), Elsevier, NY, 1991, pg 1019-21
- ↑ 2.0 2.1 Villarreal et al Nature neurosciences 5:48, 2001
- ↑ 3.0 3.1 3.2 Castellani GC, Quinlan EM, Bersani F, Cooper LN, Shouval HZ. A model of bidirectional synaptic plasticity: From signaling network to channel conductance. Learn Mem. 2005 Jul 18; [Epub ahead of print] PMID: https://www.ncbi.nlm.nih.gov/pubmed/16027175
- ↑ 4.0 4.1 Takagi H et al, Time-sharing contributions of A- and D-type K channels in EPSP integration at a model dendrite Neurosci Lett 1998, 254:164 PMID: https://www.ncbi.nlm.nih.gov/pubmed/10214983