Longterm potentiation

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Long-term potentiation is the strengthening of synapses between two neurones due to persistent use; this is caused by a long lasting increasing signal transmission. Longterm potentiation is related to the increase in the number of receptors and their permeability to ions.

Glutamate is an excitatory neurotransmitter in the central nervous system which is released as a chemical messenger from the pre-synaptic membrane and binds to receptors on the post synaptic membrane[1]. N-methyl-D-aspartate receptor (NMDA receptor) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) are glutamate receptor and are crucial in the formation of synaptic plasticity. The AMPA channel is paired with an ion channel so that when glutamate binds to the receptor the ion channel is able to let sodium in this allows the depolarisation of the neuron axon[2]. The NMDA receptor is paired with an ion channel it allows calcium to move into the cell. During resting potential, the Ca2+ ion is blocked by a Mg2+ ion when glutamate binds to the NMDA receptor and the membrane is slightly polarised it allows the influx of Ca2+.

This leads to the activation of calcium/calmodulin-dependent protein kinase II (CaMKII) which leads to the phosphorylation of the AMPA receptor and increases the AMPA receptor conductance increasing their permeability to Na2+ in addition it also increase in the number of AMPA receptors therefore increases the excitability of the neurones[3].

References

  1. [Internet]. 2017 [cited 6 December 2017]. Available from: https://www.researchgate.net/figure/23974890_fig3_Figure-3-Noradrenergic-signalling-mechanisms-for-short-and-long-lasting-plasticityThe
  2. Long-Term Potentiation [Internet]. Biology-pages.info. 2017 [cited 2 December 2017]. Available from: http://www.biology-pages.info/L/LTP.html
  3. Lisman J, Yasuda R, Raghavachari S. Mechanisms of CaMKII action in long-term potentiation. 2017.
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