Notes
LTP, in short, relies on the successful activation of a ‘cell B’ in a network, either by a high-intensity stimulus or a summation of lower-intensity stimuli in rapid succession. In the synapse between A and B, this leads to an efflux of glutamate from the presynaptic cell, which bind to AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors on the postsynaptic membrane, causing an influx of sodium ions into cell B. The consequent change in potential in cell B, along with the presence of glutamate in the synapse, shifts a magnesium blockage in a second type of postsynaptic receptor, NMDA-R (N-methyl-d-aspartate receptor). NMDA-R subsequently becomes permeable to calcium ions, which crucially promote the activity of transcription factors, leading to the expression of more AMPA receptors (leading to increased synaptic efficiency) and nerve growth factors (leading to neurogenesis and increased dendritic density) (Bliss and Lomo 1970).
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Acknowledgements
I would like to thank Professor V Nanjundiah for supporting this work and providing critical advice at every stage, EL Swingler for her indispensable insight, and Professor H Sharat Chandra and the team at the Centre for Human Genetics in Bangalore for originally providing the opportunity to present these ideas.
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Bhat, A. Unraveling the mystery of cognitive reserve. J Biosci 40, 205–208 (2015). https://doi.org/10.1007/s12038-015-9511-y
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DOI: https://doi.org/10.1007/s12038-015-9511-y