long-term potentiation

Dendrite spine synapses can have long-lasting changes {long-term potentiation} (LTP).

process

Presynaptic glutamate release activates N-methyl-D-aspartate (NMDA) postsynaptic receptors, causing Ca++ entry into postsynaptic neurons, which activates calcium/calmodulin protein kinase II (CaM kinase II), protein kinase C, and/or tyrosine kinase, which changes spine shape, synapse shape, or receptors. Perhaps, CaM kinase II adds AMPA receptors to postsynaptic membrane. Spine shape alteration exposes NMDA receptors and changes spine electrical properties. Short spine neck has high electrical resistance that amplifies depolarization. Lengthening neck permits increased Ca++ influx.

time

High-frequency hippocampus or cortex nerve stimulation increases synapse depolarization for hours {early LTP}, and, if repeated, up to weeks {late LTP}.

purposes

LTP aids space representation and affects spatial memory.

protein

Cell-membrane binding integrin protein maintains long-term potentiation and so aids memory.

locations

In hippocampus, Schaffer collateral pathway, from hippocampus region CA3 pyramidal cells to hippocampus region CA1, uses glutamate, is associative, and has post-synaptic NMDA receptor modulation. Hippocampus region CA3 pyramidal cells receive from dentate gyrus. Mossy fiber pathway, from dentate gyrus granule cells to hippocampus region CA3, uses glutamate, is non-associative, has norepinephrine interneuron modulation, and seems not to affect declarative memory. Dentate-gyrus granule cells receive from entorhinal cortex.

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4-Zoology-Organ-Nerve-Neuron-Physiology

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Date Modified: 2022.0224