Synaptic Plasticity - Theoretical Mechanisms

Theoretical Mechanisms

A bidirectional model, describing both LTP and LTD, of synaptic plasticity has proved necessary for a number of different learning mechanisms in computational neuroscience, neural networks, and biophysics. Three major hypotheses for the molecular nature of this plasticity have been well-studied, and none are required to be the exclusive mechanism:

1. Change in the probability of glutamate release.
2. Insertion or removal of post-synaptic AMPA receptors.
3. Phosphorylation and de-phosphorylation inducing a change in AMPA receptor conductance.

Of these, the first two hypotheses have been recently mathematically examined to have identical calcium-dependent dynamics which provides strong theoretical evidence for a calcium-based model of plasticity, which in a linear model where the total number of receptors are conserved looks like

where is the synaptic weight of the th input axon, is a time constant dependent on the insertion and removal rates of neurotransmitter receptors, which is dependent on, the concentration of calcium. is also a function of the concentration of calcium that depends linearly on the number of receptors on the membrane of the neuron at some fixed point. Both and are found experimentally and agree on results from both hypotheses. The model makes important simplifications that make it unsuited for actual experimental predictions, but provides a significant basis for the hypothesis of a calcium-based synaptic plasticity dependence.