On synaptic plasticity: Modelling molecular kinases involved in transmitter release

The neurotransmitter release depends, in principal, on two neuronal events. One is the influx of Calcium in the active zone due to polarization, and the other is the amount of fusion available neurotransmitter vesicles. We state a model of the phosphorylation of the Synapsins (I and II), which creates a pool of fusion available vesicles. The exocytosis of vesicles is stated by Calcium on and off rates, modelling the complex of the fusion pore. The aim here is to model paired pulse facilitation due to phosphorylation of the Synapsins, and post-tetanic potentiation due to increased kinetic activity of the cAMP complex. In addition we show that the regulation of fusion competent vesicles in post-tetanic potentiation is highly correlated to Calcium residues released by organelles, i.e Calcium buffering.