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. 2018 Mar 7;13(3):e0193410. doi: 10.1371/journal.pone.0193410

Fig 2. Block diagram of different parts of the proposed model.

Fig 2

External stimulation is followed by action potential generation in the presynaptic pyramidal neuron and the interneuron. Consequently, level of presynaptic calcium is elevated through two fast and slow mechanisms. Fast calcium oscillations are due to APs, and slow ones are because of IP3 production. Gliotransmitters activate mGlurs and contribute to slow calcium oscillations by IP3 production. Calcium enhancement results in glutamate release. Interneuron’s activation modulates GABA receptors in pyramidal neuron and is sensitive to the opioid receptor’s activation. Released glutamate reaches to the postsynaptic neuron and the astrocyte. The astrocyte releases gliotransmitter which affects presynaptic and postsynaptic neurons. Functions of AMPARs and NMDARs are considered in the postsynaptic neuron. Activation of the receptors enables CaMKII phosphorylation process. Exceeding phosphorylated CaMKII from a threshold leads to NO production which retrogrades to the presynaptic neuron. Finally, postsynaptic opioid receptors modulate NMDARs activation.