Roles of Gasotransmitters in Synaptic Plasticity and Neuropsychiatric Conditions

Figure 1

Transmission of signals through the synaptic junctions. Signals or impulses at the presynaptic terminal trigger the release of glutamate that binds to glutamate receptors at the postsynaptic membrane. Activation of α-amino-3-hydroxy-5-methyl-isoxazole-4-propanoic acid (AMPA) as well as kainate receptors which subsequently transport sodium ions that trigger postsynaptic depolarization. As membrane potential changes, it initiates the release of magnesium ions which blocks N-methyl-D-aspartate (NMDA) receptors. Influx of calcium via NMDA channels sets off a chain of events which establish long-term potentiation. Kainate receptors at the presynaptic end also seem to facilitate synaptic transmission at particular synapses by accumulating neurotransmitter release.