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Fig. 5. Guanylyl cyclase, a soluble NO receptor, binds to NO and, through cGMP-mediated signaling, functions as either a pre- or post-synaptic messenger. Since synaptophysin is essential for the fusion of presynaptic vesicles, synaptophysin is phosphorylated by the cGMP-dependent protein kinase G (PKG) pathway, which is activated by NO as a neurotransmitter. This process can lead to potentiating and facilitating neurotransmission [157]. Synaptic glutamate release also triggers the activation of postsynaptic NMDA and AMPA receptors (NMDAR, AMPAR), which in turn causes Ca2+ to trigger nNOS. NO will diffuse to activate the sGC and produce cGMP, which can influence the release of presynaptic neurotransmitters and target various ion channels among other signaling tasks. An interaction between nNOS and CAPON causes a cascade of downstream MAP kinases to begin, thereby nuclear transcription

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