NO signalling in synaptic transmission

Background The NO/cGMP signaling cascade has been proposed to play a role in long-term potentiation (LTP) and the modulation of synaptic transmission. Nitric oxide is formed enzymatically by NO synthases (NOS); two NOS, the endothelial and neuronal isoform (eNOS, nNOS) produce NO as a signalling molecule. Functionally, NO has been reported to act as a retrograde messenger that is generated postsynaptically to increase the neurotransmitter release presynaptically. The NO effects are mediated by the NO-sensitive guanylyl cyclases (NO-GC), which by the formation of cGMP transduce the NO signal. Two functionally indistinguishable isoforms of the NO-GCs, NO-GC1 and NO-GC2 exist.