Endogenous presynaptic nitric oxide supports an anterograde signaling in the central nervous system.

The source size and density determine the extent of nitric oxide (NO) diffusion which critically influences NO signaling. In the brain, NO released from postsynaptic somas following NMDA-mediated activation of neuronal nitric oxide synthase (nNOS) retrogradely affects smaller presynaptic targets. By contrast, in guinea pig trigeminal motor nucleus (TMN), NO is produced presynaptically by tiny and disperse nNOS-containing terminals that innervate large nNOS-negative motoneurons expressing the soluble guanylyl-cyclase (sGC); consequently, it is uncertain whether endogenous NO supports an anterograde signaling between pre-motor terminals and postsynaptic trigeminal motoneurons.

Nitric oxide as an anterograde neurotransmitter in the trigeminal motor pool.

We demonstrate the presence of nitric oxide synthase containing fibers within the guinea pig trigeminal motor nucleus and describe the effects of nitric oxide (NO) on trigeminal motoneurons. Using immunohistochemical techniques, we observed nitrergic fibers displaying varicosities and giving rise to bouton-like structures in apposition to retrogradely labeled motoneuron processes, most of which were dendrites. NO-donors evoked a membrane depolarization (mean 7.