Does nitric oxide play a role in orofacial pain transmission?

Although the synaptology, neural connectivity, and the roles played by nitric oxide (NO) and other neurotransmitters have been extensively studied in spinal pain, such information is rather scanty with respect to orofacial pain transmission. This paper presents the findings of several investigations carried out by the author and his colleagues on the roles of NO in orofacial pain transmission in male Wistar rats, using nicotinamide adenosine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry using light and electron microscopy; and NOS immunohistochemistry and immunofluorescence using both light and confocal laser scanning microscopy. The results revealed that (1) a complicated relation existed between the nitrergic axon terminals and dendrites in the caudal part of the spinal trigeminal nucleus (cSTN); (2) the nitrergic neuronal cells bodies were not projection neurons, but rather, local circuit neurons; (3) although the thalamus projecting neurons in the cSTN did not synthesize NO, they could be modulated by NO diffused from nitrergic neurons; (4) c-fos positive neurons in the superficial laminae of the cSTN, detected following subcutaneous injection of 0.5 ml of 4% formalin into the left lateral face of the rats, respond to the release of glutamate through activation of N-methyl-D-aspartate (NMDA), alpha-amine-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) and metabotropic glutamate (mGlu) receptors expressed by these c-fos neurons; and (5) NO might play a seemingly less important role than glutamate in neural transmission.