nNOS expression following inferior alveolar nerve injury in the ferret.

Damage to the inferior alveolar nerve (IAN) may result in permanent painful dysaesthesia, and there is compelling evidence to suggest that ectopic activity from the injury site plays a crucial role in the initiation of this disorder. The aim of this study was to determine whether neuronal nitric oxide synthase (nNOS), a regulator of neuronal excitability, could be involved in the development of the abnormal activity. In seven ferrets, the left IAN was exposed and a retrograde tracer, fluorogold, was applied to the nerve for the identification of cell bodies in the trigeminal ganglion with axons in the IAN. In four animals, the nerve was sectioned distal to the injection site, and three served as controls. After 3 days, the animals were perfused with fixative, and the left and right IANs and trigeminal ganglia were processed using indirect immunofluorescence for nNOS. Image analysis was used to quantify the percentage area of staining (PAS) at the injury site. In the ganglia, counts were made of positively labelled cells in the fluorogold population. At the injury site, PAS was significantly greater in injured nerves than in either contralateral or control nerves, and contralateral PAS was elevated compared to control. In the ganglia, the proportion of nNOS-labelled cells was significantly reduced following injury. These results indicate a possible translocation of the nNOS protein from the cell body to the site of nerve injury, where it accumulates. Thus, nNOS could play a role in the development of ectopic activity at a site of trigeminal nerve injury.

Immunohistochemical analysis of neuronal nitric oxide synthase in the trigeminal ganglia of the crotaline snake Trimeresurus flavoviridis.

The expression of neuronal nitric oxide synthase (nNOS) in the trigeminal ganglia (TG) of the infrared-sensitive crotaline snake Trimeresurus flavoviridis was studied immunohistochemically. The percentage of nNOS-positive (+) neurons in the TG was significantly higher (about 3.5-fold, P<0.001) in the mandibular division than in the infrared-sensory processing area (the maxillary division and ophthalmic ganglion). nNOS was found in varying sizes of TG neurons. However, nNOS (+) neurons were more abundant in small and large neurons than in medium-sized neurons, which include most of the infrared-sensitive neurons of the TG. These findings suggest that nNOS may be involved in normal physiological functions, such as the transmission of tactile, vibrotactile, and nociceptive sensations in the TG, rather than in infrared sensory processing in this species.

Why can't you achieve adequate regional anesthesia in the presence of infection?

Observed in this study were morphologic changes in inflamed nerves, along with biochemical changes, which appear to act concurrently to deactivate or prevent activation of the local anesthetic solution. Morphologic changes were observed along the nerve fiber distant from the inflammatory site. These neuro-degenerative changes were seen at the axon and myelin sheaths level. The biochemical data support the presence in the inflamed nerve of amino acids which may be the product of lysosomal rupture and proteolytic enzyme release. These inflammatory mediators may affect either the local anesthetic or the environment of the nerve fiber. The precise mechanism of action of these catalytic products cannot be determined from this study.