Methods: To examine whether or not NGF mRNA is expressed in the TG, we were investigated using in situ hybridization method in undamaged rats' TG. Rats were anesthetized and an elastic band was inserted between their first and second upper molars. TGs were removed at 0 to 7 days after tooth movement. Cryosections were immunostained using antibodies against NGF and glutamine synthetase (GS), a marker of SGCs. Furthermore, to investigate the role of gap junctions, gap junction inhibitor were administered at TG during experimental tooth movement. The immunostaining of SGCs in the maxillary nerve region in the TG was observed using fluorescence microscopy. The number of SGCs and the size of neurons were analyzed using Scion Image.
Results: By in situ hybridization NGF mRNA expressed both in neurons and SGCs even in undamaged TG. After tooth movement, the number of NGF-immunoreactive (IR) SGCs increased significantly compared with control level and reached maximum levels at day 3, decreased at day 5. The number of NGF-IR SGCs was significantly decreased by the injection of gap junction inhibitor at day 3.
Conclusions: These results indicated that peripheral nerve damage induced the NGF expression in surrounded SGCs possibly interacted through gap junction between TG neurons and SGCs. SGCs produced and released the NGF, which would induce the restration for the damaged neuron.