Methods: Rats were anesthetized and their upper molars were extracted. Three, seven, or ten days after extraction, the animals were perfused transcardially with 4% paraformaldehyde under deep anesthesia with diethyl ether and the TG was removed. Cryosections of the ganglia were immunostained with antibodies against glutamine synthetase (GS), a glial cell marker, glial fibrillary acidic protein (GFAP), a marker of activated SGCs, protein-gene product 9.5 (PGP-9.5), a neuronal cell marker, and ATF3, a marker of damaged neurons.
Results: After tooth extraction, the number of neurons enclosed by GFAP-immunoreactive (IR) SGCs increased in a time-dependent manner in the maxillary nerve region of the TG. Three days after extraction, ATF3-IR neurons appeared in the maxillary nerve region that persisted until day 10. The ATF3-IR neurons were surrounded by GFAP-IR SGCs. After extraction, ATF3-IR neurons were not detected in the mandibular nerve regions; however, the number of GFAP-IR SGCs was increased in both maxillary and mandibular nerve regions.
Conclusions: Our results suggest that peripheral nerve injury affects the activation of TG neurons and the SGCs around the injured neurons; moreover, our data suggest the existence of a neuronal interaction between maxillary and mandibular neurons via SGC activation.