Allodynia can be induced by transection of the inferior alveolar nerve (IAN). However, even though the transected IAN is a component of the mandibular nerve in the trigeminal ganglion (TG), allodynia developes in the whisker pads, which are innervated by the uninjured infraorbital nerve (ION), a component of the maxillary nerve in the TG. Our microarray analyses have found that many gene expression levels not only in the injured IAN cell bodies, but also in the uninjured neurons were changed by IAN transection. To demonstrate the relationship between gene expression changes in ION neurons and allodynia, we investigated the expression of 22 genes that were up-regulated in the TG ION area containing ION cell bodies in IAN-transected rats. Real-time PCR, in situ hybridization and quantitative PCR analyses indicated that the myelin basic protein (MBP) mRNA was localized to the trigeminal ganglion neurons and that the expression was significantly up-regulated in the ION area of TG after IAN transection. This finding suggests that MBP or myelin sheath in the uninjured neuron plays a role in allodynia onset following nerve injury
