Abstract
Neuroma formation at sites of injury can impair peripheral nerve regeneration. Although the involvement of semaphorin 3A has been suggested in neuroma formation, this detailed process after injury is not fully understood. This study was therefore undertaken to examine the effects of semaphorin 3A on peripheral nerve regeneration during the early stage after injury. Immunohistochemistry for semaphorin 3A and PGP9.5, a general neuronal marker, was carried out for clarify chronological changes in their expressions after transection of the mouse inferior alveolar nerve thorough postoperative days 1 to 7. At postoperative day 1, the proximal stump of the damaged IAN exhibited semaphorin 3A, while the distal stump lacked any immunoreactivity. From this day on, its expression lessened, ultimately disappearing completely in all regions of the transected inferior alveolar nerve. A local administration of an antibody to semaphorin 3A into the nerve transection site at postoperative day 3 inhibited axon sprouting at the injury site. This antibody injection increased the number of trigeminal ganglion neurons labeled with DiI (paired t-test, p < 0.05). Immunoreactivity of the semaphorin 3A receptor, neuropilin-1, was also detected at the proximal stump at postoperative day 1. These results suggest that nerve injury initiates semaphorin 3A production in ganglion neurons, which is then delivered through the nerve fibers to the proximal end, thereby contributes to the inhibition of axonal sprouting from the proximal region of injured nerves in the distal direction. To our knowledge, this is the first report to reveal the involvement of Sema3A in the nerve regeneration process at its early stage.
Highlights
Dental treatments sometimes cause sensory impairment, especially in the region innervated by the third division of the trigeminal nerve, thereby leading to vulnerability to sensory deficit hypoesthesia in the orofacial region
At postoperative (PO) day 1, Sema3A expression was recognizable in the proximal stump of the inferior alveolar nerve (IAN)
At PO day 3, Sema3A immunoreactivity became weaker in the proximal stump (Fig. 1b,c), and was not found in the medial end of the distal stump
Summary
Dental treatments sometimes cause sensory impairment, especially in the region innervated by the third division of the trigeminal nerve, thereby leading to vulnerability to sensory deficit hypoesthesia in the orofacial region. It is hypothesized that local control of Sema3A is a target for adequate peripheral nerve regeneration after injury. The expression of Sema3A is recognizable in the proximal nerve end of IAN at PO day 1 (arrowhead), and was reduced at PO day 3. Involvement of Sema3A in peripheral nerve regeneration in a mouse experimental model[8,9,10] at early stage following transection of the IAN. It shall focus on; (1) changes in expression pattern of Sema3A in the injured IAN and trigeminal ganglion neurons and (2) the effects of the anti-Sema3A antibody on the IAN regeneration
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