title: Increased BrdU incorporation reflecting DNA repair, neuronal de-differentiation or possible neurogenesis in the adult cochlear nucleus following bilateral cochlear lesions in the rat.
abstract: Neurogenesis is known to occur in response to injury in the brain, for example, as a result of neurodegenerative diseases. However, there have been few investigations into how the brain responds to damage to peripheral sensory nerves, in other areas such as the brainstem. Here, we report that bilateral surgical lesions of the cochlea result in increased incorporation of the DNA replication marker, bromodeoxyuridine (BrdU), in cells of the brainstem cochlear nucleus (CN) of the adult rat, suggesting either cell proliferation or DNA repair. Some of the BrdU-labelled cells colabelled for the mature neuron marker, NeuN and the GABAergic enzyme GAD-65, suggesting the possibility that neurogenesis might have occurred and resulted in the generation of new neurons with a GABAergic phenotype. However, some of the mature neurons also re-expressed immature neuronal intermediate filament and microtuble-associated proteins, without apoptotic neuronal death, which suggests that the colabelling of BrdU with NeuN and GAD-65 may not be a true reflection of neurogenesis, but injury-stimulated neuronal dedifferentiation. These results suggest the possibility that DNA repair, neuronal de-differentiation or possible neurogenesis occurs in the cochlear nucleus, in response to damage to the peripheral auditory system.
authors.affiliation: Department of Pharmacology and Toxicology, School of Medical Sciences, University of Otago, Dunedin, Otago, New Zealand. yiwen.zheng@stonebow.otago.ac.nz
authors.forename: Yiwen
authors.initials: Y
authors.lastname: Zheng
authors.forename: Shaeza
authors.initials: S
authors.lastname: Begum
authors.forename: Chu
authors.initials: C
authors.lastname: Zhang
authors.forename: Kirk
authors.initials: K
authors.lastname: Fleming
authors.forename: Chisako
authors.initials: C
authors.lastname: Masumura
authors.forename: Ming
authors.initials: M
authors.lastname: Zhang
authors.forename: Paul
authors.initials: P
authors.lastname: Smith
authors.forename: Cynthia
authors.initials: C
authors.lastname: Darlington
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001973:Bromodeoxyuridine / Q000378:metabolism*; D039481:CD11b Antigen / Q000378:metabolism; D002452:Cell Count / Q000379:methods; D002454:Cell Differentiation / Q000502:physiology*; D049109:Cell Proliferation; D017626:Cochlear Nucleus / Q000293:injuries* / Q000503:physiopathology*; D004260:DNA Repair / Q000502:physiology*; D005786:Gene Expression Regulation / Q000502:physiology; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D017628:Microglia / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000378:metabolism; D055495:Neurogenesis / Q000502:physiology*; D009474:Neurons / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D039481:CD11b Antigen; D019394:Ki-67 Antigen; D009419:Nerve Tissue Proteins; D001973:Bromodeoxyuridine