Peripherin as a marker for degeneration of spiral ganglion neurons after aminoglycoside ototoxicity

Wang, Yucheng; Liu, Hong; Shen, Yihang; Wang, Zhengmin; Li, Huawei

doi:10.1080/00016480600672584

Cited by 6 publications

(4 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This reflects a species difference, as in the neonatal rat model, peripherin expression occurs in type I as well as type II SGNs [36,31]. We are also confident that peripherin expression remained confined to the type II SGNs following axotomy and culture, despite previous reports of in vitro peripherin re-expression in type I SGNs from rat cochlea following axotomy and culture of SGN explants [31] and in vivo following degeneration of the organ of Corti in response to neomycin treatment [38]. In particular, we did not observe peripherin expression in fibers innervating IHCs in our organotypic cultures from P7 cochleae, by which age the IHC innervation is exclusively from type I SGNs [7].…”

Section: Discussionmentioning

confidence: 71%

Type I vs type II spiral ganglion neurons exhibit differential survival and neuritogenesis during cochlear development

2011

View full text Add to dashboard Cite

BackgroundThe mechanisms that consolidate neural circuitry are a major focus of neuroscience. In the mammalian cochlea, the refinement of spiral ganglion neuron (SGN) innervation to the inner hair cells (by type I SGNs) and the outer hair cells (by type II SGNs) is accompanied by a 25% loss of SGNs.ResultsWe investigated the segregation of neuronal loss in the mouse cochlea using β-tubulin and peripherin antisera to immunolabel all SGNs and selectively type II SGNs, respectively, and discovered that it is the type II SGN population that is predominately lost within the first postnatal week. Developmental neuronal loss has been attributed to the decline in neurotrophin expression by the target hair cells during this period, so we next examined survival of SGN sub-populations using tissue culture of the mid apex-mid turn region of neonatal mouse cochleae. In organotypic culture for 48 hours from postnatal day 1, endogenous trophic support from the organ of Corti proved sufficient to maintain all type II SGNs; however, a large proportion of type I SGNs were lost. Culture of the spiral ganglion as an explant, with removal of the organ of Corti, led to loss of the majority of both SGN sub-types. Brain-derived neurotrophic factor (BDNF) added as a supplement to the media rescued a significant proportion of the SGNs, particularly the type II SGNs, which also showed increased neuritogenesis. The known decline in BDNF production by the rodent sensory epithelium after birth is therefore a likely mediator of type II neuron apoptosis.ConclusionOur study thus indicates that BDNF supply from the organ of Corti supports consolidation of type II innervation in the neonatal mouse cochlea. In contrast, type I SGNs likely rely on additional sources for trophic support.

show abstract

Section: Discussionmentioning

confidence: 71%

Type I vs type II spiral ganglion neurons exhibit differential survival and neuritogenesis during cochlear development

2011

View full text Add to dashboard Cite

show abstract

“…Peripherins are neuronal IF proteins of the peripheral as well as central nervous system. In the cochlea, peripherin expression has been used as a differentiation marker for type II neurons of the spiral ganglion . Apart from this, its expression has been correlated with axonal regeneration .…”

Section: Discussionmentioning

confidence: 99%

“…In the cochlea, peripherin expression has been used as a differentiation marker for type II neurons of the spiral ganglion. 48 Apart from this, its expression has been correlated with axonal regeneration. 49 Neurofilaments are one of the five major groups of IF, that are important components in the cytoskeleton of neurons.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Cochlear Protein Profiles of Wistar, Sprague−Dawley, and Fischer 344 Rats with Normal Hearing Function

et al. 2009

View full text Add to dashboard Cite

Differences in the expression of cochlear proteins are likely to affect the susceptibility of different animal models to specific types of auditory pathology. However, little is currently known about proteins that are abundantly expressed in inner ear. Identification of these proteins may facilitate the search for biomarkers of susceptibility and intervention targets. To begin to address this issue, we analyzed cochlear protein profiles of three strains of rats, Wistar, Sprague-Dawley, and Fischer 344, using a broad spectrum antibody microarray. Normal hearing function of the animals was ascertained using distortion product otoacoustic emissions (DPOAE). Of 725 proteins screened in whole cochlea, more than 80% were detected in all three strains. However, there were striking differences in the levels at which they occur. Among 213 proteins expressed at levels>or=2 fold of actin, only 7.5% were detected at these levels in all three strains. Myosin light chain kinase (MLCK) was immunolocalized in cuticular plate of outer hair cells (OHC) while mitogen activated protein (MAP) kinase-extracellular-signal regulated kinase1/2 (ERK1/2) was detected as foci in OHC, pillar cells, strial marginal cells, and fibroblasts of spiral ligament. A review of literature indicated that the expression of 7 (44%) of these 16 proteins were detected for the first time in the inner ear, although there were implications of the presence of some of these proteins. One of these abundant, but unstudied, proteins, MAP kinase activated protein kinase2 (MAPKAPK2), shows strong immunolabeling in pillar cells and inner hair cells (IHC). There was moderate MAPKAPK2 labeling in OHC, supporting cells, neurons, and marginal, intermediate, and basal cells. The current study provides the first, large cochlear protein profile of multiple rat strains. The diversity in expression of abundant proteins in these strains may contribute to differences in susceptibility of these strains to aging, noise, or ototoxic drugs.

show abstract

“…Therefore, it is possible that the processes growing under OHCs may be olivocochlear projections, which begin to innervate OHCs at the end of embryogenesis (Bruce et al, 1997; Lallemend et al, 2007). Additionally, peripherin is initially expressed in all spiral ganglion neurons, and even expressed weakly in Type I neurons in the adult cochlea (Wang et al , 2006). Therefore, the origin of peripherin positive projections in the sensory epithelium cannot be unambiguously assigned to Type II neurons in early postnatal animals.…”

Section: Peripheral Innervation Of Cochlear Hair Cellsmentioning

confidence: 99%

Connecting the ear to the brain: Molecular mechanisms of auditory circuit assembly

Appler

Goodrich

2011

Progress in Neurobiology

166

128

View full text Add to dashboard Cite

Our sense of hearing depends on precisely organized circuits that allow us to sense, perceive, and respond to complex sounds in our environment, from music and language to simple warning signals. Auditory processing begins in the cochlea of the inner ear, where sounds are detected by sensory hair cells and then transmitted to the central nervous system by spiral ganglion neurons, which faithfully preserve the frequency, intensity, and timing of each stimulus. During the assembly of auditory circuits, spiral ganglion neurons establish precise connections that link hair cells in the cochlea to target neurons in the auditory brainstem, develop specific firing properties, and elaborate unusual synapses both in the periphery and in the CNS. Understanding how spiral ganglion neurons acquire these unique properties is a key goal in auditory neuroscience, as these neurons represent the sole input of auditory information to the brain. In addition, the best currently available treatment for many forms of deafness is the cochlear implant, which compensates for lost hair cell function by directly stimulating the auditory nerve. Historically, studies of the auditory system have lagged behind other sensory systems due to the small size and inaccessibility of the inner ear. With the advent of new molecular genetic tools, this gap is narrowing. Here, we summarize recent insights into the cellular and molecular cues that guide the development of spiral ganglion neurons, from their origin in the proneurosensory domain of the otic vesicle to the formation of specialized synapses that ensure rapid and reliable transmission of sound information from the ear to the brain.

show abstract

Peripherin as a marker for degeneration of spiral ganglion neurons after aminoglycoside ototoxicity

Cited by 6 publications

References 22 publications

Type I vs type II spiral ganglion neurons exhibit differential survival and neuritogenesis during cochlear development

Type I vs type II spiral ganglion neurons exhibit differential survival and neuritogenesis during cochlear development

Analysis of Cochlear Protein Profiles of Wistar, Sprague−Dawley, and Fischer 344 Rats with Normal Hearing Function

Connecting the ear to the brain: Molecular mechanisms of auditory circuit assembly

Contact Info

Product

Resources

About