Degeneration of Spiral Ganglion Cells in the Chinchilla afterInner H air Cell Loss Induced by Carboplatin

Takeno, Sachio; Wake, M.; Mount, Richard J.; Harrison, Robert V.

doi:10.1159/000013800

Cited by 46 publications

(34 citation statements)

References 26 publications

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“…Damage to the organ of Corti is a wellrecognized event during suppurative labyrinthitis, 12,13,37 and hair cell loss can induce spiral ganglion neuronal death due to inactivity. 38,39 Therefore, it is conceivable that peroxynitrite-mediated damage to hair cells can indirectly lead to neuronal loss in the spiral ganglion and thus to permanent meningitis-associated hearing loss.…”

Section: Discussionmentioning

confidence: 99%

Meningitis‐associated hearing loss: Protection by adjunctive antioxidant therapy

Klein

Koedel

Pfister

et al. 2003

Annals of Neurology

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Hearing loss is the most frequent long-term complication of pneumococcal meningitis, affecting up to 40% of survivors. Unfortunately, adjuvant therapy with dexamethasone has failed to satisfactorily reduce its incidence. Therefore, we evaluated the use of antioxidants for the adjunctive therapy of meningitis-associated deafness. Eighteen hours after intracisternal injection of 7.5 x 10(5) colony-forming units of Streptococcus pneumoniae, rats were treated systemically either with ceftriaxone and the antioxidants and peroxynitrite scavengers Mn(III)tetrakis(4-benzoic acid)-porphyrin (MnTBAP) or N-acetyl-L-cysteine (NAC) or placebo (1 ml phosphate-buffered saline) for 4 days. Hearing was assessed by auditory brainstem response audiometry. Adjunctive antioxidant therapy significantly reduced the long-term hearing loss (14 days after infection) for square wave impulses (mean hearing loss +/- SD: ceftriaxone and placebo, 45+/-26 dB; ceftriaxone and MnTBAP, 9+/-23 dB; ceftriaxone and NAC, 19+/-30 dB) as well as 1 kHz (ceftriaxone and placebo, 28+/-19 dB; ceftriaxone and MnTBAP, 10+/-16 dB; ceftriaxone and NAC, 10+/-17 dB), and 10 kHz tone bursts (ceftriaxone and placebo, 62+/-27 dB; ceftriaxone and MnTBAP, 16+/-13 dB; ceftriaxone and NAC, 25+/-26 dB). Furthermore, both antioxidants attenuated the morphological correlates of meningogenic hearing loss, namely, long-term blood-labyrinth barrier disruption, spiral ganglion neuronal loss, and fibrous obliteration of the perilymphatic spaces. Adjuvant antioxidant therapy is highly otoprotective in meningitis and therefore is a promising future treatment option.

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Section: Discussionmentioning

confidence: 99%

Meningitis‐associated hearing loss: Protection by adjunctive antioxidant therapy

Klein

Koedel

Pfister

et al. 2003

Annals of Neurology

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“…In the majority of cases this occurs as a result of loss of sensory hair cells leading to a permanent sensorineural hearing loss (SNHL). Loss of hair cells sets in place a gradual but ongoing degeneration of spiral ganglion cells (SGNs), the primary afferent neurons of the cochlea (Gillespie et al, 2004;Hardie et al, 1999;Heid et al, 1998;Leake et al, 1988;Liberman et al, 1978;Mair, 1973;McGuinness et al, 2005;Ryugo et al, 1998;Shepherd et al, 1997;Shepherd et al, 2004;Shepherd et al, 2005;Steel et al, 1984;Takeno et al, 1998). SGNs are the target neurons for cochlear implants; the functional integrity of these neurons is therefore important for the success of these neural prostheses.…”

Section: Introductionmentioning

confidence: 99%

Neurotrophins and electrical stimulation for protection and repair of spiral ganglion neurons following sensorineural hearing loss

2008

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Exogenous neurotrophins (NTs) have been shown to rescue spiral ganglion neurons (SGNs) from degeneration following a sensorineural hearing loss (SNHL). Furthermore, chronic electrical stimulation (ES) has been shown to retard SGN degeneration in some studies but not others. Since there is evidence of even greater SGN rescue when NT administration is combined with ES, we examined whether chronic ES can maintain SGN survival long after cessation of NT delivery. Young adult guinea pigs were profoundly deafened using ototoxic drugs; five days later they were unilaterally implanted with an electrode array and drug delivery system. Brain derived neurotrophic factor (BDNF) was continuously delivered to the scala tympani over a four week period while the animal simultaneously received ES via bipolar electrodes in the basal turn (i.e. turn 1) scala tympani. One cohort (n=5) received ES for six weeks (i.e. including a two week period after the cessation of BDNF delivery; ES 6 ); a second cohort (n=5) received ES for 10 weeks (i.e. a six week period following cessation of BDNF delivery; ES 10 ). The cochleae were harvested for histology and SGN density determined for each cochlear turn for comparison with normal hearing controls (n=4). The withdrawal of BDNF resulted in a rapid loss of SGNs in turns 2-4 of the deafened/BDNF-treated cochleae; this was significant as early as two weeks following removal of the NT when compared with normal controls (p<0.05). Importantly, there was not a significant reduction in SGNs in turn 1 (i.e. adjacent to the electrode array) two and six weeks after NT removal, as compared with normal controls. This result suggests that chronic ES can prevent the rapid loss of SGNs that occurs after the withdrawal of exogenous NTs. Implications for the clinical delivery of NTs are discussed.

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“…Numerous studies indicate that the target hair cells release trophic factors that support SGNs (Ernfors et al, 1995;Fritzsch et al, 1997;Hossain et al, 2002). After chemical or mechanical damage of hair cells, SGNs are rapidly lost, consistent with a target-dependent mechanism of SGN survival (Takeno et al, 1998). During the aging process, however, loss of SGNs may not arise strictly as a secondary degeneration after hair cell loss, because the extent of SGN death is much greater than that of hair cells (Ryals and Westbrook, 1988).…”

Section: Introductionmentioning

confidence: 99%

Requirement of Nicotinic Acetylcholine Receptor Subunit β2 in the Maintenance of Spiral Ganglion Neurons during Aging

Bao¹,

Lei²,

Du³

et al. 2005

J. Neurosci.

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Age-related hearing loss (presbycusis) is a major health concern for the elderly. Loss of spiral ganglion neurons (SGNs), the primary sensory relay of the auditory system, is associated consistently with presbycusis. The causative molecular events responsible for agerelated loss of SGNs are unknown. Recent reports directly link age-related neuronal loss in cerebral cortex with the loss of high-affinity nicotine acetylcholine receptors (nAChRs). In cochlea, cholinergic synapses are made by olivocochlear efferent fibers on the outer hair cells that express ␣9 nAChR subunits and on the peripheral projections of SGNs that express ␣2, ␣4 -7, and ␤2-3 nAChR subunits. A significantly decreased expression of the ␤2 nAChR subunit in SGNs was found specifically in mice susceptible to presbycusis. Furthermore, mice lacking the ␤2 nAChR subunit (␤2Ϫ/Ϫ), but not mice lacking the ␣5 nAChR subunit (␣5Ϫ/Ϫ), have dramatic hearing loss and significant reduction in the number of SGNs. Our findings clearly established a requirement for ␤2 nAChR subunit in the maintenance of SGNs during aging.

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Degeneration of Spiral Ganglion Cells in the Chinchilla afterInner H air Cell Loss Induced by Carboplatin

Cited by 46 publications

References 26 publications

Meningitis‐associated hearing loss: Protection by adjunctive antioxidant therapy

Meningitis‐associated hearing loss: Protection by adjunctive antioxidant therapy

Neurotrophins and electrical stimulation for protection and repair of spiral ganglion neurons following sensorineural hearing loss

Requirement of Nicotinic Acetylcholine Receptor Subunit β2 in the Maintenance of Spiral Ganglion Neurons during Aging

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