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1.
Hear Res ; 353: 213-223, 2017 09.
Artigo em Inglês | MEDLINE | ID: mdl-28712672

RESUMO

Cochlear synaptopathy can result from various insults, including acoustic trauma, aging, ototoxicity, or chronic conductive hearing loss. For example, moderate noise exposure in mice can destroy up to ∼50% of synapses between auditory nerve fibers (ANFs) and inner hair cells (IHCs) without affecting outer hair cells (OHCs) or thresholds, because the synaptopathy occurs first in high-threshold ANFs. However, the fiber loss likely impairs temporal processing and hearing-in-noise, a classic complaint of those with sensorineural hearing loss. Non-human primates appear to be less vulnerable to noise-induced hair-cell loss than rodents, but their susceptibility to synaptopathy has not been studied. Because establishing a non-human primate model may be important in the development of diagnostics and therapeutics, we examined cochlear innervation and the damaging effects of acoustic overexposure in young adult rhesus macaques. Anesthetized animals were exposed bilaterally to narrow-band noise centered at 2 kHz at various sound-pressure levels for 4 h. Cochlear function was assayed for up to 8 weeks following exposure via auditory brainstem responses (ABRs) and otoacoustic emissions (OAEs). A moderate loss of synaptic connections (mean of 12-27% in the basal half of the cochlea) followed temporary threshold shifts (TTS), despite minimal hair-cell loss. A dramatic loss of synapses (mean of 50-75% in the basal half of the cochlea) was seen on IHCs surviving noise exposures that produced permanent threshold shifts (PTS) and widespread hair-cell loss. Higher noise levels were required to produce PTS in macaques compared to rodents, suggesting that primates are less vulnerable to hair-cell loss. However, the phenomenon of noise-induced cochlear synaptopathy in primates is similar to that seen in rodents.


Assuntos
Limiar Auditivo , Cóclea/fisiopatologia , Doenças Cocleares/fisiopatologia , Perda Auditiva Provocada por Ruído/fisiopatologia , Audição , Ruído/efeitos adversos , Sinapses , Animais , Fadiga Auditiva , Cóclea/patologia , Doenças Cocleares/etiologia , Doenças Cocleares/patologia , Doenças Cocleares/psicologia , Modelos Animais de Doenças , Potenciais Evocados Auditivos do Tronco Encefálico , Células Ciliadas Auditivas/patologia , Perda Auditiva Provocada por Ruído/etiologia , Perda Auditiva Provocada por Ruído/patologia , Perda Auditiva Provocada por Ruído/psicologia , Macaca mulatta , Emissões Otoacústicas Espontâneas , Sinapses/patologia , Transmissão Sináptica , Fatores de Tempo
2.
Hear Res ; 243(1-2): 57-68, 2008 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-18586424

RESUMO

Distortion-product otoacoustic emissions (DPOAEs) were measured in a New World primate, the common marmoset (Callithrix jacchus). We determined the optimal primary-tone frequency ratio (f(2)/f(1)) to generate DPOAEs of maximal amplitude between 3 and 24 kHz. The optimal f(2)/f(1), determined by varying f(2)/f(1) from 1.02 to 1.40 using equilevel primary tones, decreased with increasing f(2) frequency between 3 and 17 kHz, and increased at 24 kHz. The optimal f(2)/f(1) ratio increased with increasing primary-tone levels from 50 to 74 dB SPL. When all stimulus parameters were considered, the mean optimal f(2)/f(1) was 1.224-1.226. Additionally, we determined the effect of reducing L(2) below L(1). Decreasing L(2) below L(1) by 0, 5, and 10 dB (f(2)/f(1)=1.21) minimally affected DPOAE strength. DPOAE levels were stronger in females than males and stronger in the right ear than the left, just as in humans. This study is the first to measure OAEs in the marmoset, and the results indicate that the effect of varying the frequency ratio and primary-tone level difference on marmoset DPOAEs is similar to the reported effects in humans and Old World primates.


Assuntos
Callithrix/fisiologia , Emissões Otoacústicas Espontâneas , Estimulação Acústica , Animais , Cercopithecidae/fisiologia , Feminino , Humanos , Masculino , Caracteres Sexuais , Especificidade da Espécie
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