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Medial olivocochlear efferent terminals are protected by sound conditioning.
Canlon, B; Fransson, A; Viberg, A.
Afiliação
  • Canlon B; Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. barbara.canlon@fyfa.ki.se
Brain Res ; 850(1-2): 253-60, 1999 Dec 11.
Article em En | MEDLINE | ID: mdl-10629772
Synaptophysin immunoreactivity was used as a marker for the olivocochlear efferent system that innervates the outer hair cells of the cochlea. An intense noise exposure at either 6.3 kHz or 1.0 kHz caused a significant reduction in anti-synaptophysin immunoreactivity within the 8-6 mm or 14-11 mm distance from the round window, respectively. In the region of the main lesion, the reduction in synaptophysin immunoreactivity for both the 6.3 and 1.0 kHz exposures correlated well with outer hair cell loss. In regions peripheral to the main lesion, some remnants of efferent nerve endings could remain even when their associated outer hair cells were missing. Pre-treatment with a low level sound conditioner (either at 6.3 tone or 1.0 kHz) effectively reduced the efferent and outer hair cell pathology induced by the 6.3 and 1.0 kHz intense noise exposures, respectively. The results demonstrate the feasibility of using anti-synaptophysin immunoreactivity as an effective means of quantifying pathological alterations to the medial cochlear efferent terminals throughout the cochlea. Furthermore, the results show that sound conditioning significantly reduces damage to the efferent terminals.
Assuntos
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Base de dados: MEDLINE Assunto principal: Estimulação Acústica / Núcleo Olivar / Cóclea / Terminações Pré-Sinápticas / Condicionamento Psicológico / Perda Auditiva Provocada por Ruído / Neurônios Eferentes Idioma: En Ano de publicação: 1999 Tipo de documento: Article
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Base de dados: MEDLINE Assunto principal: Estimulação Acústica / Núcleo Olivar / Cóclea / Terminações Pré-Sinápticas / Condicionamento Psicológico / Perda Auditiva Provocada por Ruído / Neurônios Eferentes Idioma: En Ano de publicação: 1999 Tipo de documento: Article