1
40
2
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Text
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URL Address
<a href="http://doi.org/10.1007/s10162-016-0601-9" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s10162-016-0601-9</a>
Pages
343–353
Issue
2
Volume
18
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Long-Lasting forward Suppression of Spontaneous Firing in Auditory Neurons: Implication to the Residual Inhibition of Tinnitus.
Publisher
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Journal of the Association for Research in Otolaryngology : JARO
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-04
Subject
The topic of the resource
acoustic trauma; Animals; Brain Stem – Physiology; Clinical Assessment Tools; Cochlear Nerve – Physiology; Cochlear Nerve/*physiology; Inbred CBA; Inferior Colliculi/*physiology; inferior colliculus; Male; mice; Mice; residual inhibition; Sound; Tinnitus – Physiopathology; Tinnitus/*physiopathology
Creator
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Galazyuk A V; Voytenko S V; Longenecker R J
Description
An account of the resource
Tinnitus is the perception of a sound that has no external source. Sound stimuli can suppress spontaneous firing in auditory neurons long after stimulus offset. It is unknown how changes in sound stimulus parameters affect this forward suppression. Using in vivo extracellular recording in awake mice, we found that about 40 % of spontaneously active inferior colliculus (IC) neurons exhibited forward suppression of spontaneous activity after sound offset. The duration of this suppression increased with sound duration and lasted about 40 s following a
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s10162-016-0601-9" target="_blank" rel="noreferrer noopener">10.1007/s10162-016-0601-9</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Acoustic trauma
Animals
Brain Stem – Physiology
Clinical Assessment Tools
Cochlear Nerve – Physiology
Cochlear Nerve/*physiology
Department of Anatomy & Neurobiology
Galazyuk A V
Inbred CBA
Inferior Colliculi/*physiology
inferior colliculus
Journal of the Association for Research in Otolaryngology : JARO
Longenecker R J
Male
Mice
NEOMED College of Medicine
residual inhibition
Sound
Tinnitus – Physiopathology
Tinnitus/*physiopathology
Voytenko S V
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1186/2193-1801-3-542" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/2193-1801-3-542</a>
Pages
542–542
Volume
3
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Age effects on tinnitus and hearing loss in CBA/CaJ mice following sound exposure.
Publisher
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SpringerPlus
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
1905-7
Subject
The topic of the resource
Acoustic trauma; Age-related hearing loss; Gap-induced suppression of the acoustic startle reflex; Tinnitus development
Creator
An entity primarily responsible for making the resource
Longenecker Ryan J; Chonko Kurt T; Maricich Steve M; Galazyuk Alexander V
Description
An account of the resource
Tinnitus is a maladaptive neuropathic condition that develops in humans and laboratory animals following auditory insult. In our previous study we demonstrated that sound exposure leads to development of behavioral evidence of tinnitus in a sample of exposed mice. However, this tinnitus mouse model did not account for long-term maladaptive plasticity or aging, factors that are commonly linked to the human tinnitus population. Therefore the same group of mice was monitored for tinnitus for 360 days post exposure. Tinnitus was assessed behaviorally by measuring gap-induced pre-pulse suppression of the acoustic startle (GPIAS). Cochlear histology was performed on both control (unexposed) and experimental mice to determine whether sound exposure caused any evident cochlear damage. We found that 360 days after exposure the vast majority of exposed mice exhibited similar gap detection deficits as detected at 84 days post exposure. These mice did not demonstrate significant loss of inner/outer hair cells or spiral ganglion neurons compared to the control sample. Lastly, we demonstrated that GPIAS deficits observed in exposed animals were unlikely exclusively caused by cochlear damage, but could be a result of central auditory maladaptive plasticity. We conclude that CBA/CaJ mice can be considered a good animal model to study the possible contribution of age effects on tinnitus development following auditory insult.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/2193-1801-3-542" target="_blank" rel="noreferrer noopener">10.1186/2193-1801-3-542</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Acoustic trauma
Age-related hearing loss
Chonko Kurt T
Department of Anatomy & Neurobiology
Galazyuk Alexander V
Gap-induced suppression of the acoustic startle reflex
Longenecker Ryan J
Maricich Steve M
NEOMED College of Medicine
SpringerPlus
Tinnitus development