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              <text>&lt;a href="http://doi.org/10.1016/j.neurobiolaging.2019.04.007" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/j.neurobiolaging.2019.04.007&lt;/a&gt;</text>
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              <text>99-110</text>
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                <text>GABAergic and glutamatergic cells in the inferior colliculus dynamically express the GABAAR γ1 subunit during aging</text>
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                <text>Neurobiology of Aging</text>
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                <text>Age-related hearing loss; GABAA receptor; GABAAR γ1 subunit; GABAergic; Glutamatergic; Inferior colliculus</text>
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                <text>Robinson Lauren C; Barat Oren; Mellott Jeffrey G</text>
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                <text>Age-related hearing loss may result, in part, from declining levels of γ-amino butyric acid (GABA) in the aging inferior colliculus (IC). An upregulation of the GABAAR γ1 subunit, which has been shown to increase sensitivity to GABA, occurs in the aging IC. We sought to determine whether the upregulation of the GABAAR γ1 subunit was specific to GABAergic or glutamatergic IC cells. We used immunohistochemistry for glutamic acid decarboxylase and the GABAAR γ1 subunit at 4 age groups in the IC of Fisher Brown Norway rats. The percentage of somas that expressed the γ1 subunit and the number of subunits on each soma were quantified. Our results show that GABAergic and glutamatergic IC cells increasingly expressed the γ1 subunit from young age until expression peaked during middle age. At old age (∼77% of life span), the number of GABAAR γ1 subunits per cell sharply decreased for both cell types. These results, along with previous studies, suggest inhibitory and excitatory IC circuits may express the GABAAR γ1 subunit in response to the age-related decline of available GABA.</text>
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                <text>&lt;a href="http://doi.org/10.1016/j.neurobiolaging.2019.04.007" target="_blank" rel="noreferrer noopener"&gt;10.1016/j.neurobiolaging.2019.04.007&lt;/a&gt;</text>
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        <name>Barat Oren</name>
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        <name>June 2019 Update</name>
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        <name>Mellott Jeffrey G</name>
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