Tracking the expression of excitatory and inhibitory neurotransmission-related proteins and neuroplasticity markers after noise induced hearing loss
Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These pathologies coincide with a range of CNS changes including reorganisation of frequency representation, alterations in the pattern of spontaneous activity and changed expression of excitatory and inhibitory neuro...
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| description | Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These pathologies coincide with a range of CNS changes including reorganisation of frequency representation, alterations in the pattern of spontaneous activity and changed expression of excitatory and inhibitory neurotransmitters. Moreover, damage to the cochlea is often accompanied by acoustic disorders such as hyperacusis and tinnitus, suggesting that one or more of these neuronal changes may be involved in these disorders, although the mechanisms remain unknown. We tested the hypothesis that excessive noise exposure increases expression of markers of excitation and plasticity, and decreases expression of inhibitory markers over a 32-day recovery period. Adult rats (n = 25) were monaurally exposed to a loud noise (16 kHz, 1/10(th) octave band pass (115 dB SPL)) for 1-hour, or left as non-exposed controls (n = 5). Animals were euthanased at either 0, 4, 8, 16 or 32 days following acoustic trauma. We used Western Blots to quantify protein levels of GABA(A) receptor subunit α1 (GABA(A)α1), Glutamic-Acid Decarboxylase-67 (GAD-67), N-Methyl-D-Aspartate receptor subunit 2A (NR2A), Calbindin (Calb1) and Growth Associated Protein 43 (GAP-43) in the Auditory Cortex (AC), Inferior Colliculus (IC) and Dorsal Cochlear Nucleus (DCN). Compared to sham-exposed controls, noise-exposed animals had significantly (p |
| doi_str_mv | 10.1371/journal.pone.0033272 |
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These pathologies coincide with a range of CNS changes including reorganisation of frequency representation, alterations in the pattern of spontaneous activity and changed expression of excitatory and inhibitory neurotransmitters. Moreover, damage to the cochlea is often accompanied by acoustic disorders such as hyperacusis and tinnitus, suggesting that one or more of these neuronal changes may be involved in these disorders, although the mechanisms remain unknown. We tested the hypothesis that excessive noise exposure increases expression of markers of excitation and plasticity, and decreases expression of inhibitory markers over a 32-day recovery period. Adult rats (n = 25) were monaurally exposed to a loud noise (16 kHz, 1/10(th) octave band pass (115 dB SPL)) for 1-hour, or left as non-exposed controls (n = 5). Animals were euthanased at either 0, 4, 8, 16 or 32 days following acoustic trauma. We used Western Blots to quantify protein levels of GABA(A) receptor subunit α1 (GABA(A)α1), Glutamic-Acid Decarboxylase-67 (GAD-67), N-Methyl-D-Aspartate receptor subunit 2A (NR2A), Calbindin (Calb1) and Growth Associated Protein 43 (GAP-43) in the Auditory Cortex (AC), Inferior Colliculus (IC) and Dorsal Cochlear Nucleus (DCN). Compared to sham-exposed controls, noise-exposed animals had significantly (p<0.05): lower levels of GABA(A)α1 in the contralateral AC at day-16 and day-32, lower levels of GAD-67 in the ipsilateral DCN at day-4, lower levels of Calb1 in the ipsilateral DCN at day-0, lower levels of GABA(A)α1 in the ipsilateral AC at day-4 and day-32. GAP-43 was reduced in the ipsilateral AC for the duration of the experiment. These complex fluctuations in protein expression suggests that for at least a month following acoustic trauma the auditory system is adapting to a new pattern of sensory input.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0033272</identifier><identifier>PMID: 22428005</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acoustic noise ; Acoustic properties ; Acoustic Stimulation ; Acoustics ; Analysis of Variance ; Animals ; Auditory plasticity ; Auditory system ; Biology ; Biomarkers - metabolism ; Blotting, Western ; Calbindin ; Calbindin 1 ; Calbindins ; Central nervous system ; Cochlea ; Cochlear nuclei ; Cochlear Nucleus - metabolism ; Colliculus ; Cortex (auditory) ; Cortex (somatosensory) ; Disorders ; Evoked Potentials, Auditory, Brain Stem - physiology ; Exposure ; GAP-43 protein ; GAP-43 Protein - metabolism ; Glutamate decarboxylase ; Glutamate Decarboxylase - metabolism ; Glutamate receptors ; Glutamic acid receptors ; Hearing loss ; Hearing Loss, Noise-Induced - metabolism ; Hearing protection ; Inferior colliculus ; Markers ; Medicine ; N-Methyl-D-aspartic acid receptors ; Nerve Tissue Proteins - metabolism ; Neuronal Plasticity - genetics ; Neuronal Plasticity - physiology ; Neuroplasticity ; Neurotransmission ; Neurotransmitters ; Noise ; Noise control ; Noise levels ; Polypeptides ; Proteins ; Rats ; Receptors, GABA-A - metabolism ; Receptors, N-Methyl-D-Aspartate - metabolism ; Rodents ; S100 Calcium Binding Protein G - metabolism ; Somatosensory cortex ; Studies ; Synaptic Transmission - genetics ; Synaptic Transmission - physiology ; Tinnitus ; Trauma ; Trends ; Western blotting ; γ-Aminobutyric acid A receptors</subject><ispartof>PloS one, 2012-03, Vol.7 (3), p.e33272-e33272</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Browne et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Browne et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c691t-bf0cf972e9fa774768430329e403e63a31d504f2641d1f18223babbfac4b1bb53</citedby><cites>FETCH-LOGICAL-c691t-bf0cf972e9fa774768430329e403e63a31d504f2641d1f18223babbfac4b1bb53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299769/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299769/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22428005$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gilestro, Giorgio F.</contributor><creatorcontrib>Browne, Cherylea J</creatorcontrib><creatorcontrib>Morley, John W</creatorcontrib><creatorcontrib>Parsons, Carl H</creatorcontrib><title>Tracking the expression of excitatory and inhibitory neurotransmission-related proteins and neuroplasticity markers after noise induced hearing loss</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These pathologies coincide with a range of CNS changes including reorganisation of frequency representation, alterations in the pattern of spontaneous activity and changed expression of excitatory and inhibitory neurotransmitters. Moreover, damage to the cochlea is often accompanied by acoustic disorders such as hyperacusis and tinnitus, suggesting that one or more of these neuronal changes may be involved in these disorders, although the mechanisms remain unknown. We tested the hypothesis that excessive noise exposure increases expression of markers of excitation and plasticity, and decreases expression of inhibitory markers over a 32-day recovery period. Adult rats (n = 25) were monaurally exposed to a loud noise (16 kHz, 1/10(th) octave band pass (115 dB SPL)) for 1-hour, or left as non-exposed controls (n = 5). Animals were euthanased at either 0, 4, 8, 16 or 32 days following acoustic trauma. We used Western Blots to quantify protein levels of GABA(A) receptor subunit α1 (GABA(A)α1), Glutamic-Acid Decarboxylase-67 (GAD-67), N-Methyl-D-Aspartate receptor subunit 2A (NR2A), Calbindin (Calb1) and Growth Associated Protein 43 (GAP-43) in the Auditory Cortex (AC), Inferior Colliculus (IC) and Dorsal Cochlear Nucleus (DCN). Compared to sham-exposed controls, noise-exposed animals had significantly (p<0.05): lower levels of GABA(A)α1 in the contralateral AC at day-16 and day-32, lower levels of GAD-67 in the ipsilateral DCN at day-4, lower levels of Calb1 in the ipsilateral DCN at day-0, lower levels of GABA(A)α1 in the ipsilateral AC at day-4 and day-32. GAP-43 was reduced in the ipsilateral AC for the duration of the experiment. These complex fluctuations in protein expression suggests that for at least a month following acoustic trauma the auditory system is adapting to a new pattern of sensory input.</description><subject>Acoustic noise</subject><subject>Acoustic properties</subject><subject>Acoustic Stimulation</subject><subject>Acoustics</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Auditory plasticity</subject><subject>Auditory system</subject><subject>Biology</subject><subject>Biomarkers - metabolism</subject><subject>Blotting, Western</subject><subject>Calbindin</subject><subject>Calbindin 1</subject><subject>Calbindins</subject><subject>Central nervous system</subject><subject>Cochlea</subject><subject>Cochlear nuclei</subject><subject>Cochlear Nucleus - metabolism</subject><subject>Colliculus</subject><subject>Cortex (auditory)</subject><subject>Cortex (somatosensory)</subject><subject>Disorders</subject><subject>Evoked Potentials, Auditory, Brain Stem - physiology</subject><subject>Exposure</subject><subject>GAP-43 protein</subject><subject>GAP-43 Protein - metabolism</subject><subject>Glutamate decarboxylase</subject><subject>Glutamate Decarboxylase - metabolism</subject><subject>Glutamate receptors</subject><subject>Glutamic acid receptors</subject><subject>Hearing loss</subject><subject>Hearing Loss, Noise-Induced - metabolism</subject><subject>Hearing protection</subject><subject>Inferior colliculus</subject><subject>Markers</subject><subject>Medicine</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neuronal Plasticity - genetics</subject><subject>Neuronal Plasticity - physiology</subject><subject>Neuroplasticity</subject><subject>Neurotransmission</subject><subject>Neurotransmitters</subject><subject>Noise</subject><subject>Noise control</subject><subject>Noise levels</subject><subject>Polypeptides</subject><subject>Proteins</subject><subject>Rats</subject><subject>Receptors, GABA-A - metabolism</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Rodents</subject><subject>S100 Calcium Binding Protein G - metabolism</subject><subject>Somatosensory cortex</subject><subject>Studies</subject><subject>Synaptic Transmission - genetics</subject><subject>Synaptic Transmission - physiology</subject><subject>Tinnitus</subject><subject>Trauma</subject><subject>Trends</subject><subject>Western blotting</subject><subject>γ-Aminobutyric acid A receptors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk9tu1DAQhiMEoqXwBggiIYG42CU-JI5vkKqKw0qVKkHh1nKc8a7brL3YDmrfgwdm9tBqF_UC5cKZ8Te_PeOZonhJqilhgny4CmP0epiugodpVTFGBX1UHBPJ6KShFXu8939UPEvpqqpq1jbN0-KIUk5bNI-LP5dRm2vn52VeQAk3qwgpueDLYNEyLusc4m2pfV86v3Cd25gexhhy1D4t3QafRBh0hr5coR-cT5uIDbYadMoOlW7LpY7XEHHPZoilDy4BqvajwcAF6Li-xhBSel48sXpI8GK3nhQ_Pn-6PPs6Ob_4Mjs7PZ-YRpI86WxlrBQUpNVCcNG0nFWMSuAVg4ZpRvq64pY2nPTEkpZS1umus9rwjnRdzU6K11vdFZ6qdgVNijDKpJScMSRmW6IP-kqtosMUblXQTm0cIc6VjpjdAIoQUwMQVgNvuJZCtjXhQnNTN4JbC6j1cXfa2C2hN-CxgsOB6OGOdws1D78VpiRFI1Hg3U4ghl8jpKyw-gaGQXsIY1KSSkJJ27ZIvvmHfDi5HTXXeH_n7fpJzVpTnXIhCGOtWFPTByj8elg6g81nHfoPAt4fBCCT4SbP9ZiSmn3_9v_sxc9D9u0ei_0y5EUKw5ix_9IhyLegidhMEex9jUml1rNzVw21nh21mx0Me7X_PvdBd8PC_gIPnhgm</recordid><startdate>20120312</startdate><enddate>20120312</enddate><creator>Browne, Cherylea J</creator><creator>Morley, John W</creator><creator>Parsons, Carl H</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120312</creationdate><title>Tracking the expression of excitatory and inhibitory neurotransmission-related proteins and neuroplasticity markers after noise induced hearing loss</title><author>Browne, Cherylea J ; Morley, John W ; Parsons, Carl H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c691t-bf0cf972e9fa774768430329e403e63a31d504f2641d1f18223babbfac4b1bb53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acoustic noise</topic><topic>Acoustic properties</topic><topic>Acoustic Stimulation</topic><topic>Acoustics</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Auditory plasticity</topic><topic>Auditory system</topic><topic>Biology</topic><topic>Biomarkers - metabolism</topic><topic>Blotting, Western</topic><topic>Calbindin</topic><topic>Calbindin 1</topic><topic>Calbindins</topic><topic>Central nervous system</topic><topic>Cochlea</topic><topic>Cochlear nuclei</topic><topic>Cochlear Nucleus - metabolism</topic><topic>Colliculus</topic><topic>Cortex (auditory)</topic><topic>Cortex (somatosensory)</topic><topic>Disorders</topic><topic>Evoked Potentials, Auditory, Brain Stem - physiology</topic><topic>Exposure</topic><topic>GAP-43 protein</topic><topic>GAP-43 Protein - metabolism</topic><topic>Glutamate decarboxylase</topic><topic>Glutamate Decarboxylase - metabolism</topic><topic>Glutamate receptors</topic><topic>Glutamic acid receptors</topic><topic>Hearing loss</topic><topic>Hearing Loss, Noise-Induced - metabolism</topic><topic>Hearing protection</topic><topic>Inferior colliculus</topic><topic>Markers</topic><topic>Medicine</topic><topic>N-Methyl-D-aspartic acid receptors</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Neuronal Plasticity - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Browne, Cherylea J</au><au>Morley, John W</au><au>Parsons, Carl H</au><au>Gilestro, Giorgio F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tracking the expression of excitatory and inhibitory neurotransmission-related proteins and neuroplasticity markers after noise induced hearing loss</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-03-12</date><risdate>2012</risdate><volume>7</volume><issue>3</issue><spage>e33272</spage><epage>e33272</epage><pages>e33272-e33272</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These pathologies coincide with a range of CNS changes including reorganisation of frequency representation, alterations in the pattern of spontaneous activity and changed expression of excitatory and inhibitory neurotransmitters. Moreover, damage to the cochlea is often accompanied by acoustic disorders such as hyperacusis and tinnitus, suggesting that one or more of these neuronal changes may be involved in these disorders, although the mechanisms remain unknown. We tested the hypothesis that excessive noise exposure increases expression of markers of excitation and plasticity, and decreases expression of inhibitory markers over a 32-day recovery period. Adult rats (n = 25) were monaurally exposed to a loud noise (16 kHz, 1/10(th) octave band pass (115 dB SPL)) for 1-hour, or left as non-exposed controls (n = 5). Animals were euthanased at either 0, 4, 8, 16 or 32 days following acoustic trauma. We used Western Blots to quantify protein levels of GABA(A) receptor subunit α1 (GABA(A)α1), Glutamic-Acid Decarboxylase-67 (GAD-67), N-Methyl-D-Aspartate receptor subunit 2A (NR2A), Calbindin (Calb1) and Growth Associated Protein 43 (GAP-43) in the Auditory Cortex (AC), Inferior Colliculus (IC) and Dorsal Cochlear Nucleus (DCN). Compared to sham-exposed controls, noise-exposed animals had significantly (p<0.05): lower levels of GABA(A)α1 in the contralateral AC at day-16 and day-32, lower levels of GAD-67 in the ipsilateral DCN at day-4, lower levels of Calb1 in the ipsilateral DCN at day-0, lower levels of GABA(A)α1 in the ipsilateral AC at day-4 and day-32. GAP-43 was reduced in the ipsilateral AC for the duration of the experiment. These complex fluctuations in protein expression suggests that for at least a month following acoustic trauma the auditory system is adapting to a new pattern of sensory input.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22428005</pmid><doi>10.1371/journal.pone.0033272</doi><tpages>e33272</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2012-03, Vol.7 (3), p.e33272-e33272 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1323999433 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Acoustic noise Acoustic properties Acoustic Stimulation Acoustics Analysis of Variance Animals Auditory plasticity Auditory system Biology Biomarkers - metabolism Blotting, Western Calbindin Calbindin 1 Calbindins Central nervous system Cochlea Cochlear nuclei Cochlear Nucleus - metabolism Colliculus Cortex (auditory) Cortex (somatosensory) Disorders Evoked Potentials, Auditory, Brain Stem - physiology Exposure GAP-43 protein GAP-43 Protein - metabolism Glutamate decarboxylase Glutamate Decarboxylase - metabolism Glutamate receptors Glutamic acid receptors Hearing loss Hearing Loss, Noise-Induced - metabolism Hearing protection Inferior colliculus Markers Medicine N-Methyl-D-aspartic acid receptors Nerve Tissue Proteins - metabolism Neuronal Plasticity - genetics Neuronal Plasticity - physiology Neuroplasticity Neurotransmission Neurotransmitters Noise Noise control Noise levels Polypeptides Proteins Rats Receptors, GABA-A - metabolism Receptors, N-Methyl-D-Aspartate - metabolism Rodents S100 Calcium Binding Protein G - metabolism Somatosensory cortex Studies Synaptic Transmission - genetics Synaptic Transmission - physiology Tinnitus Trauma Trends Western blotting γ-Aminobutyric acid A receptors |
| title | Tracking the expression of excitatory and inhibitory neurotransmission-related proteins and neuroplasticity markers after noise induced hearing loss |
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