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Protein kinase A and C signaling induces bilirubin potentiation of GABA/glycinergic synaptic transmission in rat ventral cochlear nucleus neurons
Abstract Previous studies have suggested that bilirubin can potentiate GABA/glycinergic synaptic transmission in lateral superior olivary nucleus neurons, but the cellular mechanism has not been defined. The present study evaluated the possible roles of protein kinase A (PKA) and C (PKC) in bilirubi...
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| Published in: | Brain research 2010-08, Vol.1348, p.30-41 |
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| creator | Li, Chun-Yan Shi, Hai-Bo Chen, Zheng-Nong Ye, Hai-Bo Song, Ning-ying Yin, Shan-Kai |
| description | Abstract Previous studies have suggested that bilirubin can potentiate GABA/glycinergic synaptic transmission in lateral superior olivary nucleus neurons, but the cellular mechanism has not been defined. The present study evaluated the possible roles of protein kinase A (PKA) and C (PKC) in bilirubin potentiation of GABA/glycinergic synaptic transmission in rat ventral cochlear nucleus (VCN) neurons. VCN neurons were acutely isolated from postnatal 10-12-day-old (P10-12) rats and were voltage-clamped in whole-cell mode. Miniature inhibitory postsynaptic currents (mIPSC) frequencies, but not amplitude, were increased by bilirubin. Forskolin (PKA activator) and H-89 (PKA inhibitor) also individually increased mIPSCs frequency, with an additional increase induced by co-incubation with bilirubin and H-89. Pretreatment with forskolin blocked bilirubin potentiation. mIPSC frequency was not altered by phorbol 12,13-diacetate (PKC activator), but mIPSC frequency was increased following co-application of bilirubin. The mIPSC frequency was increased by chelerythrine (PKC inhibitor), and then further increased after the addition of bilirubin. Neither H-89, forskolin, nor PDA, nor their co-application with bilirubin affected mIPSC amplitudes of GABA-activated (IGABA )/glycine-activated (Igly ) currents, suggesting a presynaptic locus of activity. Chelerythrine decreased the mIPSC amplitudes and IGABA /Igly , suggesting a postsynaptic locus of activity. These data suggest that both PKA and PKC can modulate GABA and glycine release in rat VCN neurons. Bilirubin facilitates transmitter release via presynaptic PKA activation, which might provide insight into the cellular mechanism underlying bilirubin-induced hearing dysfunction. |
| doi_str_mv | 10.1016/j.brainres.2010.06.022 |
| format | article |
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The present study evaluated the possible roles of protein kinase A (PKA) and C (PKC) in bilirubin potentiation of GABA/glycinergic synaptic transmission in rat ventral cochlear nucleus (VCN) neurons. VCN neurons were acutely isolated from postnatal 10-12-day-old (P10-12) rats and were voltage-clamped in whole-cell mode. Miniature inhibitory postsynaptic currents (mIPSC) frequencies, but not amplitude, were increased by bilirubin. Forskolin (PKA activator) and H-89 (PKA inhibitor) also individually increased mIPSCs frequency, with an additional increase induced by co-incubation with bilirubin and H-89. Pretreatment with forskolin blocked bilirubin potentiation. mIPSC frequency was not altered by phorbol 12,13-diacetate (PKC activator), but mIPSC frequency was increased following co-application of bilirubin. The mIPSC frequency was increased by chelerythrine (PKC inhibitor), and then further increased after the addition of bilirubin. Neither H-89, forskolin, nor PDA, nor their co-application with bilirubin affected mIPSC amplitudes of GABA-activated (IGABA )/glycine-activated (Igly ) currents, suggesting a presynaptic locus of activity. Chelerythrine decreased the mIPSC amplitudes and IGABA /Igly , suggesting a postsynaptic locus of activity. These data suggest that both PKA and PKC can modulate GABA and glycine release in rat VCN neurons. Bilirubin facilitates transmitter release via presynaptic PKA activation, which might provide insight into the cellular mechanism underlying bilirubin-induced hearing dysfunction.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2010.06.022</identifier><identifier>PMID: 20561511</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Animals, Newborn ; Antioxidants - pharmacology ; Benzophenanthridines - pharmacology ; Bilirubin ; Bilirubin - pharmacology ; Cochlear Nucleus - cytology ; Colforsin - pharmacology ; Cyclic AMP-Dependent Protein Kinases - metabolism ; Enzyme Activation - drug effects ; GABAergic ; gamma-Aminobutyric Acid - metabolism ; Glycine - metabolism ; Glycinergic ; In Vitro Techniques ; Isoquinolines - pharmacology ; Neural Inhibition - drug effects ; Neurology ; Neurons - drug effects ; Patch-Clamp Techniques - methods ; Phorbol Esters - pharmacology ; Protein kinase A ; Protein kinase C ; Protein Kinase C - metabolism ; Rats ; Signal Transduction - drug effects ; Sulfonamides - pharmacology ; Synaptic Transmission - drug effects ; Ventral cochlear nucleus</subject><ispartof>Brain research, 2010-08, Vol.1348, p.30-41</ispartof><rights>Elsevier B.V.</rights><rights>2010 Elsevier B.V.</rights><rights>Copyright 2010 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-b503cdffb5eb7c731ee236ef7fbd64d50f25e75a4b50c5742375b5352c890a3e3</citedby><cites>FETCH-LOGICAL-c454t-b503cdffb5eb7c731ee236ef7fbd64d50f25e75a4b50c5742375b5352c890a3e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20561511$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Chun-Yan</creatorcontrib><creatorcontrib>Shi, Hai-Bo</creatorcontrib><creatorcontrib>Chen, Zheng-Nong</creatorcontrib><creatorcontrib>Ye, Hai-Bo</creatorcontrib><creatorcontrib>Song, Ning-ying</creatorcontrib><creatorcontrib>Yin, Shan-Kai</creatorcontrib><title>Protein kinase A and C signaling induces bilirubin potentiation of GABA/glycinergic synaptic transmission in rat ventral cochlear nucleus neurons</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract Previous studies have suggested that bilirubin can potentiate GABA/glycinergic synaptic transmission in lateral superior olivary nucleus neurons, but the cellular mechanism has not been defined. The present study evaluated the possible roles of protein kinase A (PKA) and C (PKC) in bilirubin potentiation of GABA/glycinergic synaptic transmission in rat ventral cochlear nucleus (VCN) neurons. VCN neurons were acutely isolated from postnatal 10-12-day-old (P10-12) rats and were voltage-clamped in whole-cell mode. Miniature inhibitory postsynaptic currents (mIPSC) frequencies, but not amplitude, were increased by bilirubin. Forskolin (PKA activator) and H-89 (PKA inhibitor) also individually increased mIPSCs frequency, with an additional increase induced by co-incubation with bilirubin and H-89. Pretreatment with forskolin blocked bilirubin potentiation. mIPSC frequency was not altered by phorbol 12,13-diacetate (PKC activator), but mIPSC frequency was increased following co-application of bilirubin. The mIPSC frequency was increased by chelerythrine (PKC inhibitor), and then further increased after the addition of bilirubin. Neither H-89, forskolin, nor PDA, nor their co-application with bilirubin affected mIPSC amplitudes of GABA-activated (IGABA )/glycine-activated (Igly ) currents, suggesting a presynaptic locus of activity. Chelerythrine decreased the mIPSC amplitudes and IGABA /Igly , suggesting a postsynaptic locus of activity. These data suggest that both PKA and PKC can modulate GABA and glycine release in rat VCN neurons. Bilirubin facilitates transmitter release via presynaptic PKA activation, which might provide insight into the cellular mechanism underlying bilirubin-induced hearing dysfunction.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Antioxidants - pharmacology</subject><subject>Benzophenanthridines - pharmacology</subject><subject>Bilirubin</subject><subject>Bilirubin - pharmacology</subject><subject>Cochlear Nucleus - cytology</subject><subject>Colforsin - pharmacology</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>Enzyme Activation - drug effects</subject><subject>GABAergic</subject><subject>gamma-Aminobutyric Acid - metabolism</subject><subject>Glycine - metabolism</subject><subject>Glycinergic</subject><subject>In Vitro Techniques</subject><subject>Isoquinolines - pharmacology</subject><subject>Neural Inhibition - drug effects</subject><subject>Neurology</subject><subject>Neurons - drug effects</subject><subject>Patch-Clamp Techniques - methods</subject><subject>Phorbol Esters - pharmacology</subject><subject>Protein kinase A</subject><subject>Protein kinase C</subject><subject>Protein Kinase C - metabolism</subject><subject>Rats</subject><subject>Signal Transduction - drug effects</subject><subject>Sulfonamides - pharmacology</subject><subject>Synaptic Transmission - drug effects</subject><subject>Ventral cochlear nucleus</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqFks9u1DAQhyMEokvhFSrfOGU7tmM7uSCWFRSkSiABZ8txJou3WWfxJJX2MXhjHG3LgUtP_qPvN2P5m6K44rDmwPX1ft0mF2JCWgvIl6DXIMSzYsVrI0otKnherABAl3XTyIviFdE-H6Vs4GVxIUBprjhfFX--pXHCENldiI6QbZiLHdsyCrvohhB3LMRu9kisDUNIc5vRY07EKbgpjJGNPbvZfNhc74aTDxHTLnhGp-iOU95MyUU6BKKFzMnkJnafs8kNzI_-14AusTj7AWdiEec0RnpdvOjdQPjmYb0sfn76-GP7ubz9evNlu7ktfaWqqWwVSN_1fauwNd5Ijiikxt70baerTkEvFBrlqgx6ZSohjWqVVMLXDTiJ8rJ4e657TOPvGWmy-aEeh8FFHGeytTGq1lVdPUmaqgGhZa0zqc-kTyNRwt4eUzi4dLIc7OLN7u2jN7t4s6Bt9paDVw8t5vaA3b_Yo6gMvD8DmL_kPmCy5ANGj11I6CfbjeHpHu_-K-Gz4ODdcIcnpP04p6ycLLckLNjvy_Qsw8MBuFQG5F9pFcS3</recordid><startdate>20100812</startdate><enddate>20100812</enddate><creator>Li, Chun-Yan</creator><creator>Shi, Hai-Bo</creator><creator>Chen, Zheng-Nong</creator><creator>Ye, Hai-Bo</creator><creator>Song, Ning-ying</creator><creator>Yin, Shan-Kai</creator><general>Elsevier B.V</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>7X8</scope><scope>7TK</scope></search><sort><creationdate>20100812</creationdate><title>Protein kinase A and C signaling induces bilirubin potentiation of GABA/glycinergic synaptic transmission in rat ventral cochlear nucleus neurons</title><author>Li, Chun-Yan ; Shi, Hai-Bo ; Chen, Zheng-Nong ; Ye, Hai-Bo ; Song, Ning-ying ; Yin, Shan-Kai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-b503cdffb5eb7c731ee236ef7fbd64d50f25e75a4b50c5742375b5352c890a3e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Antioxidants - pharmacology</topic><topic>Benzophenanthridines - pharmacology</topic><topic>Bilirubin</topic><topic>Bilirubin - pharmacology</topic><topic>Cochlear Nucleus - cytology</topic><topic>Colforsin - pharmacology</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>Enzyme Activation - drug effects</topic><topic>GABAergic</topic><topic>gamma-Aminobutyric Acid - metabolism</topic><topic>Glycine - metabolism</topic><topic>Glycinergic</topic><topic>In Vitro Techniques</topic><topic>Isoquinolines - pharmacology</topic><topic>Neural Inhibition - drug effects</topic><topic>Neurology</topic><topic>Neurons - drug effects</topic><topic>Patch-Clamp Techniques - methods</topic><topic>Phorbol Esters - pharmacology</topic><topic>Protein kinase A</topic><topic>Protein kinase C</topic><topic>Protein Kinase C - metabolism</topic><topic>Rats</topic><topic>Signal Transduction - drug effects</topic><topic>Sulfonamides - pharmacology</topic><topic>Synaptic Transmission - drug effects</topic><topic>Ventral cochlear nucleus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Chun-Yan</creatorcontrib><creatorcontrib>Shi, Hai-Bo</creatorcontrib><creatorcontrib>Chen, Zheng-Nong</creatorcontrib><creatorcontrib>Ye, Hai-Bo</creatorcontrib><creatorcontrib>Song, Ning-ying</creatorcontrib><creatorcontrib>Yin, Shan-Kai</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Chun-Yan</au><au>Shi, Hai-Bo</au><au>Chen, Zheng-Nong</au><au>Ye, Hai-Bo</au><au>Song, Ning-ying</au><au>Yin, Shan-Kai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protein kinase A and C signaling induces bilirubin potentiation of GABA/glycinergic synaptic transmission in rat ventral cochlear nucleus neurons</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2010-08-12</date><risdate>2010</risdate><volume>1348</volume><spage>30</spage><epage>41</epage><pages>30-41</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><notes>ObjectType-Article-2</notes><notes>ObjectType-Feature-1</notes><abstract>Abstract Previous studies have suggested that bilirubin can potentiate GABA/glycinergic synaptic transmission in lateral superior olivary nucleus neurons, but the cellular mechanism has not been defined. The present study evaluated the possible roles of protein kinase A (PKA) and C (PKC) in bilirubin potentiation of GABA/glycinergic synaptic transmission in rat ventral cochlear nucleus (VCN) neurons. VCN neurons were acutely isolated from postnatal 10-12-day-old (P10-12) rats and were voltage-clamped in whole-cell mode. Miniature inhibitory postsynaptic currents (mIPSC) frequencies, but not amplitude, were increased by bilirubin. Forskolin (PKA activator) and H-89 (PKA inhibitor) also individually increased mIPSCs frequency, with an additional increase induced by co-incubation with bilirubin and H-89. Pretreatment with forskolin blocked bilirubin potentiation. mIPSC frequency was not altered by phorbol 12,13-diacetate (PKC activator), but mIPSC frequency was increased following co-application of bilirubin. The mIPSC frequency was increased by chelerythrine (PKC inhibitor), and then further increased after the addition of bilirubin. Neither H-89, forskolin, nor PDA, nor their co-application with bilirubin affected mIPSC amplitudes of GABA-activated (IGABA )/glycine-activated (Igly ) currents, suggesting a presynaptic locus of activity. Chelerythrine decreased the mIPSC amplitudes and IGABA /Igly , suggesting a postsynaptic locus of activity. These data suggest that both PKA and PKC can modulate GABA and glycine release in rat VCN neurons. Bilirubin facilitates transmitter release via presynaptic PKA activation, which might provide insight into the cellular mechanism underlying bilirubin-induced hearing dysfunction.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>20561511</pmid><doi>10.1016/j.brainres.2010.06.022</doi><tpages>12</tpages></addata></record> |
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| subjects | Animals Animals, Newborn Antioxidants - pharmacology Benzophenanthridines - pharmacology Bilirubin Bilirubin - pharmacology Cochlear Nucleus - cytology Colforsin - pharmacology Cyclic AMP-Dependent Protein Kinases - metabolism Enzyme Activation - drug effects GABAergic gamma-Aminobutyric Acid - metabolism Glycine - metabolism Glycinergic In Vitro Techniques Isoquinolines - pharmacology Neural Inhibition - drug effects Neurology Neurons - drug effects Patch-Clamp Techniques - methods Phorbol Esters - pharmacology Protein kinase A Protein kinase C Protein Kinase C - metabolism Rats Signal Transduction - drug effects Sulfonamides - pharmacology Synaptic Transmission - drug effects Ventral cochlear nucleus |
| title | Protein kinase A and C signaling induces bilirubin potentiation of GABA/glycinergic synaptic transmission in rat ventral cochlear nucleus neurons |
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