Transient Receptor Potential Vanilloid 4 Activation-Induced Increase in Glycine-Activated Current in Mouse Hippocampal Pyramidal Neurons
Background/Aims: Glycine plays an important role in regulating hippocampal inhibitory/ excitatory neurotransmission through activating glycine receptors (GlyRs) and acting as a co-agonist of N-methyl-d-aspartate-type glutamate receptors. Activation of transient receptor potential vanilloid 4 (TRPV4)...
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| Veröffentlicht in: | Cellular physiology and biochemistry 2018-01, Vol.45 (3), p.1084-1096 |
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| creator | Qi, Mengwen Wu, Chunfeng Wang, Zhouqing Zhou, Li Men, Chen Du, Yimei Huang, Songming Chen, Lei Chen, Ling |
| description | Background/Aims: Glycine plays an important role in regulating hippocampal inhibitory/ excitatory neurotransmission through activating glycine receptors (GlyRs) and acting as a co-agonist of N-methyl-d-aspartate-type glutamate receptors. Activation of transient receptor potential vanilloid 4 (TRPV4) is reported to inhibit hippocampal A-type γ-aminobutyric acid receptor, a ligand-gated chloride ion channel. GlyRs are also ligand-gated chloride ion channels and this paper aimed to explore whether activation of TRPV4 could modulate GlyRs. Methods: Whole-cell patch clamp recording was employed to record glycine-activated current (I Gly ) and Western blot was conducted to assess GlyRs subunits protein expression. Results: Application of TRPV4 agonist (GSK1016790A or 5,6-EET) increased I Gly in mouse hippocampal CA1 pyramidal neurons. This action was blocked by specific antagonists of TRPV4 (RN-1734 or HC-067047) and GlyR (strychnine), indicating that activation of TRPV4 increases strychnine-sensitive GlyR function in mouse hippocampal pyramidal neurons. GSK1016790A-induced increase in I Gly was significantly attenuated by protein kinase C (PKC) (BIM II or D-sphingosine) or calcium/calmodulin-dependent protein kinase II (CaMKII) (KN-62 or KN-93) antagonists but was unaffected by protein kinase A or protein tyrosine kinase antagonists. Finally, hippocampal protein levels of GlyR α1 α2, α3 and β subunits were not changed by treatment with GSK1016790A for 30 min or 1 h, but GlyR α2, α3 and β subunits protein levels increased in mice that were intracerebroventricularly (icv.) injected with GSK1016790A for 5 d. Conclusion: Activation of TRPV4 increases GlyR function and expression, and PKC and CaMKII signaling pathways are involved in TRPV4 activation-induced increase in I Gly . This study indicates that GlyRs may be effective targets for TRPV4-induced modulation of hippocampal inhibitory neurotransmission. |
| doi_str_mv | 10.1159/000487350 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_proquest_journals_2117159962</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_9bfc588b8d8b4dd9a9315d08d700e9eb</doaj_id><sourcerecordid>2117159962</sourcerecordid><originalsourceid>FETCH-LOGICAL-c463t-236fd3223322ca7f30f763628e152965cb5bd2317532824d5ceb66fcec5bb45a3</originalsourceid><addsrcrecordid>eNptkUtv1DAUhSMEog9YsEcoUjdlEfAjju1lGUE7UoERKmwtx76pPCR2sBOk-Qf8bFwyZIFYWL7X57tHvjpF8QKjNxgz-RYhVAtOGXpUnOKa4EpyLh7nGmFWCSn4SXGW0h7llkvytDghsqaS1OK0-HUXtU8O_FR-AQPjFGK5C1Pune7Lb9q7vg_OlnV5ZSb3U08u-Grr7WzAlltvIugEpfPldX8wzkN1xLK6mWN88M3ixzBn6saNYzB6GLPz7hD14GyuPsEcg0_Piied7hM8P97nxdcP7-82N9Xt5-vt5uq2MnVDp4rQprOUEJqP0byjqOMNbYgAzIhsmGlZawnFnFEiSG2ZgbZpOgOGtW3NND0vtouvDXqvxugGHQ8qaKf-PIR4r3ScnOlBybYzTIhWWNHW1kotKWYWCcsRAglt9rpcvMYYfsyQJjW4ZKDvtYe8sSIIEYKpxE1GL_5B92GOPm-qCMY8pygbkqnXC2ViSClCt34QI_UQtVqjzuyro-PcDmBX8m-2GXi5AN91vIe4Auv8xX_lze7dQqjRdvQ3e3G4oQ</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2117159962</pqid></control><display><type>article</type><title>Transient Receptor Potential Vanilloid 4 Activation-Induced Increase in Glycine-Activated Current in Mouse Hippocampal Pyramidal Neurons</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Karger Open Access</source><creator>Qi, Mengwen ; Wu, Chunfeng ; Wang, Zhouqing ; Zhou, Li ; Men, Chen ; Du, Yimei ; Huang, Songming ; Chen, Lei ; Chen, Ling</creator><creatorcontrib>Qi, Mengwen ; Wu, Chunfeng ; Wang, Zhouqing ; Zhou, Li ; Men, Chen ; Du, Yimei ; Huang, Songming ; Chen, Lei ; Chen, Ling</creatorcontrib><description>Background/Aims: Glycine plays an important role in regulating hippocampal inhibitory/ excitatory neurotransmission through activating glycine receptors (GlyRs) and acting as a co-agonist of N-methyl-d-aspartate-type glutamate receptors. Activation of transient receptor potential vanilloid 4 (TRPV4) is reported to inhibit hippocampal A-type γ-aminobutyric acid receptor, a ligand-gated chloride ion channel. GlyRs are also ligand-gated chloride ion channels and this paper aimed to explore whether activation of TRPV4 could modulate GlyRs. Methods: Whole-cell patch clamp recording was employed to record glycine-activated current (I Gly ) and Western blot was conducted to assess GlyRs subunits protein expression. Results: Application of TRPV4 agonist (GSK1016790A or 5,6-EET) increased I Gly in mouse hippocampal CA1 pyramidal neurons. This action was blocked by specific antagonists of TRPV4 (RN-1734 or HC-067047) and GlyR (strychnine), indicating that activation of TRPV4 increases strychnine-sensitive GlyR function in mouse hippocampal pyramidal neurons. GSK1016790A-induced increase in I Gly was significantly attenuated by protein kinase C (PKC) (BIM II or D-sphingosine) or calcium/calmodulin-dependent protein kinase II (CaMKII) (KN-62 or KN-93) antagonists but was unaffected by protein kinase A or protein tyrosine kinase antagonists. Finally, hippocampal protein levels of GlyR α1 α2, α3 and β subunits were not changed by treatment with GSK1016790A for 30 min or 1 h, but GlyR α2, α3 and β subunits protein levels increased in mice that were intracerebroventricularly (icv.) injected with GSK1016790A for 5 d. Conclusion: Activation of TRPV4 increases GlyR function and expression, and PKC and CaMKII signaling pathways are involved in TRPV4 activation-induced increase in I Gly . This study indicates that GlyRs may be effective targets for TRPV4-induced modulation of hippocampal inhibitory neurotransmission.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000487350</identifier><identifier>PMID: 29439248</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject><![CDATA[1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives ; 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology ; Animals ; Benzylamines - pharmacology ; Brain ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism ; Calcium/calmodulin-dependent protein kinase II ; Evoked Potentials - drug effects ; Glycine - pharmacology ; Glycine receptor ; Glycine receptor subunit expression ; Hippocampus - drug effects ; Hippocampus - metabolism ; Kinases ; Laboratory animals ; Leucine - analogs & derivatives ; Leucine - pharmacology ; Ligands ; Mice ; Mice, Inbred ICR ; Morpholines - pharmacology ; Neurosciences ; Original Paper ; Patch-Clamp Techniques ; Phosphorylation ; Protein kinase C ; Protein Kinase C - antagonists & inhibitors ; Protein Kinase C - metabolism ; Proteins ; Pyramidal Cells - drug effects ; Pyramidal Cells - metabolism ; Pyrroles - pharmacology ; Receptors, Glycine - antagonists & inhibitors ; Receptors, Glycine - genetics ; Receptors, Glycine - metabolism ; Signal Transduction - drug effects ; Spinal cord ; Strychnine - pharmacology ; Sulfonamides - pharmacology ; Transient receptor potential vanilloid 4 ; TRPV Cation Channels - agonists ; TRPV Cation Channels - antagonists & inhibitors ; TRPV Cation Channels - metabolism]]></subject><ispartof>Cellular physiology and biochemistry, 2018-01, Vol.45 (3), p.1084-1096</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-236fd3223322ca7f30f763628e152965cb5bd2317532824d5ceb66fcec5bb45a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2102,27635,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29439248$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Qi, Mengwen</creatorcontrib><creatorcontrib>Wu, Chunfeng</creatorcontrib><creatorcontrib>Wang, Zhouqing</creatorcontrib><creatorcontrib>Zhou, Li</creatorcontrib><creatorcontrib>Men, Chen</creatorcontrib><creatorcontrib>Du, Yimei</creatorcontrib><creatorcontrib>Huang, Songming</creatorcontrib><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Chen, Ling</creatorcontrib><title>Transient Receptor Potential Vanilloid 4 Activation-Induced Increase in Glycine-Activated Current in Mouse Hippocampal Pyramidal Neurons</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Glycine plays an important role in regulating hippocampal inhibitory/ excitatory neurotransmission through activating glycine receptors (GlyRs) and acting as a co-agonist of N-methyl-d-aspartate-type glutamate receptors. Activation of transient receptor potential vanilloid 4 (TRPV4) is reported to inhibit hippocampal A-type γ-aminobutyric acid receptor, a ligand-gated chloride ion channel. GlyRs are also ligand-gated chloride ion channels and this paper aimed to explore whether activation of TRPV4 could modulate GlyRs. Methods: Whole-cell patch clamp recording was employed to record glycine-activated current (I Gly ) and Western blot was conducted to assess GlyRs subunits protein expression. Results: Application of TRPV4 agonist (GSK1016790A or 5,6-EET) increased I Gly in mouse hippocampal CA1 pyramidal neurons. This action was blocked by specific antagonists of TRPV4 (RN-1734 or HC-067047) and GlyR (strychnine), indicating that activation of TRPV4 increases strychnine-sensitive GlyR function in mouse hippocampal pyramidal neurons. GSK1016790A-induced increase in I Gly was significantly attenuated by protein kinase C (PKC) (BIM II or D-sphingosine) or calcium/calmodulin-dependent protein kinase II (CaMKII) (KN-62 or KN-93) antagonists but was unaffected by protein kinase A or protein tyrosine kinase antagonists. Finally, hippocampal protein levels of GlyR α1 α2, α3 and β subunits were not changed by treatment with GSK1016790A for 30 min or 1 h, but GlyR α2, α3 and β subunits protein levels increased in mice that were intracerebroventricularly (icv.) injected with GSK1016790A for 5 d. Conclusion: Activation of TRPV4 increases GlyR function and expression, and PKC and CaMKII signaling pathways are involved in TRPV4 activation-induced increase in I Gly . This study indicates that GlyRs may be effective targets for TRPV4-induced modulation of hippocampal inhibitory neurotransmission.</description><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives</subject><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology</subject><subject>Animals</subject><subject>Benzylamines - pharmacology</subject><subject>Brain</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism</subject><subject>Calcium/calmodulin-dependent protein kinase II</subject><subject>Evoked Potentials - drug effects</subject><subject>Glycine - pharmacology</subject><subject>Glycine receptor</subject><subject>Glycine receptor subunit expression</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Leucine - analogs & derivatives</subject><subject>Leucine - pharmacology</subject><subject>Ligands</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Morpholines - pharmacology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Patch-Clamp Techniques</subject><subject>Phosphorylation</subject><subject>Protein kinase C</subject><subject>Protein Kinase C - antagonists & inhibitors</subject><subject>Protein Kinase C - metabolism</subject><subject>Proteins</subject><subject>Pyramidal Cells - drug effects</subject><subject>Pyramidal Cells - metabolism</subject><subject>Pyrroles - pharmacology</subject><subject>Receptors, Glycine - antagonists & inhibitors</subject><subject>Receptors, Glycine - genetics</subject><subject>Receptors, Glycine - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Spinal cord</subject><subject>Strychnine - pharmacology</subject><subject>Sulfonamides - pharmacology</subject><subject>Transient receptor potential vanilloid 4</subject><subject>TRPV Cation Channels - agonists</subject><subject>TRPV Cation Channels - antagonists & inhibitors</subject><subject>TRPV Cation Channels - metabolism</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkUtv1DAUhSMEog9YsEcoUjdlEfAjju1lGUE7UoERKmwtx76pPCR2sBOk-Qf8bFwyZIFYWL7X57tHvjpF8QKjNxgz-RYhVAtOGXpUnOKa4EpyLh7nGmFWCSn4SXGW0h7llkvytDghsqaS1OK0-HUXtU8O_FR-AQPjFGK5C1Pune7Lb9q7vg_OlnV5ZSb3U08u-Grr7WzAlltvIugEpfPldX8wzkN1xLK6mWN88M3ixzBn6saNYzB6GLPz7hD14GyuPsEcg0_Piied7hM8P97nxdcP7-82N9Xt5-vt5uq2MnVDp4rQprOUEJqP0byjqOMNbYgAzIhsmGlZawnFnFEiSG2ZgbZpOgOGtW3NND0vtouvDXqvxugGHQ8qaKf-PIR4r3ScnOlBybYzTIhWWNHW1kotKWYWCcsRAglt9rpcvMYYfsyQJjW4ZKDvtYe8sSIIEYKpxE1GL_5B92GOPm-qCMY8pygbkqnXC2ViSClCt34QI_UQtVqjzuyro-PcDmBX8m-2GXi5AN91vIe4Auv8xX_lze7dQqjRdvQ3e3G4oQ</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Qi, Mengwen</creator><creator>Wu, Chunfeng</creator><creator>Wang, Zhouqing</creator><creator>Zhou, Li</creator><creator>Men, Chen</creator><creator>Du, Yimei</creator><creator>Huang, Songming</creator><creator>Chen, Lei</creator><creator>Chen, Ling</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>Transient Receptor Potential Vanilloid 4 Activation-Induced Increase in Glycine-Activated Current in Mouse Hippocampal Pyramidal Neurons</title><author>Qi, Mengwen ; Wu, Chunfeng ; Wang, Zhouqing ; Zhou, Li ; Men, Chen ; Du, Yimei ; Huang, Songming ; Chen, Lei ; Chen, Ling</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-236fd3223322ca7f30f763628e152965cb5bd2317532824d5ceb66fcec5bb45a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives</topic><topic>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology</topic><topic>Animals</topic><topic>Benzylamines - pharmacology</topic><topic>Brain</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism</topic><topic>Calcium/calmodulin-dependent protein kinase II</topic><topic>Evoked Potentials - drug effects</topic><topic>Glycine - pharmacology</topic><topic>Glycine receptor</topic><topic>Glycine receptor subunit expression</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Leucine - analogs & derivatives</topic><topic>Leucine - pharmacology</topic><topic>Ligands</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>Morpholines - pharmacology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Patch-Clamp Techniques</topic><topic>Phosphorylation</topic><topic>Protein kinase C</topic><topic>Protein Kinase C - antagonists & inhibitors</topic><topic>Protein Kinase C - metabolism</topic><topic>Proteins</topic><topic>Pyramidal Cells - drug effects</topic><topic>Pyramidal Cells - metabolism</topic><topic>Pyrroles - pharmacology</topic><topic>Receptors, Glycine - antagonists & inhibitors</topic><topic>Receptors, Glycine - genetics</topic><topic>Receptors, Glycine - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Spinal cord</topic><topic>Strychnine - pharmacology</topic><topic>Sulfonamides - pharmacology</topic><topic>Transient receptor potential vanilloid 4</topic><topic>TRPV Cation Channels - agonists</topic><topic>TRPV Cation Channels - antagonists & inhibitors</topic><topic>TRPV Cation Channels - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Qi, Mengwen</creatorcontrib><creatorcontrib>Wu, Chunfeng</creatorcontrib><creatorcontrib>Wang, Zhouqing</creatorcontrib><creatorcontrib>Zhou, Li</creatorcontrib><creatorcontrib>Men, Chen</creatorcontrib><creatorcontrib>Du, Yimei</creatorcontrib><creatorcontrib>Huang, Songming</creatorcontrib><creatorcontrib>Chen, Lei</creatorcontrib><creatorcontrib>Chen, Ling</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Qi, Mengwen</au><au>Wu, Chunfeng</au><au>Wang, Zhouqing</au><au>Zhou, Li</au><au>Men, Chen</au><au>Du, Yimei</au><au>Huang, Songming</au><au>Chen, Lei</au><au>Chen, Ling</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transient Receptor Potential Vanilloid 4 Activation-Induced Increase in Glycine-Activated Current in Mouse Hippocampal Pyramidal Neurons</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>45</volume><issue>3</issue><spage>1084</spage><epage>1096</epage><pages>1084-1096</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Glycine plays an important role in regulating hippocampal inhibitory/ excitatory neurotransmission through activating glycine receptors (GlyRs) and acting as a co-agonist of N-methyl-d-aspartate-type glutamate receptors. Activation of transient receptor potential vanilloid 4 (TRPV4) is reported to inhibit hippocampal A-type γ-aminobutyric acid receptor, a ligand-gated chloride ion channel. GlyRs are also ligand-gated chloride ion channels and this paper aimed to explore whether activation of TRPV4 could modulate GlyRs. Methods: Whole-cell patch clamp recording was employed to record glycine-activated current (I Gly ) and Western blot was conducted to assess GlyRs subunits protein expression. Results: Application of TRPV4 agonist (GSK1016790A or 5,6-EET) increased I Gly in mouse hippocampal CA1 pyramidal neurons. This action was blocked by specific antagonists of TRPV4 (RN-1734 or HC-067047) and GlyR (strychnine), indicating that activation of TRPV4 increases strychnine-sensitive GlyR function in mouse hippocampal pyramidal neurons. GSK1016790A-induced increase in I Gly was significantly attenuated by protein kinase C (PKC) (BIM II or D-sphingosine) or calcium/calmodulin-dependent protein kinase II (CaMKII) (KN-62 or KN-93) antagonists but was unaffected by protein kinase A or protein tyrosine kinase antagonists. Finally, hippocampal protein levels of GlyR α1 α2, α3 and β subunits were not changed by treatment with GSK1016790A for 30 min or 1 h, but GlyR α2, α3 and β subunits protein levels increased in mice that were intracerebroventricularly (icv.) injected with GSK1016790A for 5 d. Conclusion: Activation of TRPV4 increases GlyR function and expression, and PKC and CaMKII signaling pathways are involved in TRPV4 activation-induced increase in I Gly . This study indicates that GlyRs may be effective targets for TRPV4-induced modulation of hippocampal inhibitory neurotransmission.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>29439248</pmid><doi>10.1159/000487350</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivatives 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology Animals Benzylamines - pharmacology Brain Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism Calcium/calmodulin-dependent protein kinase II Evoked Potentials - drug effects Glycine - pharmacology Glycine receptor Glycine receptor subunit expression Hippocampus - drug effects Hippocampus - metabolism Kinases Laboratory animals Leucine - analogs & derivatives Leucine - pharmacology Ligands Mice Mice, Inbred ICR Morpholines - pharmacology Neurosciences Original Paper Patch-Clamp Techniques Phosphorylation Protein kinase C Protein Kinase C - antagonists & inhibitors Protein Kinase C - metabolism Proteins Pyramidal Cells - drug effects Pyramidal Cells - metabolism Pyrroles - pharmacology Receptors, Glycine - antagonists & inhibitors Receptors, Glycine - genetics Receptors, Glycine - metabolism Signal Transduction - drug effects Spinal cord Strychnine - pharmacology Sulfonamides - pharmacology Transient receptor potential vanilloid 4 TRPV Cation Channels - agonists TRPV Cation Channels - antagonists & inhibitors TRPV Cation Channels - metabolism |
| title | Transient Receptor Potential Vanilloid 4 Activation-Induced Increase in Glycine-Activated Current in Mouse Hippocampal Pyramidal Neurons |
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