Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats
Calcium ions (Ca 2+ ) are important second messengers in neurons. Ketamine (KETAM) is an anesthetic and analgesic, with psychotomimetic effects and abuse potential. KETAM modulates the entry of Ca 2+ in neurons through glutamate receptors, but its effect on transient receptor potential melastatin 2...
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| Veröffentlicht in: | Cellular and molecular neurobiology 2017, Vol.37 (1), p.133-144 |
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| creator | Demirdaş, Arif Nazıroğlu, Mustafa Övey, Ishak Suat |
| description | Calcium ions (Ca
2+
) are important second messengers in neurons. Ketamine (KETAM) is an anesthetic and analgesic, with psychotomimetic effects and abuse potential. KETAM modulates the entry of Ca
2+
in neurons through glutamate receptors, but its effect on transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) channels has not been clarified. This study investigated the short-term effects of KETAM on oxidative stress and TRPM2 and TRPV1 channel gating in hippocampal and dorsal root ganglion (DRG) neurons of rats. Freshly isolated hippocampal and DRG neurons were incubated for 24 h with KETAM (0.3 mM). The TRPM2 channel antagonist,
N
-(
p
-amylcinnamoyl)anthranilic acid (ACA), inhibited cumene hydroperoxide and ADP-ribose-induced TRPM2 currents in the neurons, and capsazepine (CPZ) inhibited capsaicin-induced TRPV1 currents. The TRPM2 and TRPV1 channel current densities and intracellular free calcium ion concentration of the neurons were lower in the neurons exposed to ACA and CPZ compared to the control neurons, respectively. However, the values were not further decreased by the KETAM + CPZ and KETAM + ACA treatments. KETAM decreased lipid peroxidation levels in the neurons but increased glutathione peroxidase activity. In conclusion, short-term KETAM treatment decreased oxidative stress levels but did not seem to influence TRPM2- and TRPV1-mediated Ca
2+
entry. |
| doi_str_mv | 10.1007/s10571-016-0353-4 |
| format | Article |
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2+
) are important second messengers in neurons. Ketamine (KETAM) is an anesthetic and analgesic, with psychotomimetic effects and abuse potential. KETAM modulates the entry of Ca
2+
in neurons through glutamate receptors, but its effect on transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) channels has not been clarified. This study investigated the short-term effects of KETAM on oxidative stress and TRPM2 and TRPV1 channel gating in hippocampal and dorsal root ganglion (DRG) neurons of rats. Freshly isolated hippocampal and DRG neurons were incubated for 24 h with KETAM (0.3 mM). The TRPM2 channel antagonist,
N
-(
p
-amylcinnamoyl)anthranilic acid (ACA), inhibited cumene hydroperoxide and ADP-ribose-induced TRPM2 currents in the neurons, and capsazepine (CPZ) inhibited capsaicin-induced TRPV1 currents. The TRPM2 and TRPV1 channel current densities and intracellular free calcium ion concentration of the neurons were lower in the neurons exposed to ACA and CPZ compared to the control neurons, respectively. However, the values were not further decreased by the KETAM + CPZ and KETAM + ACA treatments. KETAM decreased lipid peroxidation levels in the neurons but increased glutathione peroxidase activity. In conclusion, short-term KETAM treatment decreased oxidative stress levels but did not seem to influence TRPM2- and TRPV1-mediated Ca
2+
entry.</description><identifier>ISSN: 0272-4340</identifier><identifier>ISSN: 1573-6830</identifier><identifier>EISSN: 1573-6830</identifier><identifier>DOI: 10.1007/s10571-016-0353-4</identifier><identifier>PMID: 26935063</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Analgesics - administration & dosage ; Animals ; Anthranilic acid ; Biomedical and Life Sciences ; Biomedicine ; Calcium (intracellular) ; Calcium influx ; Calcium Signaling - drug effects ; Calcium Signaling - physiology ; Capsaicin ; Capsaicin receptors ; Capsazepine ; Cell Biology ; Channel gating ; Cumene hydroperoxide ; Dorsal root ganglia ; Drug abuse ; Drug Administration Schedule ; Ganglia, Spinal - drug effects ; Ganglia, Spinal - metabolism ; Glutamic acid receptors ; Glutathione peroxidase ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - metabolism ; Ion Channel Gating - drug effects ; Ion Channel Gating - physiology ; Ketamine ; Ketamine - administration & dosage ; Lipid peroxidation ; Male ; Neurobiology ; Neurons ; Neurosciences ; Original Research ; Oxidative stress ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Rats ; Rats, Wistar ; Ribose ; Rodents ; Second messengers ; Short term ; Transient receptor potential proteins ; Treatment Outcome ; TRPM Cation Channels - metabolism ; TRPV Cation Channels - metabolism</subject><ispartof>Cellular and molecular neurobiology, 2017, Vol.37 (1), p.133-144</ispartof><rights>Springer Science+Business Media New York 2016</rights><rights>Copyright Springer Science & Business Media 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-3147488e88af36cc953aca7c3710651db03a4b84a00b83b7072c53ab9b2af4e13</citedby><cites>FETCH-LOGICAL-c372t-3147488e88af36cc953aca7c3710651db03a4b84a00b83b7072c53ab9b2af4e13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10571-016-0353-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10571-016-0353-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27928,27929,41492,42561,51323</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26935063$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Demirdaş, Arif</creatorcontrib><creatorcontrib>Nazıroğlu, Mustafa</creatorcontrib><creatorcontrib>Övey, Ishak Suat</creatorcontrib><title>Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats</title><title>Cellular and molecular neurobiology</title><addtitle>Cell Mol Neurobiol</addtitle><addtitle>Cell Mol Neurobiol</addtitle><description>Calcium ions (Ca
2+
) are important second messengers in neurons. Ketamine (KETAM) is an anesthetic and analgesic, with psychotomimetic effects and abuse potential. KETAM modulates the entry of Ca
2+
in neurons through glutamate receptors, but its effect on transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) channels has not been clarified. This study investigated the short-term effects of KETAM on oxidative stress and TRPM2 and TRPV1 channel gating in hippocampal and dorsal root ganglion (DRG) neurons of rats. Freshly isolated hippocampal and DRG neurons were incubated for 24 h with KETAM (0.3 mM). The TRPM2 channel antagonist,
N
-(
p
-amylcinnamoyl)anthranilic acid (ACA), inhibited cumene hydroperoxide and ADP-ribose-induced TRPM2 currents in the neurons, and capsazepine (CPZ) inhibited capsaicin-induced TRPV1 currents. The TRPM2 and TRPV1 channel current densities and intracellular free calcium ion concentration of the neurons were lower in the neurons exposed to ACA and CPZ compared to the control neurons, respectively. However, the values were not further decreased by the KETAM + CPZ and KETAM + ACA treatments. KETAM decreased lipid peroxidation levels in the neurons but increased glutathione peroxidase activity. In conclusion, short-term KETAM treatment decreased oxidative stress levels but did not seem to influence TRPM2- and TRPV1-mediated Ca
2+
entry.</description><subject>Analgesics - administration & dosage</subject><subject>Animals</subject><subject>Anthranilic acid</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Calcium (intracellular)</subject><subject>Calcium influx</subject><subject>Calcium Signaling - drug effects</subject><subject>Calcium Signaling - physiology</subject><subject>Capsaicin</subject><subject>Capsaicin receptors</subject><subject>Capsazepine</subject><subject>Cell Biology</subject><subject>Channel gating</subject><subject>Cumene hydroperoxide</subject><subject>Dorsal root ganglia</subject><subject>Drug abuse</subject><subject>Drug Administration Schedule</subject><subject>Ganglia, Spinal - drug effects</subject><subject>Ganglia, Spinal - metabolism</subject><subject>Glutamic acid receptors</subject><subject>Glutathione peroxidase</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Ion Channel Gating - drug effects</subject><subject>Ion Channel Gating - physiology</subject><subject>Ketamine</subject><subject>Ketamine - administration & dosage</subject><subject>Lipid peroxidation</subject><subject>Male</subject><subject>Neurobiology</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Original Research</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Ribose</subject><subject>Rodents</subject><subject>Second messengers</subject><subject>Short term</subject><subject>Transient receptor potential proteins</subject><subject>Treatment Outcome</subject><subject>TRPM Cation Channels - metabolism</subject><subject>TRPV Cation Channels - metabolism</subject><issn>0272-4340</issn><issn>1573-6830</issn><issn>1573-6830</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1DAUhS0EokPhAdggS2y6Cb3-SeIs0ZT-qEVF0wGWkeO5mXGV2MF2EDwNr4qHKQghsbpXOt851_Ih5CWDNwygPo0MypoVwKoCRCkK-YgsWFmLolICHpMF8JoXUkg4Is9ivAeABqB8So541YgSKrEgP-52PqRijWGk15j0aB3SdUCdRnSJnqHJe8RIb7_ZjU72K9K7FDBG-tmmnZ8TvXL9MKMz1m3pevXhPafabfbbJ0aXO-0cDvQiO7NsHU07pJd2mrzR4zTHX-yZD1EPdOV9yqTbDtY76nu60ik-J096PUR88TCPycfzd-vlZXFze3G1fHtTGFHzVAgma6kUKqV7URnTlEIbXWeRQVWyTQdCy05JDdAp0dVQc5ORrum47iUycUxODrlT8F9mjKkdbTQ4DNqhn2PLFK-qSkq-R1__g977Obj8ukwpUPmbZZMpdqBM8DEG7Nsp2FGH7y2Ddt9ee2ivze21-_ZamT2vHpLnbsTNH8fvujLAD0DMktti-Ov0f1N_Aow3pKU</recordid><startdate>2017</startdate><enddate>2017</enddate><creator>Demirdaş, Arif</creator><creator>Nazıroğlu, Mustafa</creator><creator>Övey, Ishak Suat</creator><general>Springer US</general><general>Springer Nature 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></search><sort><creationdate>2017</creationdate><title>Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats</title><author>Demirdaş, Arif ; Nazıroğlu, Mustafa ; Övey, Ishak Suat</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-3147488e88af36cc953aca7c3710651db03a4b84a00b83b7072c53ab9b2af4e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Analgesics - administration & dosage</topic><topic>Animals</topic><topic>Anthranilic acid</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Calcium (intracellular)</topic><topic>Calcium influx</topic><topic>Calcium Signaling - drug effects</topic><topic>Calcium Signaling - physiology</topic><topic>Capsaicin</topic><topic>Capsaicin receptors</topic><topic>Capsazepine</topic><topic>Cell Biology</topic><topic>Channel gating</topic><topic>Cumene hydroperoxide</topic><topic>Dorsal root ganglia</topic><topic>Drug abuse</topic><topic>Drug Administration Schedule</topic><topic>Ganglia, Spinal - drug effects</topic><topic>Ganglia, Spinal - metabolism</topic><topic>Glutamic acid receptors</topic><topic>Glutathione peroxidase</topic><topic>Hippocampus</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Ion Channel Gating - drug effects</topic><topic>Ion Channel Gating - physiology</topic><topic>Ketamine</topic><topic>Ketamine - administration & dosage</topic><topic>Lipid peroxidation</topic><topic>Male</topic><topic>Neurobiology</topic><topic>Neurons</topic><topic>Neurosciences</topic><topic>Original Research</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Ribose</topic><topic>Rodents</topic><topic>Second messengers</topic><topic>Short term</topic><topic>Transient receptor potential proteins</topic><topic>Treatment Outcome</topic><topic>TRPM Cation Channels - metabolism</topic><topic>TRPV Cation Channels - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Demirdaş, Arif</creatorcontrib><creatorcontrib>Nazıroğlu, Mustafa</creatorcontrib><creatorcontrib>Övey, Ishak Suat</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><jtitle>Cellular and molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Demirdaş, Arif</au><au>Nazıroğlu, Mustafa</au><au>Övey, Ishak Suat</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats</atitle><jtitle>Cellular and molecular neurobiology</jtitle><stitle>Cell Mol Neurobiol</stitle><addtitle>Cell Mol Neurobiol</addtitle><date>2017</date><risdate>2017</risdate><volume>37</volume><issue>1</issue><spage>133</spage><epage>144</epage><pages>133-144</pages><issn>0272-4340</issn><issn>1573-6830</issn><eissn>1573-6830</eissn><abstract>Calcium ions (Ca
2+
) are important second messengers in neurons. Ketamine (KETAM) is an anesthetic and analgesic, with psychotomimetic effects and abuse potential. KETAM modulates the entry of Ca
2+
in neurons through glutamate receptors, but its effect on transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) channels has not been clarified. This study investigated the short-term effects of KETAM on oxidative stress and TRPM2 and TRPV1 channel gating in hippocampal and dorsal root ganglion (DRG) neurons of rats. Freshly isolated hippocampal and DRG neurons were incubated for 24 h with KETAM (0.3 mM). The TRPM2 channel antagonist,
N
-(
p
-amylcinnamoyl)anthranilic acid (ACA), inhibited cumene hydroperoxide and ADP-ribose-induced TRPM2 currents in the neurons, and capsazepine (CPZ) inhibited capsaicin-induced TRPV1 currents. The TRPM2 and TRPV1 channel current densities and intracellular free calcium ion concentration of the neurons were lower in the neurons exposed to ACA and CPZ compared to the control neurons, respectively. However, the values were not further decreased by the KETAM + CPZ and KETAM + ACA treatments. KETAM decreased lipid peroxidation levels in the neurons but increased glutathione peroxidase activity. In conclusion, short-term KETAM treatment decreased oxidative stress levels but did not seem to influence TRPM2- and TRPV1-mediated Ca
2+
entry.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>26935063</pmid><doi>10.1007/s10571-016-0353-4</doi><tpages>12</tpages></addata></record> |
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| subjects | Analgesics - administration & dosage Animals Anthranilic acid Biomedical and Life Sciences Biomedicine Calcium (intracellular) Calcium influx Calcium Signaling - drug effects Calcium Signaling - physiology Capsaicin Capsaicin receptors Capsazepine Cell Biology Channel gating Cumene hydroperoxide Dorsal root ganglia Drug abuse Drug Administration Schedule Ganglia, Spinal - drug effects Ganglia, Spinal - metabolism Glutamic acid receptors Glutathione peroxidase Hippocampus Hippocampus - drug effects Hippocampus - metabolism Ion Channel Gating - drug effects Ion Channel Gating - physiology Ketamine Ketamine - administration & dosage Lipid peroxidation Male Neurobiology Neurons Neurosciences Original Research Oxidative stress Oxidative Stress - drug effects Oxidative Stress - physiology Rats Rats, Wistar Ribose Rodents Second messengers Short term Transient receptor potential proteins Treatment Outcome TRPM Cation Channels - metabolism TRPV Cation Channels - metabolism |
| title | Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats |
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