Protein kinase-mediated reciprocal modulatory changes in anesthetic sensitivity of (BK)-K +- and GABA-A receptor-gated conductances in guinea-pig sympathetic neurons
(1) The interaction of substance P (SP)-mediated synaptic transmission with general anesthetics remains unknown. (2) Intracellular recordings were obtained from guinea-pig inferior mesenteric ganglion neurons to study monosynaptic responses to exogenous SP and GABA. (3) Propofol (1–100 μM) caused an...
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| Veröffentlicht in: | Toxicology letters 1998-11, Vol.100, p.97-102 |
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| creator | Stapelfeldt, Wolf H Oleszewski, Jan M |
| description | (1) The interaction of substance P (SP)-mediated synaptic transmission with general anesthetics remains unknown. (2) Intracellular recordings were obtained from guinea-pig inferior mesenteric ganglion neurons to study monosynaptic responses to exogenous SP and GABA. (3) Propofol (1–100
μM) caused an increase in SP-evoked inward current responses and a concurrent decrease in peak amplitude of the afterspike hyperpolarization of intermittently evoked action potentials. These effects were occluded by the (BK)-K
+-channel-selective blocker charybdotoxin (10 nM), and prevented by the protein kinase inhibitor staurosporine (100 nM). (4) Propofol also increased GABA-evoked current (
I
GABA) responses. (5) When elicited during a SP response,
I
GABA was significantly diminished compared to control. In the presence of staurosporine (100 nM), the inhibitory effect of SP upon
I
GABA was abolished, and the propofol-induced augmentation of
I
GABA was significantly increased. (6) Thus, SP-evoked protein kinase activity produced reciprocal changes in anesthetic sensitivity of (BK)-K
+- and GABA A-receptor-gated currents of these sympathetic neurons. |
| doi_str_mv | 10.1016/S0378-4274(98)00171-4 |
| format | Article |
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μM) caused an increase in SP-evoked inward current responses and a concurrent decrease in peak amplitude of the afterspike hyperpolarization of intermittently evoked action potentials. These effects were occluded by the (BK)-K
+-channel-selective blocker charybdotoxin (10 nM), and prevented by the protein kinase inhibitor staurosporine (100 nM). (4) Propofol also increased GABA-evoked current (
I
GABA) responses. (5) When elicited during a SP response,
I
GABA was significantly diminished compared to control. In the presence of staurosporine (100 nM), the inhibitory effect of SP upon
I
GABA was abolished, and the propofol-induced augmentation of
I
GABA was significantly increased. (6) Thus, SP-evoked protein kinase activity produced reciprocal changes in anesthetic sensitivity of (BK)-K
+- and GABA A-receptor-gated currents of these sympathetic neurons.</description><identifier>ISSN: 0378-4274</identifier><identifier>EISSN: 1879-3169</identifier><identifier>DOI: 10.1016/S0378-4274(98)00171-4</identifier><identifier>PMID: 10049188</identifier><language>eng</language><publisher>Netherlands: Elsevier Ireland Ltd</publisher><subject>Action Potentials - drug effects ; Anesthetic ; Anesthetics - pharmacology ; Anesthetics, Intravenous - pharmacology ; Animals ; Guinea Pigs ; In Vitro Techniques ; Ion Channel Gating - drug effects ; Ion Channel Gating - physiology ; Male ; Membrane Potentials - drug effects ; Neurons - drug effects ; Neurons - metabolism ; Potassium Channels - drug effects ; Potassium Channels - physiology ; Propofol - pharmacology ; Protein kinase ; Protein Kinases - metabolism ; Receptors, GABA-A - drug effects ; Receptors, GABA-A - physiology ; Sensitivity ; Substance P - physiology ; Sympathetic Nervous System - cytology ; Sympathetic Nervous System - drug effects ; Sympathetic Nervous System - metabolism ; Sympathetic neurons</subject><ispartof>Toxicology letters, 1998-11, Vol.100, p.97-102</ispartof><rights>1998 Elsevier Science Ireland Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c361t-fe050e71618a4abd199dd0daa300a0e10abe31982ecce08e3a28440662f13ff53</citedby><cites>FETCH-LOGICAL-c361t-fe050e71618a4abd199dd0daa300a0e10abe31982ecce08e3a28440662f13ff53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0378-4274(98)00171-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3541,27915,27916,45986</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10049188$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stapelfeldt, Wolf H</creatorcontrib><creatorcontrib>Oleszewski, Jan M</creatorcontrib><title>Protein kinase-mediated reciprocal modulatory changes in anesthetic sensitivity of (BK)-K +- and GABA-A receptor-gated conductances in guinea-pig sympathetic neurons</title><title>Toxicology letters</title><addtitle>Toxicol Lett</addtitle><description>(1) The interaction of substance P (SP)-mediated synaptic transmission with general anesthetics remains unknown. (2) Intracellular recordings were obtained from guinea-pig inferior mesenteric ganglion neurons to study monosynaptic responses to exogenous SP and GABA. (3) Propofol (1–100
μM) caused an increase in SP-evoked inward current responses and a concurrent decrease in peak amplitude of the afterspike hyperpolarization of intermittently evoked action potentials. These effects were occluded by the (BK)-K
+-channel-selective blocker charybdotoxin (10 nM), and prevented by the protein kinase inhibitor staurosporine (100 nM). (4) Propofol also increased GABA-evoked current (
I
GABA) responses. (5) When elicited during a SP response,
I
GABA was significantly diminished compared to control. In the presence of staurosporine (100 nM), the inhibitory effect of SP upon
I
GABA was abolished, and the propofol-induced augmentation of
I
GABA was significantly increased. (6) Thus, SP-evoked protein kinase activity produced reciprocal changes in anesthetic sensitivity of (BK)-K
+- and GABA A-receptor-gated currents of these sympathetic neurons.</description><subject>Action Potentials - drug effects</subject><subject>Anesthetic</subject><subject>Anesthetics - pharmacology</subject><subject>Anesthetics, Intravenous - pharmacology</subject><subject>Animals</subject><subject>Guinea Pigs</subject><subject>In Vitro Techniques</subject><subject>Ion Channel Gating - drug effects</subject><subject>Ion Channel Gating - physiology</subject><subject>Male</subject><subject>Membrane Potentials - drug effects</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Potassium Channels - drug effects</subject><subject>Potassium Channels - physiology</subject><subject>Propofol - pharmacology</subject><subject>Protein kinase</subject><subject>Protein Kinases - metabolism</subject><subject>Receptors, GABA-A - drug effects</subject><subject>Receptors, GABA-A - physiology</subject><subject>Sensitivity</subject><subject>Substance P - physiology</subject><subject>Sympathetic Nervous System - cytology</subject><subject>Sympathetic Nervous System - drug effects</subject><subject>Sympathetic Nervous System - metabolism</subject><subject>Sympathetic neurons</subject><issn>0378-4274</issn><issn>1879-3169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFv1DAUhC0EokvhJ4B8Qq0qw_Mm6zgntK2goFYCCThbXvtla0js1HYq7Q_if-LdrCpunN5l5nuaGUJec3jHgYv336FqJKuXTX3WynMA3nBWPyELLpuWVVy0T8niUXJCXqT0CwBELVbPyQkHqFsu5YL8-RZDRufpb-d1QjagdTqjpRGNG2MwuqdDsFOvc4g7au6032KixaA9pnyH2Rma0CeX3YPLOxo6enZ5c85u6AUrGkuv15drtt7zcCwMtj3gTfB2Mll7M9O2k_Oo2ei2NO2GUR_JHqcYfHpJnnW6T_jqeE_Jz08ff1x9Zrdfr79crW-ZqQTPrENYATZccKlrvbG8ba0Fq3UFoAE56A1WvJVLNAZBYqWXsq5BiGXHq65bVafk7cwtye-nkk8NLhns-xI2TEmJthRb1aIIV7PQxJBSxE6N0Q067hQHtd9HHfZR-_JVK9VhH1UX35vjg2lTqv7HNQ9SBB9mAZaYDw6jSsZhacm60mBWNrj_vPgL1CKiaw</recordid><startdate>19981123</startdate><enddate>19981123</enddate><creator>Stapelfeldt, Wolf H</creator><creator>Oleszewski, Jan M</creator><general>Elsevier Ireland Ltd</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>19981123</creationdate><title>Protein kinase-mediated reciprocal modulatory changes in anesthetic sensitivity of (BK)-K +- and GABA-A receptor-gated conductances in guinea-pig sympathetic neurons</title><author>Stapelfeldt, Wolf H ; Oleszewski, Jan M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c361t-fe050e71618a4abd199dd0daa300a0e10abe31982ecce08e3a28440662f13ff53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Action Potentials - drug effects</topic><topic>Anesthetic</topic><topic>Anesthetics - pharmacology</topic><topic>Anesthetics, Intravenous - pharmacology</topic><topic>Animals</topic><topic>Guinea Pigs</topic><topic>In Vitro Techniques</topic><topic>Ion Channel Gating - drug effects</topic><topic>Ion Channel Gating - physiology</topic><topic>Male</topic><topic>Membrane Potentials - drug effects</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Potassium Channels - drug effects</topic><topic>Potassium Channels - physiology</topic><topic>Propofol - pharmacology</topic><topic>Protein kinase</topic><topic>Protein Kinases - metabolism</topic><topic>Receptors, GABA-A - drug effects</topic><topic>Receptors, GABA-A - physiology</topic><topic>Sensitivity</topic><topic>Substance P - physiology</topic><topic>Sympathetic Nervous System - cytology</topic><topic>Sympathetic Nervous System - drug effects</topic><topic>Sympathetic Nervous System - metabolism</topic><topic>Sympathetic neurons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stapelfeldt, Wolf H</creatorcontrib><creatorcontrib>Oleszewski, Jan M</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>Toxicology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stapelfeldt, Wolf H</au><au>Oleszewski, Jan M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protein kinase-mediated reciprocal modulatory changes in anesthetic sensitivity of (BK)-K +- and GABA-A receptor-gated conductances in guinea-pig sympathetic neurons</atitle><jtitle>Toxicology letters</jtitle><addtitle>Toxicol Lett</addtitle><date>1998-11-23</date><risdate>1998</risdate><volume>100</volume><spage>97</spage><epage>102</epage><pages>97-102</pages><issn>0378-4274</issn><eissn>1879-3169</eissn><abstract>(1) The interaction of substance P (SP)-mediated synaptic transmission with general anesthetics remains unknown. (2) Intracellular recordings were obtained from guinea-pig inferior mesenteric ganglion neurons to study monosynaptic responses to exogenous SP and GABA. (3) Propofol (1–100
μM) caused an increase in SP-evoked inward current responses and a concurrent decrease in peak amplitude of the afterspike hyperpolarization of intermittently evoked action potentials. These effects were occluded by the (BK)-K
+-channel-selective blocker charybdotoxin (10 nM), and prevented by the protein kinase inhibitor staurosporine (100 nM). (4) Propofol also increased GABA-evoked current (
I
GABA) responses. (5) When elicited during a SP response,
I
GABA was significantly diminished compared to control. In the presence of staurosporine (100 nM), the inhibitory effect of SP upon
I
GABA was abolished, and the propofol-induced augmentation of
I
GABA was significantly increased. (6) Thus, SP-evoked protein kinase activity produced reciprocal changes in anesthetic sensitivity of (BK)-K
+- and GABA A-receptor-gated currents of these sympathetic neurons.</abstract><cop>Netherlands</cop><pub>Elsevier Ireland Ltd</pub><pmid>10049188</pmid><doi>10.1016/S0378-4274(98)00171-4</doi><tpages>6</tpages></addata></record> |
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| issn | 0378-4274 1879-3169 |
| language | eng |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Action Potentials - drug effects Anesthetic Anesthetics - pharmacology Anesthetics, Intravenous - pharmacology Animals Guinea Pigs In Vitro Techniques Ion Channel Gating - drug effects Ion Channel Gating - physiology Male Membrane Potentials - drug effects Neurons - drug effects Neurons - metabolism Potassium Channels - drug effects Potassium Channels - physiology Propofol - pharmacology Protein kinase Protein Kinases - metabolism Receptors, GABA-A - drug effects Receptors, GABA-A - physiology Sensitivity Substance P - physiology Sympathetic Nervous System - cytology Sympathetic Nervous System - drug effects Sympathetic Nervous System - metabolism Sympathetic neurons |
| title | Protein kinase-mediated reciprocal modulatory changes in anesthetic sensitivity of (BK)-K +- and GABA-A receptor-gated conductances in guinea-pig sympathetic neurons |
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