An analysis of the depolarization produced in guinea-pig hippocampus by cholinergic receptor stimulation
1. The effects of carbachol on hippocampal pyramidal neurones were studied in tissue slices in vitro with intracellular microelectrodes, employing current clamp and voltage clamp methods. 2. The calcium-dependent potassium current, IAHP, and the voltage-dependent potassium current, IM, were both rev...
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| Veröffentlicht in: | The Journal of physiology 1988-10, Vol.404 (1), p.479-496 |
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| description | 1. The effects of carbachol on hippocampal pyramidal neurones were studied in tissue slices in vitro with intracellular microelectrodes,
employing current clamp and voltage clamp methods. 2. The calcium-dependent potassium current, IAHP, and the voltage-dependent
potassium current, IM, were both reversibly blocked by the application of carbachol (5-10 microM). 3. Carbachol (1-10 microM)
induced a steady inward current under circumstances in which both IAHP and IM were inactive. This inward current was sometimes
difficult to reverse upon carbachol wash-out, an effect possibly related to receptor desensitization. 4. The depolarizing
effect of carbachol was reversed by 0.1 microM-atropine, and exhibited an apparent dissociation coefficient of 1.2 microM
for carbachol and 18 nM for pirenzepine, indicating that it is mediated by activation of an M1 muscarinic receptor. 5. The
depolarizing effect or inward current induced by carbachol was completely blocked by the potassium channel blockers caesium,
tetraethylammonium and barium. 6. The slope of the current-voltage (I-V) plots in carbachol was reduced in the majority of
cells, and crossed the control I-V plots at a negative membrane potential. The reversal potentials in carbachol shifted in
a positive direction when bathing potassium concentration was increased. 7. In a number of cells, the I-V curves in carbachol
were parallel to or converged positively with the control I-V curves. 8. The effects of carbachol were compared to those of
serotonin, which increases a 'pure' potassium conductance. Serotonin (10 microM) produced an increase in the slope of the
I-V curve, with a reversal potential sensitive to changes in bathing potassium concentration. The carbachol reversal potential
values were negative to those of serotonin at 5 and 10 mM-potassium. The equilibrium potentials for carbachol and serotonin
were equal at 25 mM-potassium. 9. The negative values of the reversal potential at 5 and 10 mM-potassium and the occurrence
of non-crossing I-V characteristics in carbachol could be explained by postulating a second effect of carbachol: namely, a
non-specific conductance increase in the dendrites. 10. It is concluded that carbachol depolarizes pyramidal cells in the
hippocampus by blocking a voltage-insensitive potassium leak channel and does so by activating M1 muscarinic receptors. In
addition, carbachol may also activate a second conductance in the dendrites, which could account for the anomalous I-V characteris |
| doi_str_mv | 10.1113/jphysiol.1988.sp017301 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1190837</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>78769179</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5939-d66c5d139e07639e03a13d72d61059fcc304a5b859ff5a8795cb0bea727f909e3</originalsourceid><addsrcrecordid>eNqNkV-P1CAUxYnRrOPoR9DwYNSXjtxSSnkxWTf-zSb6sD4TSumUDVMQWjfjp5fuzE70RX0Bwvndw-UehJ4B2QAAfX0dhn2y3m1ANM0mBQKcEriHVlDVouBc0PtoRUhZFpQzeIgepXRNCFAixBk6oyWjFRUrNJyPWI3KZa-EfY-nweDOBO9UtD_VZP2IQ_TdrE2H7Yi3sx2NKoLd4sGG4LXahTnhdo_14F3W4tZqHI02YfIRp8nuZndr8xg96JVL5slxX6Nv799dXXwsLr98-HRxflloJqgourrWrAMqDOH1slIFtONlVwNhoteakkqxtsnnnqmGC6Zb0hrFS94LIgxdozcH3zC3O9NpM05RORmi3am4l15Z-acy2kFu_Q8JIEhDeTZ4cTSI_vts0iR3NmnjnBqNn5PkDa8F5Pmu0au_gsBJ5qrc-D89gREGNWMZrA-gjj6laPpT40Dkkru8y10uucu73HPh09-_fSo7Bp3150ddJa1cH9WobTphHGhTN2XG3h6wG-vM_j8fl1efvy4XFamguh3My4PJYLfDjY1GHsqS19ZMe5k5CXIhfwHNTN5f</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>15051655</pqid></control><display><type>article</type><title>An analysis of the depolarization produced in guinea-pig hippocampus by cholinergic receptor stimulation</title><source>MEDLINE</source><source>IngentaConnect Free/Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Benson, D M ; Blitzer, R D ; Landau, E M</creator><creatorcontrib>Benson, D M ; Blitzer, R D ; Landau, E M</creatorcontrib><description>1. The effects of carbachol on hippocampal pyramidal neurones were studied in tissue slices in vitro with intracellular microelectrodes,
employing current clamp and voltage clamp methods. 2. The calcium-dependent potassium current, IAHP, and the voltage-dependent
potassium current, IM, were both reversibly blocked by the application of carbachol (5-10 microM). 3. Carbachol (1-10 microM)
induced a steady inward current under circumstances in which both IAHP and IM were inactive. This inward current was sometimes
difficult to reverse upon carbachol wash-out, an effect possibly related to receptor desensitization. 4. The depolarizing
effect of carbachol was reversed by 0.1 microM-atropine, and exhibited an apparent dissociation coefficient of 1.2 microM
for carbachol and 18 nM for pirenzepine, indicating that it is mediated by activation of an M1 muscarinic receptor. 5. The
depolarizing effect or inward current induced by carbachol was completely blocked by the potassium channel blockers caesium,
tetraethylammonium and barium. 6. The slope of the current-voltage (I-V) plots in carbachol was reduced in the majority of
cells, and crossed the control I-V plots at a negative membrane potential. The reversal potentials in carbachol shifted in
a positive direction when bathing potassium concentration was increased. 7. In a number of cells, the I-V curves in carbachol
were parallel to or converged positively with the control I-V curves. 8. The effects of carbachol were compared to those of
serotonin, which increases a 'pure' potassium conductance. Serotonin (10 microM) produced an increase in the slope of the
I-V curve, with a reversal potential sensitive to changes in bathing potassium concentration. The carbachol reversal potential
values were negative to those of serotonin at 5 and 10 mM-potassium. The equilibrium potentials for carbachol and serotonin
were equal at 25 mM-potassium. 9. The negative values of the reversal potential at 5 and 10 mM-potassium and the occurrence
of non-crossing I-V characteristics in carbachol could be explained by postulating a second effect of carbachol: namely, a
non-specific conductance increase in the dendrites. 10. It is concluded that carbachol depolarizes pyramidal cells in the
hippocampus by blocking a voltage-insensitive potassium leak channel and does so by activating M1 muscarinic receptors. In
addition, carbachol may also activate a second conductance in the dendrites, which could account for the anomalous I-V characteristics
sometimes seen in response to carbachol in these cells.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.1988.sp017301</identifier><identifier>PMID: 3253439</identifier><identifier>CODEN: JPHYA7</identifier><language>eng</language><publisher>Oxford: The Physiological Society</publisher><subject>Animals ; Atropine - pharmacology ; Barium - pharmacology ; Biological and medical sciences ; Cadmium - pharmacology ; carbachol ; Carbachol - pharmacology ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Cesium - pharmacology ; Dose-Response Relationship, Drug ; Fundamental and applied biological sciences. Psychology ; Guinea Pigs ; hippocampus ; Hippocampus - physiology ; In Vitro Techniques ; membrane potential ; Membrane Potentials ; Pirenzepine - pharmacology ; Potassium Channels - drug effects ; pyramidal cells ; Receptors, Cholinergic - drug effects ; Serotonin - pharmacology ; Vertebrates: nervous system and sense organs</subject><ispartof>The Journal of physiology, 1988-10, Vol.404 (1), p.479-496</ispartof><rights>1988 The Physiological Society</rights><rights>1989 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5939-d66c5d139e07639e03a13d72d61059fcc304a5b859ff5a8795cb0bea727f909e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1190837/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1190837/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,27901,27902,45550,45551,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7138682$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3253439$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Benson, D M</creatorcontrib><creatorcontrib>Blitzer, R D</creatorcontrib><creatorcontrib>Landau, E M</creatorcontrib><title>An analysis of the depolarization produced in guinea-pig hippocampus by cholinergic receptor stimulation</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>1. The effects of carbachol on hippocampal pyramidal neurones were studied in tissue slices in vitro with intracellular microelectrodes,
employing current clamp and voltage clamp methods. 2. The calcium-dependent potassium current, IAHP, and the voltage-dependent
potassium current, IM, were both reversibly blocked by the application of carbachol (5-10 microM). 3. Carbachol (1-10 microM)
induced a steady inward current under circumstances in which both IAHP and IM were inactive. This inward current was sometimes
difficult to reverse upon carbachol wash-out, an effect possibly related to receptor desensitization. 4. The depolarizing
effect of carbachol was reversed by 0.1 microM-atropine, and exhibited an apparent dissociation coefficient of 1.2 microM
for carbachol and 18 nM for pirenzepine, indicating that it is mediated by activation of an M1 muscarinic receptor. 5. The
depolarizing effect or inward current induced by carbachol was completely blocked by the potassium channel blockers caesium,
tetraethylammonium and barium. 6. The slope of the current-voltage (I-V) plots in carbachol was reduced in the majority of
cells, and crossed the control I-V plots at a negative membrane potential. The reversal potentials in carbachol shifted in
a positive direction when bathing potassium concentration was increased. 7. In a number of cells, the I-V curves in carbachol
were parallel to or converged positively with the control I-V curves. 8. The effects of carbachol were compared to those of
serotonin, which increases a 'pure' potassium conductance. Serotonin (10 microM) produced an increase in the slope of the
I-V curve, with a reversal potential sensitive to changes in bathing potassium concentration. The carbachol reversal potential
values were negative to those of serotonin at 5 and 10 mM-potassium. The equilibrium potentials for carbachol and serotonin
were equal at 25 mM-potassium. 9. The negative values of the reversal potential at 5 and 10 mM-potassium and the occurrence
of non-crossing I-V characteristics in carbachol could be explained by postulating a second effect of carbachol: namely, a
non-specific conductance increase in the dendrites. 10. It is concluded that carbachol depolarizes pyramidal cells in the
hippocampus by blocking a voltage-insensitive potassium leak channel and does so by activating M1 muscarinic receptors. In
addition, carbachol may also activate a second conductance in the dendrites, which could account for the anomalous I-V characteristics
sometimes seen in response to carbachol in these cells.</description><subject>Animals</subject><subject>Atropine - pharmacology</subject><subject>Barium - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cadmium - pharmacology</subject><subject>carbachol</subject><subject>Carbachol - pharmacology</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Cesium - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Guinea Pigs</subject><subject>hippocampus</subject><subject>Hippocampus - physiology</subject><subject>In Vitro Techniques</subject><subject>membrane potential</subject><subject>Membrane Potentials</subject><subject>Pirenzepine - pharmacology</subject><subject>Potassium Channels - drug effects</subject><subject>pyramidal cells</subject><subject>Receptors, Cholinergic - drug effects</subject><subject>Serotonin - pharmacology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV-P1CAUxYnRrOPoR9DwYNSXjtxSSnkxWTf-zSb6sD4TSumUDVMQWjfjp5fuzE70RX0Bwvndw-UehJ4B2QAAfX0dhn2y3m1ANM0mBQKcEriHVlDVouBc0PtoRUhZFpQzeIgepXRNCFAixBk6oyWjFRUrNJyPWI3KZa-EfY-nweDOBO9UtD_VZP2IQ_TdrE2H7Yi3sx2NKoLd4sGG4LXahTnhdo_14F3W4tZqHI02YfIRp8nuZndr8xg96JVL5slxX6Nv799dXXwsLr98-HRxflloJqgourrWrAMqDOH1slIFtONlVwNhoteakkqxtsnnnqmGC6Zb0hrFS94LIgxdozcH3zC3O9NpM05RORmi3am4l15Z-acy2kFu_Q8JIEhDeTZ4cTSI_vts0iR3NmnjnBqNn5PkDa8F5Pmu0au_gsBJ5qrc-D89gREGNWMZrA-gjj6laPpT40Dkkru8y10uucu73HPh09-_fSo7Bp3150ddJa1cH9WobTphHGhTN2XG3h6wG-vM_j8fl1efvy4XFamguh3My4PJYLfDjY1GHsqS19ZMe5k5CXIhfwHNTN5f</recordid><startdate>19881001</startdate><enddate>19881001</enddate><creator>Benson, D M</creator><creator>Blitzer, R D</creator><creator>Landau, E M</creator><general>The Physiological Society</general><general>Blackwell</general><scope>IQODW</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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19881001</creationdate><title>An analysis of the depolarization produced in guinea-pig hippocampus by cholinergic receptor stimulation</title><author>Benson, D M ; Blitzer, R D ; Landau, E M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5939-d66c5d139e07639e03a13d72d61059fcc304a5b859ff5a8795cb0bea727f909e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Animals</topic><topic>Atropine - pharmacology</topic><topic>Barium - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cadmium - pharmacology</topic><topic>carbachol</topic><topic>Carbachol - pharmacology</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Cesium - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Guinea Pigs</topic><topic>hippocampus</topic><topic>Hippocampus - physiology</topic><topic>In Vitro Techniques</topic><topic>membrane potential</topic><topic>Membrane Potentials</topic><topic>Pirenzepine - pharmacology</topic><topic>Potassium Channels - drug effects</topic><topic>pyramidal cells</topic><topic>Receptors, Cholinergic - drug effects</topic><topic>Serotonin - pharmacology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Benson, D M</creatorcontrib><creatorcontrib>Blitzer, R D</creatorcontrib><creatorcontrib>Landau, E M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Benson, D M</au><au>Blitzer, R D</au><au>Landau, E M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An analysis of the depolarization produced in guinea-pig hippocampus by cholinergic receptor stimulation</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1988-10-01</date><risdate>1988</risdate><volume>404</volume><issue>1</issue><spage>479</spage><epage>496</epage><pages>479-496</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><coden>JPHYA7</coden><abstract>1. The effects of carbachol on hippocampal pyramidal neurones were studied in tissue slices in vitro with intracellular microelectrodes,
employing current clamp and voltage clamp methods. 2. The calcium-dependent potassium current, IAHP, and the voltage-dependent
potassium current, IM, were both reversibly blocked by the application of carbachol (5-10 microM). 3. Carbachol (1-10 microM)
induced a steady inward current under circumstances in which both IAHP and IM were inactive. This inward current was sometimes
difficult to reverse upon carbachol wash-out, an effect possibly related to receptor desensitization. 4. The depolarizing
effect of carbachol was reversed by 0.1 microM-atropine, and exhibited an apparent dissociation coefficient of 1.2 microM
for carbachol and 18 nM for pirenzepine, indicating that it is mediated by activation of an M1 muscarinic receptor. 5. The
depolarizing effect or inward current induced by carbachol was completely blocked by the potassium channel blockers caesium,
tetraethylammonium and barium. 6. The slope of the current-voltage (I-V) plots in carbachol was reduced in the majority of
cells, and crossed the control I-V plots at a negative membrane potential. The reversal potentials in carbachol shifted in
a positive direction when bathing potassium concentration was increased. 7. In a number of cells, the I-V curves in carbachol
were parallel to or converged positively with the control I-V curves. 8. The effects of carbachol were compared to those of
serotonin, which increases a 'pure' potassium conductance. Serotonin (10 microM) produced an increase in the slope of the
I-V curve, with a reversal potential sensitive to changes in bathing potassium concentration. The carbachol reversal potential
values were negative to those of serotonin at 5 and 10 mM-potassium. The equilibrium potentials for carbachol and serotonin
were equal at 25 mM-potassium. 9. The negative values of the reversal potential at 5 and 10 mM-potassium and the occurrence
of non-crossing I-V characteristics in carbachol could be explained by postulating a second effect of carbachol: namely, a
non-specific conductance increase in the dendrites. 10. It is concluded that carbachol depolarizes pyramidal cells in the
hippocampus by blocking a voltage-insensitive potassium leak channel and does so by activating M1 muscarinic receptors. In
addition, carbachol may also activate a second conductance in the dendrites, which could account for the anomalous I-V characteristics
sometimes seen in response to carbachol in these cells.</abstract><cop>Oxford</cop><pub>The Physiological Society</pub><pmid>3253439</pmid><doi>10.1113/jphysiol.1988.sp017301</doi><tpages>18</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of physiology, 1988-10, Vol.404 (1), p.479-496 |
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| language | eng |
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| source | MEDLINE; IngentaConnect Free/Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Atropine - pharmacology Barium - pharmacology Biological and medical sciences Cadmium - pharmacology carbachol Carbachol - pharmacology Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Cesium - pharmacology Dose-Response Relationship, Drug Fundamental and applied biological sciences. Psychology Guinea Pigs hippocampus Hippocampus - physiology In Vitro Techniques membrane potential Membrane Potentials Pirenzepine - pharmacology Potassium Channels - drug effects pyramidal cells Receptors, Cholinergic - drug effects Serotonin - pharmacology Vertebrates: nervous system and sense organs |
| title | An analysis of the depolarization produced in guinea-pig hippocampus by cholinergic receptor stimulation |
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