Stimulation of a nicotinic ACh receptor causes depolarization and activation of L-type Ca2+ channels in rat pinealocytes
1. Membrane voltage (Vm) recordings were obtained from isolated rat pinealocytes using the patch-clamp technique. In parallel to the electrophysiological experiments, intracellular Ca2+ measurements were performed using fura-2. 2. The resting Vm averaged -43 mV and replacement of extracellular NaCl...
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| Veröffentlicht in: | The Journal of physiology 1997-03, Vol.499 (Pt 2), p.329-340 |
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| creator | Letz, B Schomerus, C Maronde, E Korf, H W Korbmacher, C |
| description | 1. Membrane voltage (Vm) recordings were obtained from isolated rat pinealocytes using the patch-clamp technique. In parallel
to the electrophysiological experiments, intracellular Ca2+ measurements were performed using fura-2. 2. The resting Vm averaged
-43 mV and replacement of extracellular NaCl by KCl completely depolarized the cells. This indicates that the resting Vm is
dominated by a K+ conductance. Single-channel recordings revealed the presence of a large conductance Ca(2+)-activated charybdotoxin-sensitive
K+ channel. 3. Application of ACh (100 microM) depolarized the pinealocytes on average by 16 mV. The depolarizing effect of
ACh was mimicked by nicotine (50 microM) and was prevented by tubocurarine (100 microM). 4. The ACh-induced depolarization
was largely abolished in the absence of extracellular Na+, but was not significantly affected by extracellular Ca2+ removal.
5. Application of ACh (100 microM) caused an increase in [Ca2+]i. This increase was completely dependent on the presence of
extracellular Ca2+ and was largely reduced after extracellular Na+ removal. Nifedipine (1 microM) reduced the ACh-induced
increase in [Ca2+]i by about 50%. 6. Our findings indicate that in rat pinealocytes stimulation of a nicotinic ACh receptor
(nAChR) induces depolarization mainly by Na+ influx via the nAChR. The depolarization then activates L-type Ca2+ channels,
which are responsible for the nifedipine-sensitive portion of the intracellular Ca2+ increase. Ca2+ influx via the nAChR probably
also contributes to the observed rise in [Ca2+]i. |
| doi_str_mv | 10.1113/jphysiol.1997.sp021930 |
| format | Article |
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to the electrophysiological experiments, intracellular Ca2+ measurements were performed using fura-2. 2. The resting Vm averaged
-43 mV and replacement of extracellular NaCl by KCl completely depolarized the cells. This indicates that the resting Vm is
dominated by a K+ conductance. Single-channel recordings revealed the presence of a large conductance Ca(2+)-activated charybdotoxin-sensitive
K+ channel. 3. Application of ACh (100 microM) depolarized the pinealocytes on average by 16 mV. The depolarizing effect of
ACh was mimicked by nicotine (50 microM) and was prevented by tubocurarine (100 microM). 4. The ACh-induced depolarization
was largely abolished in the absence of extracellular Na+, but was not significantly affected by extracellular Ca2+ removal.
5. Application of ACh (100 microM) caused an increase in [Ca2+]i. This increase was completely dependent on the presence of
extracellular Ca2+ and was largely reduced after extracellular Na+ removal. Nifedipine (1 microM) reduced the ACh-induced
increase in [Ca2+]i by about 50%. 6. Our findings indicate that in rat pinealocytes stimulation of a nicotinic ACh receptor
(nAChR) induces depolarization mainly by Na+ influx via the nAChR. The depolarization then activates L-type Ca2+ channels,
which are responsible for the nifedipine-sensitive portion of the intracellular Ca2+ increase. Ca2+ influx via the nAChR probably
also contributes to the observed rise in [Ca2+]i.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.1997.sp021930</identifier><identifier>PMID: 9080363</identifier><language>eng</language><publisher>England: The Physiological Society</publisher><subject>Acetylcholine - metabolism ; Animals ; Calcium - metabolism ; Calcium Channels - metabolism ; Charybdotoxin - pharmacology ; Large-Conductance Calcium-Activated Potassium Channels ; Microscopy, Fluorescence ; Nicotine - metabolism ; Nifedipine - metabolism ; Pineal Gland - cytology ; Pineal Gland - metabolism ; Potassium Channels - metabolism ; Potassium Channels, Calcium-Activated ; Potassium Chloride - metabolism ; Rats ; Receptors, Nicotinic - metabolism ; Sodium Chloride - metabolism</subject><ispartof>The Journal of physiology, 1997-03, Vol.499 (Pt 2), p.329-340</ispartof><rights>1997 The Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5349-c8844f55a9a0af3ca972b3e1ffb3683783e6cf76a50e972a8ce1b9500026aa033</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/PMC1159308/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1159308/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1416,1432,27915,27916,45565,45566,46400,46824,53782,53784</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9080363$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Letz, B</creatorcontrib><creatorcontrib>Schomerus, C</creatorcontrib><creatorcontrib>Maronde, E</creatorcontrib><creatorcontrib>Korf, H W</creatorcontrib><creatorcontrib>Korbmacher, C</creatorcontrib><title>Stimulation of a nicotinic ACh receptor causes depolarization and activation of L-type Ca2+ channels in rat pinealocytes</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>1. Membrane voltage (Vm) recordings were obtained from isolated rat pinealocytes using the patch-clamp technique. In parallel
to the electrophysiological experiments, intracellular Ca2+ measurements were performed using fura-2. 2. The resting Vm averaged
-43 mV and replacement of extracellular NaCl by KCl completely depolarized the cells. This indicates that the resting Vm is
dominated by a K+ conductance. Single-channel recordings revealed the presence of a large conductance Ca(2+)-activated charybdotoxin-sensitive
K+ channel. 3. Application of ACh (100 microM) depolarized the pinealocytes on average by 16 mV. The depolarizing effect of
ACh was mimicked by nicotine (50 microM) and was prevented by tubocurarine (100 microM). 4. The ACh-induced depolarization
was largely abolished in the absence of extracellular Na+, but was not significantly affected by extracellular Ca2+ removal.
5. Application of ACh (100 microM) caused an increase in [Ca2+]i. This increase was completely dependent on the presence of
extracellular Ca2+ and was largely reduced after extracellular Na+ removal. Nifedipine (1 microM) reduced the ACh-induced
increase in [Ca2+]i by about 50%. 6. Our findings indicate that in rat pinealocytes stimulation of a nicotinic ACh receptor
(nAChR) induces depolarization mainly by Na+ influx via the nAChR. The depolarization then activates L-type Ca2+ channels,
which are responsible for the nifedipine-sensitive portion of the intracellular Ca2+ increase. Ca2+ influx via the nAChR probably
also contributes to the observed rise in [Ca2+]i.</description><subject>Acetylcholine - metabolism</subject><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Calcium Channels - metabolism</subject><subject>Charybdotoxin - pharmacology</subject><subject>Large-Conductance Calcium-Activated Potassium Channels</subject><subject>Microscopy, Fluorescence</subject><subject>Nicotine - metabolism</subject><subject>Nifedipine - metabolism</subject><subject>Pineal Gland - cytology</subject><subject>Pineal Gland - metabolism</subject><subject>Potassium Channels - metabolism</subject><subject>Potassium Channels, Calcium-Activated</subject><subject>Potassium Chloride - metabolism</subject><subject>Rats</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>Sodium Chloride - metabolism</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV9v0zAUxS0EGmXwEUB-RKAUO07i-AVpq_irSkxiPFu37s3iyY2D7W6ET4-rdBW88WJLPuf8ru1DyCvOlpxz8e527KdovVtypeQyjqzkSrBHZMGrRhVSKvGYLBgry0LImj8lz2K8ZYwLptQZOVOsZaIRC_Lre7K7vYNk_UB9R4EO1vhk80ovVj0NaHBMPlAD-4iRbnH0DoL9PSdg2FIwyd6dAOsiTSPSFZRvqelhGNBFagcaINHRDgjOmylhfE6edOAivjju5-THxw_Xq8_F-tunL6uLdWFqUanCtG1VdXUNChh0woCS5UYg77qNaFohW4GN6WQDNcMsQWuQb1TN8ssbACbEOXk_c8f9Zodbg0MK4PQY7A7CpD1Y_a8y2F7f-DvNeZ0_tM2A10dA8D_3GJPe2WjQORjQ76Pmkiku65LJbG1mqwk-xoDdaQxn-tCafmhNH1rTD63l4Mu_L3mKHWvK-uWs31uH039S9fXXq8NBpVQpSpUhb2ZIb2_6extQz7HojcU06ezTV0mX-mD-A_q2vP8</recordid><startdate>19970301</startdate><enddate>19970301</enddate><creator>Letz, B</creator><creator>Schomerus, C</creator><creator>Maronde, E</creator><creator>Korf, H W</creator><creator>Korbmacher, C</creator><general>The Physiological Society</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>7QP</scope><scope>5PM</scope></search><sort><creationdate>19970301</creationdate><title>Stimulation of a nicotinic ACh receptor causes depolarization and activation of L-type Ca2+ channels in rat pinealocytes</title><author>Letz, B ; Schomerus, C ; Maronde, E ; Korf, H W ; Korbmacher, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5349-c8844f55a9a0af3ca972b3e1ffb3683783e6cf76a50e972a8ce1b9500026aa033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Acetylcholine - metabolism</topic><topic>Animals</topic><topic>Calcium - metabolism</topic><topic>Calcium Channels - metabolism</topic><topic>Charybdotoxin - pharmacology</topic><topic>Large-Conductance Calcium-Activated Potassium Channels</topic><topic>Microscopy, Fluorescence</topic><topic>Nicotine - metabolism</topic><topic>Nifedipine - metabolism</topic><topic>Pineal Gland - cytology</topic><topic>Pineal Gland - metabolism</topic><topic>Potassium Channels - metabolism</topic><topic>Potassium Channels, Calcium-Activated</topic><topic>Potassium Chloride - metabolism</topic><topic>Rats</topic><topic>Receptors, Nicotinic - metabolism</topic><topic>Sodium Chloride - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Letz, B</creatorcontrib><creatorcontrib>Schomerus, C</creatorcontrib><creatorcontrib>Maronde, E</creatorcontrib><creatorcontrib>Korf, H W</creatorcontrib><creatorcontrib>Korbmacher, C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</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>Letz, B</au><au>Schomerus, C</au><au>Maronde, E</au><au>Korf, H W</au><au>Korbmacher, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stimulation of a nicotinic ACh receptor causes depolarization and activation of L-type Ca2+ channels in rat pinealocytes</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1997-03-01</date><risdate>1997</risdate><volume>499</volume><issue>Pt 2</issue><spage>329</spage><epage>340</epage><pages>329-340</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>1. Membrane voltage (Vm) recordings were obtained from isolated rat pinealocytes using the patch-clamp technique. In parallel
to the electrophysiological experiments, intracellular Ca2+ measurements were performed using fura-2. 2. The resting Vm averaged
-43 mV and replacement of extracellular NaCl by KCl completely depolarized the cells. This indicates that the resting Vm is
dominated by a K+ conductance. Single-channel recordings revealed the presence of a large conductance Ca(2+)-activated charybdotoxin-sensitive
K+ channel. 3. Application of ACh (100 microM) depolarized the pinealocytes on average by 16 mV. The depolarizing effect of
ACh was mimicked by nicotine (50 microM) and was prevented by tubocurarine (100 microM). 4. The ACh-induced depolarization
was largely abolished in the absence of extracellular Na+, but was not significantly affected by extracellular Ca2+ removal.
5. Application of ACh (100 microM) caused an increase in [Ca2+]i. This increase was completely dependent on the presence of
extracellular Ca2+ and was largely reduced after extracellular Na+ removal. Nifedipine (1 microM) reduced the ACh-induced
increase in [Ca2+]i by about 50%. 6. Our findings indicate that in rat pinealocytes stimulation of a nicotinic ACh receptor
(nAChR) induces depolarization mainly by Na+ influx via the nAChR. The depolarization then activates L-type Ca2+ channels,
which are responsible for the nifedipine-sensitive portion of the intracellular Ca2+ increase. Ca2+ influx via the nAChR probably
also contributes to the observed rise in [Ca2+]i.</abstract><cop>England</cop><pub>The Physiological Society</pub><pmid>9080363</pmid><doi>10.1113/jphysiol.1997.sp021930</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1159308 |
| source | MEDLINE; Wiley Online Library Journals; Wiley Free Archive; IngentaConnect Open Access; PubMed Central; EZB Electronic Journals Library |
| subjects | Acetylcholine - metabolism Animals Calcium - metabolism Calcium Channels - metabolism Charybdotoxin - pharmacology Large-Conductance Calcium-Activated Potassium Channels Microscopy, Fluorescence Nicotine - metabolism Nifedipine - metabolism Pineal Gland - cytology Pineal Gland - metabolism Potassium Channels - metabolism Potassium Channels, Calcium-Activated Potassium Chloride - metabolism Rats Receptors, Nicotinic - metabolism Sodium Chloride - metabolism |
| title | Stimulation of a nicotinic ACh receptor causes depolarization and activation of L-type Ca2+ channels in rat pinealocytes |
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