Delayed expression of large conductance K+ channels reshaping agonist-induced currents in mouse pancreatic acinar cells

Epithelial secretory cells display cell-specific mechanisms of fluid secretion and express large conductance voltage- and Ca 2+ -activated K + (Maxi-K) channels that generate the membrane negativity for effective Cl − exit to the lumen. Rat and mouse pancreatic acinar cells had been thought to be...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:The Journal of physiology 2005-03, Vol.563 (2), p.379-391
Hauptverfasser: Oshiro, Takako, Takahashi, Hidenori, Ohsaga, Atsushi, Ebihara, Satoru, Sasaki, Hidetada, Maruyama, Yoshio
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 391
container_issue 2
container_start_page 379
container_title The Journal of physiology
container_volume 563
creator Oshiro, Takako
Takahashi, Hidenori
Ohsaga, Atsushi
Ebihara, Satoru
Sasaki, Hidetada
Maruyama, Yoshio
description Epithelial secretory cells display cell-specific mechanisms of fluid secretion and express large conductance voltage- and Ca 2+ -activated K + (Maxi-K) channels that generate the membrane negativity for effective Cl − exit to the lumen. Rat and mouse pancreatic acinar cells had been thought to be peculiar in this sense because of the previously reported lack of Maxi-K channels. However, this view is not entirely correct as evidenced in the present paper. Searching for their presence in pancreatic acinar cells in mice from 5 to 84 weeks of age with patch-clamp current measurements, we demonstrated that the expression of Maxi-K channels is regulated in an age-associated manner after birth. The expression started at approximately 12 postnatal weeks and increased steadily up to 84 weeks. In support of this, RT-PCR could not detect mSlo mRNA, the Maxi-K gene, at either 7 or 8 weeks but could at 58 and 64 postnatal weeks. These results suggest that a key steering element for fluid secretion, the Maxi-K channel, is progressively re-organized in rodent pancreas. A pancreatic secretagogue, acetylcholine, evoked Maxi-K channel current overlapping to various degrees on the previously known current response. This suggests that the rise in internal Ca 2+ activates Maxi-K channels which reshape the mode of secretagogue-evoked current response and contribute to Cl − driving in fluid secretion in an age-associated fashion.
doi_str_mv 10.1113/jphysiol.2004.077834
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1665597</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67468515</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5534-59f0967088d9652771878e5ee7e54179b30750efc5a45a9e2432ca9d3ded90e33</originalsourceid><addsrcrecordid>eNqNkk2P1SAUhonRONfRf2AMK11MeoVSoGxMzDh-TqKLcU0Yetoy6YUKrdf-e2l6_dq5YsHzPpyTF4SeUrKnlLKXd2O_JBeGfUlItSdS1qy6h3a0EqqQUrH7aEdIWRZMcnqGHqV0RwhlRKmH6IxyQSkp6x06voHBLNBg-DFGSFnocWjxYGIH2AbfzHYy3gL-dIFtb7yHIeEM9mZ0vsOmC96lqXArmC12jhH8lLDz-BDmBHjM6QhmchYb67yJ2MIwpMfoQWuGBE9O5zn6-vbq5vJ9cf353YfL19eF5ZxVBVctUUKSum6U4KWUtJY1cAAJvKJS3TIiOYHWclNxo6CsWGmNalgDjSLA2Dl6tXnH-fYAjc3DRTPoMbqDiYsOxul_b7zrdRe-ayoE50pmwfOTIIZvM6RJH1xaVzAe8oJayErUnPIMVhtoY0gpQvv7EUr02pj-1ZheG9NbYzn27O8B_4ROFWWg3oCjG2D5L6m--fhF0tX9Yov2ruuPLoLe4BSsg2nRXDBdapY_y0948bdO</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67468515</pqid></control><display><type>article</type><title>Delayed expression of large conductance K+ channels reshaping agonist-induced currents in mouse pancreatic acinar cells</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Access via Wiley Online Library</source><source>IngentaConnect Free/Open Access Journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><creator>Oshiro, Takako ; Takahashi, Hidenori ; Ohsaga, Atsushi ; Ebihara, Satoru ; Sasaki, Hidetada ; Maruyama, Yoshio</creator><creatorcontrib>Oshiro, Takako ; Takahashi, Hidenori ; Ohsaga, Atsushi ; Ebihara, Satoru ; Sasaki, Hidetada ; Maruyama, Yoshio</creatorcontrib><description>Epithelial secretory cells display cell-specific mechanisms of fluid secretion and express large conductance voltage- and Ca 2+ -activated K + (Maxi-K) channels that generate the membrane negativity for effective Cl − exit to the lumen. Rat and mouse pancreatic acinar cells had been thought to be peculiar in this sense because of the previously reported lack of Maxi-K channels. However, this view is not entirely correct as evidenced in the present paper. Searching for their presence in pancreatic acinar cells in mice from 5 to 84 weeks of age with patch-clamp current measurements, we demonstrated that the expression of Maxi-K channels is regulated in an age-associated manner after birth. The expression started at approximately 12 postnatal weeks and increased steadily up to 84 weeks. In support of this, RT-PCR could not detect mSlo mRNA, the Maxi-K gene, at either 7 or 8 weeks but could at 58 and 64 postnatal weeks. These results suggest that a key steering element for fluid secretion, the Maxi-K channel, is progressively re-organized in rodent pancreas. A pancreatic secretagogue, acetylcholine, evoked Maxi-K channel current overlapping to various degrees on the previously known current response. This suggests that the rise in internal Ca 2+ activates Maxi-K channels which reshape the mode of secretagogue-evoked current response and contribute to Cl − driving in fluid secretion in an age-associated fashion.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2004.077834</identifier><identifier>PMID: 15611028</identifier><language>eng</language><publisher>9600 Garsington Road , Oxford , OX4 2DQ , UK: The Physiological Society</publisher><subject>Acetylcholine - pharmacology ; Aging - physiology ; Animals ; Cell Physiology ; Chlorides - physiology ; Gene Expression Regulation, Developmental - physiology ; In Vitro Techniques ; Large-Conductance Calcium-Activated Potassium Channels ; Male ; Membrane Potentials - drug effects ; Membrane Potentials - physiology ; Mice ; Models, Biological ; Pancreas, Exocrine - cytology ; Pancreas, Exocrine - drug effects ; Pancreas, Exocrine - physiology ; Potassium Channels - drug effects ; Potassium Channels - physiology ; Potassium Channels, Calcium-Activated - physiology ; Protein Subunits - metabolism</subject><ispartof>The Journal of physiology, 2005-03, Vol.563 (2), p.379-391</ispartof><rights>2005 The Journal of Physiology © 2005 The Physiological Society</rights><rights>The Physiological Society 2005 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5534-59f0967088d9652771878e5ee7e54179b30750efc5a45a9e2432ca9d3ded90e33</citedby><cites>FETCH-LOGICAL-c5534-59f0967088d9652771878e5ee7e54179b30750efc5a45a9e2432ca9d3ded90e33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665597/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665597/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15611028$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oshiro, Takako</creatorcontrib><creatorcontrib>Takahashi, Hidenori</creatorcontrib><creatorcontrib>Ohsaga, Atsushi</creatorcontrib><creatorcontrib>Ebihara, Satoru</creatorcontrib><creatorcontrib>Sasaki, Hidetada</creatorcontrib><creatorcontrib>Maruyama, Yoshio</creatorcontrib><title>Delayed expression of large conductance K+ channels reshaping agonist-induced currents in mouse pancreatic acinar cells</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>Epithelial secretory cells display cell-specific mechanisms of fluid secretion and express large conductance voltage- and Ca 2+ -activated K + (Maxi-K) channels that generate the membrane negativity for effective Cl − exit to the lumen. Rat and mouse pancreatic acinar cells had been thought to be peculiar in this sense because of the previously reported lack of Maxi-K channels. However, this view is not entirely correct as evidenced in the present paper. Searching for their presence in pancreatic acinar cells in mice from 5 to 84 weeks of age with patch-clamp current measurements, we demonstrated that the expression of Maxi-K channels is regulated in an age-associated manner after birth. The expression started at approximately 12 postnatal weeks and increased steadily up to 84 weeks. In support of this, RT-PCR could not detect mSlo mRNA, the Maxi-K gene, at either 7 or 8 weeks but could at 58 and 64 postnatal weeks. These results suggest that a key steering element for fluid secretion, the Maxi-K channel, is progressively re-organized in rodent pancreas. A pancreatic secretagogue, acetylcholine, evoked Maxi-K channel current overlapping to various degrees on the previously known current response. This suggests that the rise in internal Ca 2+ activates Maxi-K channels which reshape the mode of secretagogue-evoked current response and contribute to Cl − driving in fluid secretion in an age-associated fashion.</description><subject>Acetylcholine - pharmacology</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Cell Physiology</subject><subject>Chlorides - physiology</subject><subject>Gene Expression Regulation, Developmental - physiology</subject><subject>In Vitro Techniques</subject><subject>Large-Conductance Calcium-Activated Potassium Channels</subject><subject>Male</subject><subject>Membrane Potentials - drug effects</subject><subject>Membrane Potentials - physiology</subject><subject>Mice</subject><subject>Models, Biological</subject><subject>Pancreas, Exocrine - cytology</subject><subject>Pancreas, Exocrine - drug effects</subject><subject>Pancreas, Exocrine - physiology</subject><subject>Potassium Channels - drug effects</subject><subject>Potassium Channels - physiology</subject><subject>Potassium Channels, Calcium-Activated - physiology</subject><subject>Protein Subunits - metabolism</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkk2P1SAUhonRONfRf2AMK11MeoVSoGxMzDh-TqKLcU0Yetoy6YUKrdf-e2l6_dq5YsHzPpyTF4SeUrKnlLKXd2O_JBeGfUlItSdS1qy6h3a0EqqQUrH7aEdIWRZMcnqGHqV0RwhlRKmH6IxyQSkp6x06voHBLNBg-DFGSFnocWjxYGIH2AbfzHYy3gL-dIFtb7yHIeEM9mZ0vsOmC96lqXArmC12jhH8lLDz-BDmBHjM6QhmchYb67yJ2MIwpMfoQWuGBE9O5zn6-vbq5vJ9cf353YfL19eF5ZxVBVctUUKSum6U4KWUtJY1cAAJvKJS3TIiOYHWclNxo6CsWGmNalgDjSLA2Dl6tXnH-fYAjc3DRTPoMbqDiYsOxul_b7zrdRe-ayoE50pmwfOTIIZvM6RJH1xaVzAe8oJayErUnPIMVhtoY0gpQvv7EUr02pj-1ZheG9NbYzn27O8B_4ROFWWg3oCjG2D5L6m--fhF0tX9Yov2ruuPLoLe4BSsg2nRXDBdapY_y0948bdO</recordid><startdate>200503</startdate><enddate>200503</enddate><creator>Oshiro, Takako</creator><creator>Takahashi, Hidenori</creator><creator>Ohsaga, Atsushi</creator><creator>Ebihara, Satoru</creator><creator>Sasaki, Hidetada</creator><creator>Maruyama, Yoshio</creator><general>The Physiological Society</general><general>Blackwell Science Ltd</general><general>Blackwell Science Inc</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><scope>5PM</scope></search><sort><creationdate>200503</creationdate><title>Delayed expression of large conductance K+ channels reshaping agonist-induced currents in mouse pancreatic acinar cells</title><author>Oshiro, Takako ; Takahashi, Hidenori ; Ohsaga, Atsushi ; Ebihara, Satoru ; Sasaki, Hidetada ; Maruyama, Yoshio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5534-59f0967088d9652771878e5ee7e54179b30750efc5a45a9e2432ca9d3ded90e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Aging - physiology</topic><topic>Animals</topic><topic>Cell Physiology</topic><topic>Chlorides - physiology</topic><topic>Gene Expression Regulation, Developmental - physiology</topic><topic>In Vitro Techniques</topic><topic>Large-Conductance Calcium-Activated Potassium Channels</topic><topic>Male</topic><topic>Membrane Potentials - drug effects</topic><topic>Membrane Potentials - physiology</topic><topic>Mice</topic><topic>Models, Biological</topic><topic>Pancreas, Exocrine - cytology</topic><topic>Pancreas, Exocrine - drug effects</topic><topic>Pancreas, Exocrine - physiology</topic><topic>Potassium Channels - drug effects</topic><topic>Potassium Channels - physiology</topic><topic>Potassium Channels, Calcium-Activated - physiology</topic><topic>Protein Subunits - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oshiro, Takako</creatorcontrib><creatorcontrib>Takahashi, Hidenori</creatorcontrib><creatorcontrib>Ohsaga, Atsushi</creatorcontrib><creatorcontrib>Ebihara, Satoru</creatorcontrib><creatorcontrib>Sasaki, Hidetada</creatorcontrib><creatorcontrib>Maruyama, Yoshio</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><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>Oshiro, Takako</au><au>Takahashi, Hidenori</au><au>Ohsaga, Atsushi</au><au>Ebihara, Satoru</au><au>Sasaki, Hidetada</au><au>Maruyama, Yoshio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Delayed expression of large conductance K+ channels reshaping agonist-induced currents in mouse pancreatic acinar cells</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2005-03</date><risdate>2005</risdate><volume>563</volume><issue>2</issue><spage>379</spage><epage>391</epage><pages>379-391</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>Epithelial secretory cells display cell-specific mechanisms of fluid secretion and express large conductance voltage- and Ca 2+ -activated K + (Maxi-K) channels that generate the membrane negativity for effective Cl − exit to the lumen. Rat and mouse pancreatic acinar cells had been thought to be peculiar in this sense because of the previously reported lack of Maxi-K channels. However, this view is not entirely correct as evidenced in the present paper. Searching for their presence in pancreatic acinar cells in mice from 5 to 84 weeks of age with patch-clamp current measurements, we demonstrated that the expression of Maxi-K channels is regulated in an age-associated manner after birth. The expression started at approximately 12 postnatal weeks and increased steadily up to 84 weeks. In support of this, RT-PCR could not detect mSlo mRNA, the Maxi-K gene, at either 7 or 8 weeks but could at 58 and 64 postnatal weeks. These results suggest that a key steering element for fluid secretion, the Maxi-K channel, is progressively re-organized in rodent pancreas. A pancreatic secretagogue, acetylcholine, evoked Maxi-K channel current overlapping to various degrees on the previously known current response. This suggests that the rise in internal Ca 2+ activates Maxi-K channels which reshape the mode of secretagogue-evoked current response and contribute to Cl − driving in fluid secretion in an age-associated fashion.</abstract><cop>9600 Garsington Road , Oxford , OX4 2DQ , UK</cop><pub>The Physiological Society</pub><pmid>15611028</pmid><doi>10.1113/jphysiol.2004.077834</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0022-3751
ispartof The Journal of physiology, 2005-03, Vol.563 (2), p.379-391
issn 0022-3751
1469-7793
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1665597
source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Access via Wiley Online Library; IngentaConnect Free/Open Access Journals; Wiley Online Library (Open Access Collection); PubMed Central
subjects Acetylcholine - pharmacology
Aging - physiology
Animals
Cell Physiology
Chlorides - physiology
Gene Expression Regulation, Developmental - physiology
In Vitro Techniques
Large-Conductance Calcium-Activated Potassium Channels
Male
Membrane Potentials - drug effects
Membrane Potentials - physiology
Mice
Models, Biological
Pancreas, Exocrine - cytology
Pancreas, Exocrine - drug effects
Pancreas, Exocrine - physiology
Potassium Channels - drug effects
Potassium Channels - physiology
Potassium Channels, Calcium-Activated - physiology
Protein Subunits - metabolism
title Delayed expression of large conductance K+ channels reshaping agonist-induced currents in mouse pancreatic acinar cells
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T17%3A04%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Delayed%20expression%20of%20large%20conductance%20K+%20channels%20reshaping%20agonist-induced%20currents%20in%20mouse%20pancreatic%20acinar%20cells&rft.jtitle=The%20Journal%20of%20physiology&rft.au=Oshiro,%20Takako&rft.date=2005-03&rft.volume=563&rft.issue=2&rft.spage=379&rft.epage=391&rft.pages=379-391&rft.issn=0022-3751&rft.eissn=1469-7793&rft_id=info:doi/10.1113/jphysiol.2004.077834&rft_dat=%3Cproquest_pubme%3E67468515%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=67468515&rft_id=info:pmid/15611028&rfr_iscdi=true