Ca2+- and Metabolism-Related Changes of Mitochondrial Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ
1 II. Physiologisches Institut, Universität Göttingen, D-37073 Göttingen; and 2 Institut für Physiologie, Humboldt-Universität Berlin, Universitätsklinikum Charité, D-10117 Berlin, Germany Schuchmann, S., M. Lückermann, A. Kulik, U. Heinemann, and K. Ballanyi. Ca 2+ - and Metabolism-Related Chan...
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| description | 1 II. Physiologisches Institut,
Universität Göttingen, D-37073 Göttingen; and
2 Institut für Physiologie,
Humboldt-Universität Berlin, Universitätsklinikum
Charité, D-10117 Berlin, Germany
Schuchmann, S.,
M. Lückermann,
A. Kulik,
U. Heinemann, and
K. Ballanyi.
Ca 2+ - and Metabolism-Related Changes of Mitochondrial
Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ. J. Neurophysiol. 83: 1710-1721, 2000. In
hippocampal slices from rats, dialysis with rhodamine-123 (Rh-123)
and/or fura-2 via the patch electrode allowed monitoring of
mitochondrial potential ( ) changes and intracellular
Ca 2+ ([Ca 2+ ] i ) of CA1 pyramidal
neurons. Plasmalemmal depolarization to 0 mV caused a mean
[Ca 2+ ] i rise of 300 nM and increased Rh-123
fluorescence signal (RFS) by 50% of control. The evoked RFS,
indicating depolarization of , and the
[Ca 2+ ] i transient were abolished by
Ca 2+ -free superfusate or exposure of
Ni 2+ /Cd 2+ . Simultaneous measurements of RFS and
[Ca 2+ ] i showed that the kinetics of both the
Ca 2+ rise and recovery were considerably faster than those
of the depolarization. The plasmalemmal
Ca 2+ /H + pump blocker eosin-B potentiated the
peak of the depolarization-induced RFS and delayed recovery of both the
RFS and [Ca 2+ ] i transient. Thus the
depolarization due to plasmalemmal depolarization is related to
mitochondrial Ca 2+ sequestration secondary to
Ca 2+ influx through voltage-gated Ca 2+
channels. CN elevated [Ca 2+ ] i
by |
| doi_str_mv | 10.1152/jn.2000.83.3.1710 |
| format | Article |
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Universität Göttingen, D-37073 Göttingen; and
2 Institut für Physiologie,
Humboldt-Universität Berlin, Universitätsklinikum
Charité, D-10117 Berlin, Germany
Schuchmann, S.,
M. Lückermann,
A. Kulik,
U. Heinemann, and
K. Ballanyi.
Ca 2+ - and Metabolism-Related Changes of Mitochondrial
Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ. J. Neurophysiol. 83: 1710-1721, 2000. In
hippocampal slices from rats, dialysis with rhodamine-123 (Rh-123)
and/or fura-2 via the patch electrode allowed monitoring of
mitochondrial potential ( ) changes and intracellular
Ca 2+ ([Ca 2+ ] i ) of CA1 pyramidal
neurons. Plasmalemmal depolarization to 0 mV caused a mean
[Ca 2+ ] i rise of 300 nM and increased Rh-123
fluorescence signal (RFS) by 50% of control. The evoked RFS,
indicating depolarization of , and the
[Ca 2+ ] i transient were abolished by
Ca 2+ -free superfusate or exposure of
Ni 2+ /Cd 2+ . Simultaneous measurements of RFS and
[Ca 2+ ] i showed that the kinetics of both the
Ca 2+ rise and recovery were considerably faster than those
of the depolarization. The plasmalemmal
Ca 2+ /H + pump blocker eosin-B potentiated the
peak of the depolarization-induced RFS and delayed recovery of both the
RFS and [Ca 2+ ] i transient. Thus the
depolarization due to plasmalemmal depolarization is related to
mitochondrial Ca 2+ sequestration secondary to
Ca 2+ influx through voltage-gated Ca 2+
channels. CN elevated [Ca 2+ ] i
by <50 nM but increased RFS by 221% as a result of extensive depolarization of . Oligomycin decreased RFS by 52% without affecting [Ca 2+ ] i . In the presence of
oligomycin, CN and
p-trifluoromethoxy-phenylhydrazone (FCCP) elevated
[Ca 2+ ] i by <50 nM and increased RFS by 285 and 290%, respectively. Accordingly, the metabolism-related
changes are independent of [Ca 2+ ] i . Imaging
techniques revealed that evoked [Ca 2+ ] i rises
are distributed uniformly over the soma and primary dendrites, whereas
corresponding changes in RFS occur more localized in subregions within
the soma. The results show that microfluorometric measurement of the
relation between mitochondrial function and intracellular Ca 2+ is feasible in whole cell recorded mammalian neurons
in situ.</description><identifier>ISSN: 0022-3077</identifier><identifier>EISSN: 1522-1598</identifier><identifier>DOI: 10.1152/jn.2000.83.3.1710</identifier><identifier>PMID: 10712491</identifier><language>eng</language><publisher>Am Phys Soc</publisher><ispartof>Journal of neurophysiology, 2000-03, Vol.83 (3), p.1710</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids></links><search><creatorcontrib>Schuchmann, S</creatorcontrib><creatorcontrib>Luckermann, M</creatorcontrib><creatorcontrib>Kulik, A</creatorcontrib><creatorcontrib>Heinemann, U</creatorcontrib><creatorcontrib>Ballanyi, K</creatorcontrib><title>Ca2+- and Metabolism-Related Changes of Mitochondrial Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ</title><title>Journal of neurophysiology</title><description> 1 II. Physiologisches Institut,
Universität Göttingen, D-37073 Göttingen; and
2 Institut für Physiologie,
Humboldt-Universität Berlin, Universitätsklinikum
Charité, D-10117 Berlin, Germany
Schuchmann, S.,
M. Lückermann,
A. Kulik,
U. Heinemann, and
K. Ballanyi.
Ca 2+ - and Metabolism-Related Changes of Mitochondrial
Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ. J. Neurophysiol. 83: 1710-1721, 2000. In
hippocampal slices from rats, dialysis with rhodamine-123 (Rh-123)
and/or fura-2 via the patch electrode allowed monitoring of
mitochondrial potential ( ) changes and intracellular
Ca 2+ ([Ca 2+ ] i ) of CA1 pyramidal
neurons. Plasmalemmal depolarization to 0 mV caused a mean
[Ca 2+ ] i rise of 300 nM and increased Rh-123
fluorescence signal (RFS) by 50% of control. The evoked RFS,
indicating depolarization of , and the
[Ca 2+ ] i transient were abolished by
Ca 2+ -free superfusate or exposure of
Ni 2+ /Cd 2+ . Simultaneous measurements of RFS and
[Ca 2+ ] i showed that the kinetics of both the
Ca 2+ rise and recovery were considerably faster than those
of the depolarization. The plasmalemmal
Ca 2+ /H + pump blocker eosin-B potentiated the
peak of the depolarization-induced RFS and delayed recovery of both the
RFS and [Ca 2+ ] i transient. Thus the
depolarization due to plasmalemmal depolarization is related to
mitochondrial Ca 2+ sequestration secondary to
Ca 2+ influx through voltage-gated Ca 2+
channels. CN elevated [Ca 2+ ] i
by <50 nM but increased RFS by 221% as a result of extensive depolarization of . Oligomycin decreased RFS by 52% without affecting [Ca 2+ ] i . In the presence of
oligomycin, CN and
p-trifluoromethoxy-phenylhydrazone (FCCP) elevated
[Ca 2+ ] i by <50 nM and increased RFS by 285 and 290%, respectively. Accordingly, the metabolism-related
changes are independent of [Ca 2+ ] i . Imaging
techniques revealed that evoked [Ca 2+ ] i rises
are distributed uniformly over the soma and primary dendrites, whereas
corresponding changes in RFS occur more localized in subregions within
the soma. The results show that microfluorometric measurement of the
relation between mitochondrial function and intracellular Ca 2+ is feasible in whole cell recorded mammalian neurons
in situ.</description><issn>0022-3077</issn><issn>1522-1598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNp1kD1PwzAURS0EoqXwA9i8MSAHfySxPVYRhUoUKiiskVs7iSvXjhJX0H9PKhAb07u6OucOD4BrghNCMnq39QnFGCeCJSwhnOATMB56ikgmxSkYYzxkhjkfgYu-3w4ozzA9ByOCOaGpJGPQForeIqi8hgsT1To42-_Qq3EqGg2LRvna9DBUcGFj2DTB684qB5chGh-PyXr4EVxUtUGFU7v2aE0JXB46tbN6AJ7Nvgu-h3MP32zcX4KzSrneXP3eCXif3a-KR_T08jAvpk-ooTiNiGgmaL7OVFXxjJuhI6wSOdZSSJWyNM01ljqvFBU8VZJvGM6oyCXT60xizdgE3PzsNrZuPm1nyrY59Da4UB_KrS8FK1l5_NlAsv_J2d65lfmKg_JnlK2u2Dc91XCf</recordid><startdate>20000301</startdate><enddate>20000301</enddate><creator>Schuchmann, S</creator><creator>Luckermann, M</creator><creator>Kulik, A</creator><creator>Heinemann, U</creator><creator>Ballanyi, K</creator><general>Am Phys Soc</general><scope/></search><sort><creationdate>20000301</creationdate><title>Ca2+- and Metabolism-Related Changes of Mitochondrial Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ</title><author>Schuchmann, S ; Luckermann, M ; Kulik, A ; Heinemann, U ; Ballanyi, K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h204t-1d3826b5aff757e20413f860d989a43446d09d6fa2874a97c30528693db590d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schuchmann, S</creatorcontrib><creatorcontrib>Luckermann, M</creatorcontrib><creatorcontrib>Kulik, A</creatorcontrib><creatorcontrib>Heinemann, U</creatorcontrib><creatorcontrib>Ballanyi, K</creatorcontrib><jtitle>Journal of neurophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schuchmann, S</au><au>Luckermann, M</au><au>Kulik, A</au><au>Heinemann, U</au><au>Ballanyi, K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ca2+- and Metabolism-Related Changes of Mitochondrial Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ</atitle><jtitle>Journal of neurophysiology</jtitle><date>2000-03-01</date><risdate>2000</risdate><volume>83</volume><issue>3</issue><spage>1710</spage><pages>1710-</pages><issn>0022-3077</issn><eissn>1522-1598</eissn><abstract> 1 II. Physiologisches Institut,
Universität Göttingen, D-37073 Göttingen; and
2 Institut für Physiologie,
Humboldt-Universität Berlin, Universitätsklinikum
Charité, D-10117 Berlin, Germany
Schuchmann, S.,
M. Lückermann,
A. Kulik,
U. Heinemann, and
K. Ballanyi.
Ca 2+ - and Metabolism-Related Changes of Mitochondrial
Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ. J. Neurophysiol. 83: 1710-1721, 2000. In
hippocampal slices from rats, dialysis with rhodamine-123 (Rh-123)
and/or fura-2 via the patch electrode allowed monitoring of
mitochondrial potential ( ) changes and intracellular
Ca 2+ ([Ca 2+ ] i ) of CA1 pyramidal
neurons. Plasmalemmal depolarization to 0 mV caused a mean
[Ca 2+ ] i rise of 300 nM and increased Rh-123
fluorescence signal (RFS) by 50% of control. The evoked RFS,
indicating depolarization of , and the
[Ca 2+ ] i transient were abolished by
Ca 2+ -free superfusate or exposure of
Ni 2+ /Cd 2+ . Simultaneous measurements of RFS and
[Ca 2+ ] i showed that the kinetics of both the
Ca 2+ rise and recovery were considerably faster than those
of the depolarization. The plasmalemmal
Ca 2+ /H + pump blocker eosin-B potentiated the
peak of the depolarization-induced RFS and delayed recovery of both the
RFS and [Ca 2+ ] i transient. Thus the
depolarization due to plasmalemmal depolarization is related to
mitochondrial Ca 2+ sequestration secondary to
Ca 2+ influx through voltage-gated Ca 2+
channels. CN elevated [Ca 2+ ] i
by <50 nM but increased RFS by 221% as a result of extensive depolarization of . Oligomycin decreased RFS by 52% without affecting [Ca 2+ ] i . In the presence of
oligomycin, CN and
p-trifluoromethoxy-phenylhydrazone (FCCP) elevated
[Ca 2+ ] i by <50 nM and increased RFS by 285 and 290%, respectively. Accordingly, the metabolism-related
changes are independent of [Ca 2+ ] i . Imaging
techniques revealed that evoked [Ca 2+ ] i rises
are distributed uniformly over the soma and primary dendrites, whereas
corresponding changes in RFS occur more localized in subregions within
the soma. The results show that microfluorometric measurement of the
relation between mitochondrial function and intracellular Ca 2+ is feasible in whole cell recorded mammalian neurons
in situ.</abstract><pub>Am Phys Soc</pub><pmid>10712491</pmid><doi>10.1152/jn.2000.83.3.1710</doi><oa>free_for_read</oa></addata></record> |
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| title | Ca2+- and Metabolism-Related Changes of Mitochondrial Potential in Voltage-Clamped CA1 Pyramidal Neurons In Situ |
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