Characterization of Ca2+ signals induced in hippocampal CA1 neurones by the synaptic activation of NMDA receptors
1. A combination of confocal microscopy, whole-cell patch-clamp recording, intracellular dialysis and pharmacological techniques have been employed to study Ca2+ signalling in CA1 pyramidal neurones, within rat hippocampal slices. 2. In the soma of CA1 neurones, depolarizing steps applied through th...
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| Veröffentlicht in: | The Journal of physiology 1993-09, Vol.469 (1), p.693-716 |
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| description | 1. A combination of confocal microscopy, whole-cell patch-clamp recording, intracellular dialysis and pharmacological techniques
have been employed to study Ca2+ signalling in CA1 pyramidal neurones, within rat hippocampal slices. 2. In the soma of CA1
neurones, depolarizing steps applied through the patch-pipette resulted in transient increases in the fluorescence emitted
by the Ca2+ indicator fluo-3. The intensity of the fluorescence transients was proportional to the magnitude of the Ca2+ currents
recorded through the pipette. Both the somatic fluorescence transients and the voltage-activated Ca2+ currents ran down in
parallel over a period of between approximately 15-45 min. The fluorescence transients were considered, therefore, to be caused
by increases in cytosolic free Ca2+. 3. Under current-clamp conditions, high-frequency (tetanic) stimulation (100 Hz, 1 s)
of the Schaffer collateral-commissural pathway led to compound excitatory postsynaptic potentials (EPSPs) and somatic Ca2+
transients. The somatic Ca2+ transients were sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonopentanoate
(AP5; 100 microM). These transients, but not the EPSPs, disappeared with a time course similar to that of the run-down of
voltage-gated Ca2+ currents. Tetanus-induced somatic Ca2+ transients could not be elicited under voltage-clamp conditions.
4. Fluorescence images were obtained from the dendrites of CA1 pyramidal neurones starting at least 30 min after obtaining
whole-cell access to the neurone. Measurements were obtained only after voltage-gated Ca2+ channel activity had run down completely.
5. Tetanic stimulation of the Schaffer collateral-commissural pathway resulted in compound EPSPs and excitatory postsynaptic
currents (EPSCs), under current- and voltage-clamp, respectively. In both cases, these were invariably associated with dendritic
Ca2+ transients. In cells voltage-clamped at -35 mV, the fluorescent signal increased on average 2-fold during the tetanus
and decayed to baseline values with a half-time (t1/2) of approximately 5 s. 6. The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate
(AMPA) receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) partially reduced the tetanus-induced EPSC
without affecting the Ca2+ transients. In contrast, AP5, which also depressed the EPSC, substantially reduced or eliminated
the Ca2+ transients. 7. In normal (i.e. 1 mM Mg(2+)-containing) medium, NMDA receptor-medi |
| doi_str_mv | 10.1113/jphysiol.1993.sp019838 |
| format | Article |
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have been employed to study Ca2+ signalling in CA1 pyramidal neurones, within rat hippocampal slices. 2. In the soma of CA1
neurones, depolarizing steps applied through the patch-pipette resulted in transient increases in the fluorescence emitted
by the Ca2+ indicator fluo-3. The intensity of the fluorescence transients was proportional to the magnitude of the Ca2+ currents
recorded through the pipette. Both the somatic fluorescence transients and the voltage-activated Ca2+ currents ran down in
parallel over a period of between approximately 15-45 min. The fluorescence transients were considered, therefore, to be caused
by increases in cytosolic free Ca2+. 3. Under current-clamp conditions, high-frequency (tetanic) stimulation (100 Hz, 1 s)
of the Schaffer collateral-commissural pathway led to compound excitatory postsynaptic potentials (EPSPs) and somatic Ca2+
transients. The somatic Ca2+ transients were sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonopentanoate
(AP5; 100 microM). These transients, but not the EPSPs, disappeared with a time course similar to that of the run-down of
voltage-gated Ca2+ currents. Tetanus-induced somatic Ca2+ transients could not be elicited under voltage-clamp conditions.
4. Fluorescence images were obtained from the dendrites of CA1 pyramidal neurones starting at least 30 min after obtaining
whole-cell access to the neurone. Measurements were obtained only after voltage-gated Ca2+ channel activity had run down completely.
5. Tetanic stimulation of the Schaffer collateral-commissural pathway resulted in compound EPSPs and excitatory postsynaptic
currents (EPSCs), under current- and voltage-clamp, respectively. In both cases, these were invariably associated with dendritic
Ca2+ transients. In cells voltage-clamped at -35 mV, the fluorescent signal increased on average 2-fold during the tetanus
and decayed to baseline values with a half-time (t1/2) of approximately 5 s. 6. The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate
(AMPA) receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) partially reduced the tetanus-induced EPSC
without affecting the Ca2+ transients. In contrast, AP5, which also depressed the EPSC, substantially reduced or eliminated
the Ca2+ transients. 7. In normal (i.e. 1 mM Mg(2+)-containing) medium, NMDA receptor-mediated synaptic currents displayed
the typical region of negative slope conductance in the peak I-V relationship (between -90 and -35 mV). The dendritic tetanus-induced
Ca2+ transients also displayed a similar anomalous voltage dependence, decreasing in size from -35 to -90 mV.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.1993.sp019838</identifier><identifier>PMID: 8271224</identifier><identifier>CODEN: JPHYA7</identifier><language>eng</language><publisher>Oxford: The Physiological Society</publisher><subject>Animals ; Biological and medical sciences ; Calcium - physiology ; Calcium Channels - physiology ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Dendrites - physiology ; Electric Stimulation ; Evoked Potentials - drug effects ; Evoked Potentials - physiology ; Fundamental and applied biological sciences. Psychology ; Hippocampus - cytology ; Hippocampus - physiology ; In Vitro Techniques ; Ion Channel Gating - physiology ; Lasers ; Microscopy ; Neural Pathways - physiology ; Neurons - physiology ; Pyramidal Cells - metabolism ; Rats ; Receptors, Amino Acid - metabolism ; Receptors, N-Methyl-D-Aspartate - physiology ; Signal Transduction - physiology ; Spectrometry, Fluorescence ; Synapses - physiology ; Vertebrates: nervous system and sense organs</subject><ispartof>The Journal of physiology, 1993-09, Vol.469 (1), p.693-716</ispartof><rights>1993 The Physiological Society</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5433-e7eb17e4d929554fb607bdceff6106783d1a60be86bab8f1468ad4348c0030a23</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/PMC1143895/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1143895/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,725,778,782,883,1414,27907,27908,45557,45558,53774,53776</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4882573$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8271224$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alford, S</creatorcontrib><creatorcontrib>Frenguelli, B G</creatorcontrib><creatorcontrib>Schofield, J G</creatorcontrib><creatorcontrib>Collingridge, G L</creatorcontrib><title>Characterization of Ca2+ signals induced in hippocampal CA1 neurones by the synaptic activation of NMDA receptors</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>1. A combination of confocal microscopy, whole-cell patch-clamp recording, intracellular dialysis and pharmacological techniques
have been employed to study Ca2+ signalling in CA1 pyramidal neurones, within rat hippocampal slices. 2. In the soma of CA1
neurones, depolarizing steps applied through the patch-pipette resulted in transient increases in the fluorescence emitted
by the Ca2+ indicator fluo-3. The intensity of the fluorescence transients was proportional to the magnitude of the Ca2+ currents
recorded through the pipette. Both the somatic fluorescence transients and the voltage-activated Ca2+ currents ran down in
parallel over a period of between approximately 15-45 min. The fluorescence transients were considered, therefore, to be caused
by increases in cytosolic free Ca2+. 3. Under current-clamp conditions, high-frequency (tetanic) stimulation (100 Hz, 1 s)
of the Schaffer collateral-commissural pathway led to compound excitatory postsynaptic potentials (EPSPs) and somatic Ca2+
transients. The somatic Ca2+ transients were sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonopentanoate
(AP5; 100 microM). These transients, but not the EPSPs, disappeared with a time course similar to that of the run-down of
voltage-gated Ca2+ currents. Tetanus-induced somatic Ca2+ transients could not be elicited under voltage-clamp conditions.
4. Fluorescence images were obtained from the dendrites of CA1 pyramidal neurones starting at least 30 min after obtaining
whole-cell access to the neurone. Measurements were obtained only after voltage-gated Ca2+ channel activity had run down completely.
5. Tetanic stimulation of the Schaffer collateral-commissural pathway resulted in compound EPSPs and excitatory postsynaptic
currents (EPSCs), under current- and voltage-clamp, respectively. In both cases, these were invariably associated with dendritic
Ca2+ transients. In cells voltage-clamped at -35 mV, the fluorescent signal increased on average 2-fold during the tetanus
and decayed to baseline values with a half-time (t1/2) of approximately 5 s. 6. The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate
(AMPA) receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) partially reduced the tetanus-induced EPSC
without affecting the Ca2+ transients. In contrast, AP5, which also depressed the EPSC, substantially reduced or eliminated
the Ca2+ transients. 7. In normal (i.e. 1 mM Mg(2+)-containing) medium, NMDA receptor-mediated synaptic currents displayed
the typical region of negative slope conductance in the peak I-V relationship (between -90 and -35 mV). The dendritic tetanus-induced
Ca2+ transients also displayed a similar anomalous voltage dependence, decreasing in size from -35 to -90 mV.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - physiology</subject><subject>Calcium Channels - physiology</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Dendrites - physiology</subject><subject>Electric Stimulation</subject><subject>Evoked Potentials - drug effects</subject><subject>Evoked Potentials - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - physiology</subject><subject>In Vitro Techniques</subject><subject>Ion Channel Gating - physiology</subject><subject>Lasers</subject><subject>Microscopy</subject><subject>Neural Pathways - physiology</subject><subject>Neurons - physiology</subject><subject>Pyramidal Cells - metabolism</subject><subject>Rats</subject><subject>Receptors, Amino Acid - metabolism</subject><subject>Receptors, N-Methyl-D-Aspartate - physiology</subject><subject>Signal Transduction - physiology</subject><subject>Spectrometry, Fluorescence</subject><subject>Synapses - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkltv1DAQhSMEKkvhJ4D8gKAS2sUTJ768VFq2XFUuD-XZcpzJxlU2Tu1sq-XX42i3K3hBPI3kOeebGR1n2QugCwBgb6-Hdhed7xagFFvEgYKSTD7IZlBwNRdCsYfZjNI8nzNRwuPsSYzXlAKjSp1kJzIXkOfFLLtZtSYYO2Jwv8zofE98Q1Ymf0OiW_emi8T19dZinSpp3TB4azaD6chqCaTHbfA9RlLtyNgiibveDKOzJAHd7RH37evFkgS0OIw-xKfZoyZx8dmhnmY_P7y_Wn2aX37_-Hm1vJzbsmBsjgIrEFjUKldlWTQVp6KqLTYNB8qFZDUYTiuUvDKVbNLV0tQFK6SllFGTs9PsfM8dttUGk7Mfg-n0ENzGhJ32xum_O71r9drfaoCCSVUmwKsDIPibLcZRb1y02HWmR7-NWnBgueTTpLN_CkFQBVIUSiQp30tt8DEGbI77ANVTrvo-Vz3lqu9zTcbnf15ztB2CTP2Xh76J1nRNML118SgrpMxLwZLs3V525zrc_edwffXlx_SQPhZwNUFe7yGtW7d3LqDe26K3Dsc0jCsNelL-Bsf90uE</recordid><startdate>19930901</startdate><enddate>19930901</enddate><creator>Alford, S</creator><creator>Frenguelli, B G</creator><creator>Schofield, J G</creator><creator>Collingridge, G L</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>7QP</scope><scope>7TK</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19930901</creationdate><title>Characterization of Ca2+ signals induced in hippocampal CA1 neurones by the synaptic activation of NMDA receptors</title><author>Alford, S ; Frenguelli, B G ; Schofield, J G ; Collingridge, G L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5433-e7eb17e4d929554fb607bdceff6106783d1a60be86bab8f1468ad4348c0030a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium - physiology</topic><topic>Calcium Channels - physiology</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Dendrites - physiology</topic><topic>Electric Stimulation</topic><topic>Evoked Potentials - drug effects</topic><topic>Evoked Potentials - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - physiology</topic><topic>In Vitro Techniques</topic><topic>Ion Channel Gating - physiology</topic><topic>Lasers</topic><topic>Microscopy</topic><topic>Neural Pathways - physiology</topic><topic>Neurons - physiology</topic><topic>Pyramidal Cells - metabolism</topic><topic>Rats</topic><topic>Receptors, Amino Acid - metabolism</topic><topic>Receptors, N-Methyl-D-Aspartate - physiology</topic><topic>Signal Transduction - physiology</topic><topic>Spectrometry, Fluorescence</topic><topic>Synapses - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alford, S</creatorcontrib><creatorcontrib>Frenguelli, B G</creatorcontrib><creatorcontrib>Schofield, J G</creatorcontrib><creatorcontrib>Collingridge, G L</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences 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>Alford, S</au><au>Frenguelli, B G</au><au>Schofield, J G</au><au>Collingridge, G L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization of Ca2+ signals induced in hippocampal CA1 neurones by the synaptic activation of NMDA receptors</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1993-09-01</date><risdate>1993</risdate><volume>469</volume><issue>1</issue><spage>693</spage><epage>716</epage><pages>693-716</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><coden>JPHYA7</coden><abstract>1. A combination of confocal microscopy, whole-cell patch-clamp recording, intracellular dialysis and pharmacological techniques
have been employed to study Ca2+ signalling in CA1 pyramidal neurones, within rat hippocampal slices. 2. In the soma of CA1
neurones, depolarizing steps applied through the patch-pipette resulted in transient increases in the fluorescence emitted
by the Ca2+ indicator fluo-3. The intensity of the fluorescence transients was proportional to the magnitude of the Ca2+ currents
recorded through the pipette. Both the somatic fluorescence transients and the voltage-activated Ca2+ currents ran down in
parallel over a period of between approximately 15-45 min. The fluorescence transients were considered, therefore, to be caused
by increases in cytosolic free Ca2+. 3. Under current-clamp conditions, high-frequency (tetanic) stimulation (100 Hz, 1 s)
of the Schaffer collateral-commissural pathway led to compound excitatory postsynaptic potentials (EPSPs) and somatic Ca2+
transients. The somatic Ca2+ transients were sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonopentanoate
(AP5; 100 microM). These transients, but not the EPSPs, disappeared with a time course similar to that of the run-down of
voltage-gated Ca2+ currents. Tetanus-induced somatic Ca2+ transients could not be elicited under voltage-clamp conditions.
4. Fluorescence images were obtained from the dendrites of CA1 pyramidal neurones starting at least 30 min after obtaining
whole-cell access to the neurone. Measurements were obtained only after voltage-gated Ca2+ channel activity had run down completely.
5. Tetanic stimulation of the Schaffer collateral-commissural pathway resulted in compound EPSPs and excitatory postsynaptic
currents (EPSCs), under current- and voltage-clamp, respectively. In both cases, these were invariably associated with dendritic
Ca2+ transients. In cells voltage-clamped at -35 mV, the fluorescent signal increased on average 2-fold during the tetanus
and decayed to baseline values with a half-time (t1/2) of approximately 5 s. 6. The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate
(AMPA) receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) partially reduced the tetanus-induced EPSC
without affecting the Ca2+ transients. In contrast, AP5, which also depressed the EPSC, substantially reduced or eliminated
the Ca2+ transients. 7. In normal (i.e. 1 mM Mg(2+)-containing) medium, NMDA receptor-mediated synaptic currents displayed
the typical region of negative slope conductance in the peak I-V relationship (between -90 and -35 mV). The dendritic tetanus-induced
Ca2+ transients also displayed a similar anomalous voltage dependence, decreasing in size from -35 to -90 mV.</abstract><cop>Oxford</cop><pub>The Physiological Society</pub><pmid>8271224</pmid><doi>10.1113/jphysiol.1993.sp019838</doi><tpages>24</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of physiology, 1993-09, Vol.469 (1), p.693-716 |
| issn | 0022-3751 1469-7793 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1143895 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; IngentaConnect Free/Open Access Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Biological and medical sciences Calcium - physiology Calcium Channels - physiology Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Dendrites - physiology Electric Stimulation Evoked Potentials - drug effects Evoked Potentials - physiology Fundamental and applied biological sciences. Psychology Hippocampus - cytology Hippocampus - physiology In Vitro Techniques Ion Channel Gating - physiology Lasers Microscopy Neural Pathways - physiology Neurons - physiology Pyramidal Cells - metabolism Rats Receptors, Amino Acid - metabolism Receptors, N-Methyl-D-Aspartate - physiology Signal Transduction - physiology Spectrometry, Fluorescence Synapses - physiology Vertebrates: nervous system and sense organs |
| title | Characterization of Ca2+ signals induced in hippocampal CA1 neurones by the synaptic activation of NMDA receptors |
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