Participation of low-threshold calcium spikes in excitatory synaptic transmission in guinea pig medial frontal cortex
We studied the activation of low‐threshold calcium spikes (LTS) by excitatory postsynaptic potentials in pyramidal neurons from guinea pig medial frontal cortex with intracellular recording. We used extracellular bicuculline and phaclofen and intracellular QX‐314 to block inhibitory synaptic potenti...
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description | We studied the activation of low‐threshold calcium spikes (LTS) by excitatory postsynaptic potentials in pyramidal neurons from guinea pig medial frontal cortex with intracellular recording. We used extracellular bicuculline and phaclofen and intracellular QX‐314 to block inhibitory synaptic potentials and sodium currents. Postsynaptic potentials were evoked by stimulation of layer I. We found that large (> 10–15 mV) excitatory synaptic potentials evoked from membrane potentials more negative than −75 mV were able to trigger LTS. The activation of LTS resulted in an increase of the rising slope or amplitude of the synaptic potentials depending on the size of the excitatory postsynaptic potential (EPSP). We used 100 μm NiCl2 to confirm the presence of LTS as part of the EPSPs. The N‐methyl‐d‐aspartate (NMDA) and non‐NMDA components of the excitatory synaptic potentials were isolated using (±)2‐amino‐5‐phosphonovaleric acid (APV; 50 μm) or 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX; 20 μm); both components could, independently, trigger an LTS. With recordings made with K+ acetate‐filled electrodes, we show that the activation of LTS was critical to allow excitatory synaptic potentials to reach the threshold of action potential firing; also, this amplification of synaptic responses produced the firing of more than a single action potential by the postsynaptic cell. These results demonstrate that in cortical pyramidal neurons the activation of low‐threshold calcium spikes results in the amplification of synaptic responses. |
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We used extracellular bicuculline and phaclofen and intracellular QX‐314 to block inhibitory synaptic potentials and sodium currents. Postsynaptic potentials were evoked by stimulation of layer I. We found that large (> 10–15 mV) excitatory synaptic potentials evoked from membrane potentials more negative than −75 mV were able to trigger LTS. The activation of LTS resulted in an increase of the rising slope or amplitude of the synaptic potentials depending on the size of the excitatory postsynaptic potential (EPSP). We used 100 μm NiCl2 to confirm the presence of LTS as part of the EPSPs. The N‐methyl‐d‐aspartate (NMDA) and non‐NMDA components of the excitatory synaptic potentials were isolated using (±)2‐amino‐5‐phosphonovaleric acid (APV; 50 μm) or 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX; 20 μm); both components could, independently, trigger an LTS. With recordings made with K+ acetate‐filled electrodes, we show that the activation of LTS was critical to allow excitatory synaptic potentials to reach the threshold of action potential firing; also, this amplification of synaptic responses produced the firing of more than a single action potential by the postsynaptic cell. These results demonstrate that in cortical pyramidal neurons the activation of low‐threshold calcium spikes results in the amplification of synaptic responses.</description><identifier>ISSN: 0953-816X</identifier><identifier>EISSN: 1460-9568</identifier><identifier>DOI: 10.1046/j.1460-9568.2000.00061.x</identifier><identifier>PMID: 10792445</identifier><identifier>CODEN: EJONEI</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>2-Amino-5-phosphonovalerate - pharmacology ; 6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology ; Animals ; Bicuculline - pharmacology ; brain slices ; Calcium - physiology ; EPSP amplification ; Evoked Potentials - drug effects ; Evoked Potentials - physiology ; Excitatory Amino Acid Antagonists - pharmacology ; Excitatory Postsynaptic Potentials - drug effects ; Excitatory Postsynaptic Potentials - physiology ; Frontal Lobe - physiology ; glutamate receptors ; Guinea Pigs ; In Vitro Techniques ; intracellular recording ; Lidocaine - analogs & derivatives ; Lidocaine - pharmacology ; Membrane Potentials - physiology ; N-Methylaspartate - physiology ; Potassium Acetate - pharmacology ; Pyramidal Cells - drug effects ; Pyramidal Cells - physiology ; pyramidal neurons ; Synaptic Transmission - drug effects ; Synaptic Transmission - physiology</subject><ispartof>The European journal of neuroscience, 2000-05, Vol.12 (5), p.1679-1686</ispartof><rights>European Neuroscience Association</rights><rights>Copyright Oxford University Press May 2000</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5881-96e557f3c085d3df0673863070576942806d16967acee50b84b2e196d3f77ed33</citedby><cites>FETCH-LOGICAL-c5881-96e557f3c085d3df0673863070576942806d16967acee50b84b2e196d3f77ed33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1046%2Fj.1460-9568.2000.00061.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1046%2Fj.1460-9568.2000.00061.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,778,782,1414,27907,27908,45557,45558</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10792445$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de la Pena, Elvira</creatorcontrib><creatorcontrib>Geijo-Barrientos, Emilio</creatorcontrib><title>Participation of low-threshold calcium spikes in excitatory synaptic transmission in guinea pig medial frontal cortex</title><title>The European journal of neuroscience</title><addtitle>Eur J Neurosci</addtitle><description>We studied the activation of low‐threshold calcium spikes (LTS) by excitatory postsynaptic potentials in pyramidal neurons from guinea pig medial frontal cortex with intracellular recording. We used extracellular bicuculline and phaclofen and intracellular QX‐314 to block inhibitory synaptic potentials and sodium currents. Postsynaptic potentials were evoked by stimulation of layer I. We found that large (> 10–15 mV) excitatory synaptic potentials evoked from membrane potentials more negative than −75 mV were able to trigger LTS. The activation of LTS resulted in an increase of the rising slope or amplitude of the synaptic potentials depending on the size of the excitatory postsynaptic potential (EPSP). We used 100 μm NiCl2 to confirm the presence of LTS as part of the EPSPs. The N‐methyl‐d‐aspartate (NMDA) and non‐NMDA components of the excitatory synaptic potentials were isolated using (±)2‐amino‐5‐phosphonovaleric acid (APV; 50 μm) or 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX; 20 μm); both components could, independently, trigger an LTS. With recordings made with K+ acetate‐filled electrodes, we show that the activation of LTS was critical to allow excitatory synaptic potentials to reach the threshold of action potential firing; also, this amplification of synaptic responses produced the firing of more than a single action potential by the postsynaptic cell. These results demonstrate that in cortical pyramidal neurons the activation of low‐threshold calcium spikes results in the amplification of synaptic responses.</description><subject>2-Amino-5-phosphonovalerate - pharmacology</subject><subject>6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology</subject><subject>Animals</subject><subject>Bicuculline - pharmacology</subject><subject>brain slices</subject><subject>Calcium - physiology</subject><subject>EPSP amplification</subject><subject>Evoked Potentials - drug effects</subject><subject>Evoked Potentials - physiology</subject><subject>Excitatory Amino Acid Antagonists - pharmacology</subject><subject>Excitatory Postsynaptic Potentials - drug effects</subject><subject>Excitatory Postsynaptic Potentials - physiology</subject><subject>Frontal Lobe - physiology</subject><subject>glutamate receptors</subject><subject>Guinea Pigs</subject><subject>In Vitro Techniques</subject><subject>intracellular recording</subject><subject>Lidocaine - analogs & derivatives</subject><subject>Lidocaine - pharmacology</subject><subject>Membrane Potentials - physiology</subject><subject>N-Methylaspartate - physiology</subject><subject>Potassium Acetate - pharmacology</subject><subject>Pyramidal Cells - drug effects</subject><subject>Pyramidal Cells - physiology</subject><subject>pyramidal neurons</subject><subject>Synaptic Transmission - drug effects</subject><subject>Synaptic Transmission - physiology</subject><issn>0953-816X</issn><issn>1460-9568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EokPhFZDFArFJuI5_I7FBo9IWRuVHINhZHsdpPc3EwU7Umbevw1QVYgEsrGvJ3zmy_SGECZQEmHi9KQkTUNRcqLICgDIvQcrdA7S4P3iIFlBzWigifhyhJyltMqQE44_REQFZV4zxBZo-mTh66wcz-tDj0OIu3BTjVXTpKnQNtqazftriNPhrl7DvsdtZP5oxxD1O-94MOY3HaPq09SnNHZm5nHzvDB78Jd66xpsOtzH0Y542xNHtnqJHremSe3Y3j9G3dydfl2fF6uPp-fLtqrBcKVLUwnEuW2pB8YY2LQhJlaAggUtRs0qBaIiohTTWOQ5rxdaVI7VoaCulayg9Ri8PvUMMPyeXRp0vaV3Xmd6FKWlJQNFKqH-CFYGKAa0z-OqvIFGg5Py9kNEXf6CbMMU-v1dXwCrJJBEZUgfIxpBSdK0eot-auNcE9Oxab_SsVM9K9exa_3Ktdzn6_K5_Wudf_i14kJuBNwfgxndu_9_F-uT9Rd7keHGI-5SV3cdNvNbZg-T6-8Wp_gxnH77w1VKv6C3CxcbO</recordid><startdate>200005</startdate><enddate>200005</enddate><creator>de la Pena, Elvira</creator><creator>Geijo-Barrientos, Emilio</creator><general>Blackwell Science Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>200005</creationdate><title>Participation of low-threshold calcium spikes in excitatory synaptic transmission in guinea pig medial frontal cortex</title><author>de la Pena, Elvira ; Geijo-Barrientos, Emilio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5881-96e557f3c085d3df0673863070576942806d16967acee50b84b2e196d3f77ed33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>2-Amino-5-phosphonovalerate - pharmacology</topic><topic>6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology</topic><topic>Animals</topic><topic>Bicuculline - pharmacology</topic><topic>brain slices</topic><topic>Calcium - physiology</topic><topic>EPSP amplification</topic><topic>Evoked Potentials - drug effects</topic><topic>Evoked Potentials - physiology</topic><topic>Excitatory Amino Acid Antagonists - pharmacology</topic><topic>Excitatory Postsynaptic Potentials - drug effects</topic><topic>Excitatory Postsynaptic Potentials - physiology</topic><topic>Frontal Lobe - physiology</topic><topic>glutamate receptors</topic><topic>Guinea Pigs</topic><topic>In Vitro Techniques</topic><topic>intracellular recording</topic><topic>Lidocaine - analogs & derivatives</topic><topic>Lidocaine - pharmacology</topic><topic>Membrane Potentials - physiology</topic><topic>N-Methylaspartate - physiology</topic><topic>Potassium Acetate - pharmacology</topic><topic>Pyramidal Cells - drug effects</topic><topic>Pyramidal Cells - physiology</topic><topic>pyramidal neurons</topic><topic>Synaptic Transmission - drug effects</topic><topic>Synaptic Transmission - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de la Pena, Elvira</creatorcontrib><creatorcontrib>Geijo-Barrientos, Emilio</creatorcontrib><collection>Istex</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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The European journal of neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de la Pena, Elvira</au><au>Geijo-Barrientos, Emilio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Participation of low-threshold calcium spikes in excitatory synaptic transmission in guinea pig medial frontal cortex</atitle><jtitle>The European journal of neuroscience</jtitle><addtitle>Eur J Neurosci</addtitle><date>2000-05</date><risdate>2000</risdate><volume>12</volume><issue>5</issue><spage>1679</spage><epage>1686</epage><pages>1679-1686</pages><issn>0953-816X</issn><eissn>1460-9568</eissn><coden>EJONEI</coden><abstract>We studied the activation of low‐threshold calcium spikes (LTS) by excitatory postsynaptic potentials in pyramidal neurons from guinea pig medial frontal cortex with intracellular recording. We used extracellular bicuculline and phaclofen and intracellular QX‐314 to block inhibitory synaptic potentials and sodium currents. Postsynaptic potentials were evoked by stimulation of layer I. We found that large (> 10–15 mV) excitatory synaptic potentials evoked from membrane potentials more negative than −75 mV were able to trigger LTS. The activation of LTS resulted in an increase of the rising slope or amplitude of the synaptic potentials depending on the size of the excitatory postsynaptic potential (EPSP). We used 100 μm NiCl2 to confirm the presence of LTS as part of the EPSPs. The N‐methyl‐d‐aspartate (NMDA) and non‐NMDA components of the excitatory synaptic potentials were isolated using (±)2‐amino‐5‐phosphonovaleric acid (APV; 50 μm) or 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX; 20 μm); both components could, independently, trigger an LTS. With recordings made with K+ acetate‐filled electrodes, we show that the activation of LTS was critical to allow excitatory synaptic potentials to reach the threshold of action potential firing; also, this amplification of synaptic responses produced the firing of more than a single action potential by the postsynaptic cell. These results demonstrate that in cortical pyramidal neurons the activation of low‐threshold calcium spikes results in the amplification of synaptic responses.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>10792445</pmid><doi>10.1046/j.1460-9568.2000.00061.x</doi><tpages>8</tpages></addata></record> |
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subjects | 2-Amino-5-phosphonovalerate - pharmacology 6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology Animals Bicuculline - pharmacology brain slices Calcium - physiology EPSP amplification Evoked Potentials - drug effects Evoked Potentials - physiology Excitatory Amino Acid Antagonists - pharmacology Excitatory Postsynaptic Potentials - drug effects Excitatory Postsynaptic Potentials - physiology Frontal Lobe - physiology glutamate receptors Guinea Pigs In Vitro Techniques intracellular recording Lidocaine - analogs & derivatives Lidocaine - pharmacology Membrane Potentials - physiology N-Methylaspartate - physiology Potassium Acetate - pharmacology Pyramidal Cells - drug effects Pyramidal Cells - physiology pyramidal neurons Synaptic Transmission - drug effects Synaptic Transmission - physiology |
title | Participation of low-threshold calcium spikes in excitatory synaptic transmission in guinea pig medial frontal cortex |
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