Glutamatergic and non-glutamatergic responses evoked in neonatal rat lumbar motoneurons on stimulation of the lateroventral spinal cord surface
The effects on lumbar motoneurons of thoracic cord stimulation were investigated in the neonatal rat hemisected spinal cord vitro using intracellular recording. Four responses were evoked—a fast, excitatory postsynaptic potential, a second component to the fast excitatory postsynaptic potential, a f...
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description | The effects on lumbar motoneurons of thoracic cord stimulation were investigated in the neonatal rat hemisected spinal cord
vitro using intracellular recording. Four responses were evoked—a fast, excitatory postsynaptic potential, a second component to the fast excitatory postsynaptic potential, a fast inhibitory postsynaptic potential and a slow excitatory postsynaptic potential. The fast (CNQX-sensitive) excitatory postsynaptic potential was probably monosynaptic, was blocked by CNQX, (10μM) and showed a frequency-dependent run-down at stimulation frequencies between 0.1 and 1 Hz. A slower component to the fast excitatory postsynaptic potential ((±)-2-amino-5-phosphono-valeric acid-sensitive excitatory postsynaptic potential) was blocked by (±)-2-amino-5-phosphonovaleric acid (50 μM). Following fast excitatory postsynaptic potential blockade with both CNQX and (±)-2-amino-5-phospho-novaleric acid, a fast inhibitory postsynaptic potential was revealed. This reversed at a membrane potential close to resting and was incompletely blocked by either bicuculline (30 μM) or strychnine (10 μM). The slow excitatory postsynaptic potential was a delayed depolarization associated with a small increase in input resistance (20%) and was insensitive to block by CNQX and/or (±)-2-amino-5-phosphonovaleric acid. It increased in amplitude on membrane depolarization and decreased on hyperpolarization and was potentiated by cocaine (3μM) and citalopram (0.1μM), but not by desipramine (5μM). The slow excitatory postsynaptic potential was blocked by ketanserin (1μM) and by LY 53857 (1μM).
It is concluded that a non-glutamatergic transmitter is involved in generating the slow excitatory postsynaptic potential possibly 5-hydroxytryptamine acting at 5-hydroxytryptamine
2 receptors. |
doi_str_mv | 10.1016/0306-4522(93)90573-X |
format | Article |
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vitro using intracellular recording. Four responses were evoked—a fast, excitatory postsynaptic potential, a second component to the fast excitatory postsynaptic potential, a fast inhibitory postsynaptic potential and a slow excitatory postsynaptic potential. The fast (CNQX-sensitive) excitatory postsynaptic potential was probably monosynaptic, was blocked by CNQX, (10μM) and showed a frequency-dependent run-down at stimulation frequencies between 0.1 and 1 Hz. A slower component to the fast excitatory postsynaptic potential ((±)-2-amino-5-phosphono-valeric acid-sensitive excitatory postsynaptic potential) was blocked by (±)-2-amino-5-phosphonovaleric acid (50 μM). Following fast excitatory postsynaptic potential blockade with both CNQX and (±)-2-amino-5-phospho-novaleric acid, a fast inhibitory postsynaptic potential was revealed. This reversed at a membrane potential close to resting and was incompletely blocked by either bicuculline (30 μM) or strychnine (10 μM). The slow excitatory postsynaptic potential was a delayed depolarization associated with a small increase in input resistance (20%) and was insensitive to block by CNQX and/or (±)-2-amino-5-phosphonovaleric acid. It increased in amplitude on membrane depolarization and decreased on hyperpolarization and was potentiated by cocaine (3μM) and citalopram (0.1μM), but not by desipramine (5μM). The slow excitatory postsynaptic potential was blocked by ketanserin (1μM) and by LY 53857 (1μM).
It is concluded that a non-glutamatergic transmitter is involved in generating the slow excitatory postsynaptic potential possibly 5-hydroxytryptamine acting at 5-hydroxytryptamine
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vitro using intracellular recording. Four responses were evoked—a fast, excitatory postsynaptic potential, a second component to the fast excitatory postsynaptic potential, a fast inhibitory postsynaptic potential and a slow excitatory postsynaptic potential. The fast (CNQX-sensitive) excitatory postsynaptic potential was probably monosynaptic, was blocked by CNQX, (10μM) and showed a frequency-dependent run-down at stimulation frequencies between 0.1 and 1 Hz. A slower component to the fast excitatory postsynaptic potential ((±)-2-amino-5-phosphono-valeric acid-sensitive excitatory postsynaptic potential) was blocked by (±)-2-amino-5-phosphonovaleric acid (50 μM). Following fast excitatory postsynaptic potential blockade with both CNQX and (±)-2-amino-5-phospho-novaleric acid, a fast inhibitory postsynaptic potential was revealed. This reversed at a membrane potential close to resting and was incompletely blocked by either bicuculline (30 μM) or strychnine (10 μM). The slow excitatory postsynaptic potential was a delayed depolarization associated with a small increase in input resistance (20%) and was insensitive to block by CNQX and/or (±)-2-amino-5-phosphonovaleric acid. It increased in amplitude on membrane depolarization and decreased on hyperpolarization and was potentiated by cocaine (3μM) and citalopram (0.1μM), but not by desipramine (5μM). The slow excitatory postsynaptic potential was blocked by ketanserin (1μM) and by LY 53857 (1μM).
It is concluded that a non-glutamatergic transmitter is involved in generating the slow excitatory postsynaptic potential possibly 5-hydroxytryptamine acting at 5-hydroxytryptamine
2 receptors.</description><subject>2-Amino-5-phosphonovalerate - pharmacology</subject><subject>6-Cyano-7-nitroquinoxaline-2,3-dione</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Bicuculline - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Central nervous system</subject><subject>Citalopram - pharmacology</subject><subject>Cocaine - pharmacology</subject><subject>Desipramine - pharmacology</subject><subject>Electric Stimulation</subject><subject>Electrophysiology</subject><subject>Ergolines - pharmacology</subject><subject>Evoked Potentials - drug effects</subject><subject>Excitatory Amino Acid Antagonists</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>In Vitro Techniques</subject><subject>Ketanserin - pharmacology</subject><subject>Membrane Potentials - drug effects</subject><subject>Motor Neurons - drug effects</subject><subject>Motor Neurons - physiology</subject><subject>Quinoxalines - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Glutamate - physiology</subject><subject>Serotonin Antagonists - pharmacology</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - physiology</subject><subject>Strychnine - pharmacology</subject><subject>Synapses - drug effects</subject><subject>Synapses - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc-KFDEQxoMo67j6Bgo5iOihNel0-s9FkEVXYcGLwt5CdVJZo-lkTNIDPoWvbNoZBrwYCFWkfl9R-YqQp5y95oz3b5hgfdPJtn05iVcTk4Nobu-RHR9rMsiuu092Z-QheZTzd1aP7MQFuRgmxkfW78jva78WWKBgunOaQjA0xNDc_fOaMO9jyJgpHuIPNNQFGjAGKOBpgkL9usyQ6BJLDLimytIYaC5uWT0UV_NoafmG1G8t4wFDSVWa9y7UoGMyNK_JgsbH5IEFn_HJKV6Srx_ef7n62Nx8vv509e6m0R0fSqOBQz_Z3o7WMmY4ynZEibJH27aaAcxzO2O9FoTojWayWqaRsQFmM1ghLsmLY999ij9XzEUtLmv0HurH1qx4P4hp6jewO4I6xZwTWrVPboH0S3Gmtj2ozWS1mawmof7uQd1W2bNT_3Ve0JxFJ-Nr_fmpDlmDtwmCdvmMdaPsKlqxt0cMqxcHh0ll7TBoNC6hLspE9_85_gASIql7</recordid><startdate>19930901</startdate><enddate>19930901</enddate><creator>Elliott, P.</creator><creator>Wallis, D.I.</creator><general>Elsevier Ltd</general><general>Elsevier</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>7TK</scope></search><sort><creationdate>19930901</creationdate><title>Glutamatergic and non-glutamatergic responses evoked in neonatal rat lumbar motoneurons on stimulation of the lateroventral spinal cord surface</title><author>Elliott, P. ; Wallis, D.I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-ca1a69f6f8ff00d1e528e5e56ef22c0aabb2beb2bfa336dc05101ce007abd7f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>2-Amino-5-phosphonovalerate - pharmacology</topic><topic>6-Cyano-7-nitroquinoxaline-2,3-dione</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Bicuculline - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Central nervous system</topic><topic>Citalopram - pharmacology</topic><topic>Cocaine - pharmacology</topic><topic>Desipramine - pharmacology</topic><topic>Electric Stimulation</topic><topic>Electrophysiology</topic><topic>Ergolines - pharmacology</topic><topic>Evoked Potentials - drug effects</topic><topic>Excitatory Amino Acid Antagonists</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>In Vitro Techniques</topic><topic>Ketanserin - pharmacology</topic><topic>Membrane Potentials - drug effects</topic><topic>Motor Neurons - drug effects</topic><topic>Motor Neurons - physiology</topic><topic>Quinoxalines - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Glutamate - physiology</topic><topic>Serotonin Antagonists - pharmacology</topic><topic>Spinal Cord - drug effects</topic><topic>Spinal Cord - physiology</topic><topic>Strychnine - pharmacology</topic><topic>Synapses - drug effects</topic><topic>Synapses - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Elliott, P.</creatorcontrib><creatorcontrib>Wallis, D.I.</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>Neurosciences Abstracts</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Elliott, P.</au><au>Wallis, D.I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glutamatergic and non-glutamatergic responses evoked in neonatal rat lumbar motoneurons on stimulation of the lateroventral spinal cord surface</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>1993-09-01</date><risdate>1993</risdate><volume>56</volume><issue>1</issue><spage>189</spage><epage>197</epage><pages>189-197</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>The effects on lumbar motoneurons of thoracic cord stimulation were investigated in the neonatal rat hemisected spinal cord
vitro using intracellular recording. Four responses were evoked—a fast, excitatory postsynaptic potential, a second component to the fast excitatory postsynaptic potential, a fast inhibitory postsynaptic potential and a slow excitatory postsynaptic potential. The fast (CNQX-sensitive) excitatory postsynaptic potential was probably monosynaptic, was blocked by CNQX, (10μM) and showed a frequency-dependent run-down at stimulation frequencies between 0.1 and 1 Hz. A slower component to the fast excitatory postsynaptic potential ((±)-2-amino-5-phosphono-valeric acid-sensitive excitatory postsynaptic potential) was blocked by (±)-2-amino-5-phosphonovaleric acid (50 μM). Following fast excitatory postsynaptic potential blockade with both CNQX and (±)-2-amino-5-phospho-novaleric acid, a fast inhibitory postsynaptic potential was revealed. This reversed at a membrane potential close to resting and was incompletely blocked by either bicuculline (30 μM) or strychnine (10 μM). The slow excitatory postsynaptic potential was a delayed depolarization associated with a small increase in input resistance (20%) and was insensitive to block by CNQX and/or (±)-2-amino-5-phosphonovaleric acid. It increased in amplitude on membrane depolarization and decreased on hyperpolarization and was potentiated by cocaine (3μM) and citalopram (0.1μM), but not by desipramine (5μM). The slow excitatory postsynaptic potential was blocked by ketanserin (1μM) and by LY 53857 (1μM).
It is concluded that a non-glutamatergic transmitter is involved in generating the slow excitatory postsynaptic potential possibly 5-hydroxytryptamine acting at 5-hydroxytryptamine
2 receptors.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>7901806</pmid><doi>10.1016/0306-4522(93)90573-X</doi><tpages>9</tpages></addata></record> |
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subjects | 2-Amino-5-phosphonovalerate - pharmacology 6-Cyano-7-nitroquinoxaline-2,3-dione Animals Animals, Newborn Bicuculline - pharmacology Biological and medical sciences Central nervous system Citalopram - pharmacology Cocaine - pharmacology Desipramine - pharmacology Electric Stimulation Electrophysiology Ergolines - pharmacology Evoked Potentials - drug effects Excitatory Amino Acid Antagonists Fundamental and applied biological sciences. Psychology In Vitro Techniques Ketanserin - pharmacology Membrane Potentials - drug effects Motor Neurons - drug effects Motor Neurons - physiology Quinoxalines - pharmacology Rats Rats, Wistar Receptors, Glutamate - physiology Serotonin Antagonists - pharmacology Spinal Cord - drug effects Spinal Cord - physiology Strychnine - pharmacology Synapses - drug effects Synapses - physiology Vertebrates: nervous system and sense organs |
title | Glutamatergic and non-glutamatergic responses evoked in neonatal rat lumbar motoneurons on stimulation of the lateroventral spinal cord surface |
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