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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Veröffentlicht in:Neuroscience 1993-09, Vol.56 (1), p.189-197
Hauptverfasser: Elliott, P., Wallis, D.I.
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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.
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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). 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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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identifier ISSN: 0306-4522
ispartof Neuroscience, 1993-09, Vol.56 (1), p.189-197
issn 0306-4522
1873-7544
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source MEDLINE; Elsevier ScienceDirect Journals
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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