Effects of selective serotonergic ligands on posthypoxic audiogenic myoclonus.
Identifieur interne : 004A52 ( Ncbi/Curation ); précédent : 004A51; suivant : 004A53Effects of selective serotonergic ligands on posthypoxic audiogenic myoclonus.
Auteurs : R R Matsumoto [États-Unis] ; M J Hussong ; D D TruongSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1995.
English descriptors
- KwdEn :
- Animals, Anoxia (complications), Behavior, Animal (drug effects), Brain Stem (drug effects), Brain Stem (physiopathology), Heart Arrest (complications), Male, Myoclonus (drug therapy), Myoclonus (etiology), Rats, Rats, Sprague-Dawley, Receptors, Serotonin (drug effects), Serotonin Agents (pharmacology), Serotonin Agents (therapeutic use), Synaptic Transmission (drug effects).
- MESH :
- chemical , drug effects : Receptors, Serotonin.
- complications : Anoxia, Heart Arrest.
- drug effects : Behavior, Animal, Brain Stem, Synaptic Transmission.
- drug therapy : Myoclonus.
- etiology : Myoclonus.
- chemical , pharmacology : Serotonin Agents.
- physiopathology : Brain Stem.
- chemical , therapeutic use : Serotonin Agents.
- Animals, Male, Rats, Rats, Sprague-Dawley.
Abstract
Male Sprague-Dawley rats underwent cardiac arrest and resuscitation, subsequently exhibiting posthypoxic myoclonus. The audiogenic posthypoxic myoclonus in these animals could be attenuated with the following drugs: 5-hydroxytryptophan (5-HTP, serotonin [5-HT] precursor), N-(3-trifluoro-methylphenyl)piperazine hydrochloride (TFMPP, 5-HT1B/1C/2 agonist), (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrobromide (DOI, 5-HT2 agonist), and 1-(m-chlorophenyl)-biguanide hydrochloride (m-CPBG, 5-HT3 agonist). In contrast, the following drugs were ineffective: (+/-)-8-hydroxy-dipropylaminotetralin hydrobromide (8-OH-DPAT, 5-HT1A agonist), buspirone hydrochloride (5-HT1A agonist), 7-trifluoromethyl-4(4-methyl-l-piperazinyl)-pyrrolo[1,2- a]quinoxaline maleate (CGS 12066B, 5-HT1B agonist), ketanserin tartrate (5-HT2 antagonist), methysergide maleate (5-HT2 antagonist), fluoxetine (5-HT uptake blocker), and saline (vehicle). The data suggest that enhancement of serotonergic activity, particularly through 5-HT2 and 5-HT3 receptors, have therapeutic potential for the treatment of posthypoxic myoclonus.
DOI: 10.1002/mds.870100514
PubMed: 8552114
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Effects of selective serotonergic ligands on posthypoxic audiogenic myoclonus.</title><author><name sortKey="Matsumoto, R R" sort="Matsumoto, R R" uniqKey="Matsumoto R" first="R R" last="Matsumoto">R R Matsumoto</name><affiliation wicri:level="1"><nlm:affiliation>Parkinson and Movement Disorders Program, Department of Neurology, University of California-Irvine 92717, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Parkinson and Movement Disorders Program, Department of Neurology, University of California-Irvine 92717</wicri:regionArea><wicri:noRegion>University of California-Irvine 92717</wicri:noRegion></affiliation></author><author><name sortKey="Hussong, M J" sort="Hussong, M J" uniqKey="Hussong M" first="M J" last="Hussong">M J Hussong</name></author><author><name sortKey="Truong, D D" sort="Truong, D D" uniqKey="Truong D" first="D D" last="Truong">D D Truong</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1995">1995</date><idno type="RBID">pubmed:8552114</idno><idno type="pmid">8552114</idno><idno type="doi">10.1002/mds.870100514</idno><idno type="wicri:Area/PubMed/Corpus">004931</idno><idno type="wicri:Area/PubMed/Curation">004931</idno><idno type="wicri:Area/PubMed/Checkpoint">004988</idno><idno type="wicri:Area/Ncbi/Merge">004A52</idno><idno type="wicri:Area/Ncbi/Curation">004A52</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effects of selective serotonergic ligands on posthypoxic audiogenic myoclonus.</title><author><name sortKey="Matsumoto, R R" sort="Matsumoto, R R" uniqKey="Matsumoto R" first="R R" last="Matsumoto">R R Matsumoto</name><affiliation wicri:level="1"><nlm:affiliation>Parkinson and Movement Disorders Program, Department of Neurology, University of California-Irvine 92717, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Parkinson and Movement Disorders Program, Department of Neurology, University of California-Irvine 92717</wicri:regionArea><wicri:noRegion>University of California-Irvine 92717</wicri:noRegion></affiliation></author><author><name sortKey="Hussong, M J" sort="Hussong, M J" uniqKey="Hussong M" first="M J" last="Hussong">M J Hussong</name></author><author><name sortKey="Truong, D D" sort="Truong, D D" uniqKey="Truong D" first="D D" last="Truong">D D Truong</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1995" type="published">1995</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Anoxia (complications)</term><term>Behavior, Animal (drug effects)</term><term>Brain Stem (drug effects)</term><term>Brain Stem (physiopathology)</term><term>Heart Arrest (complications)</term><term>Male</term><term>Myoclonus (drug therapy)</term><term>Myoclonus (etiology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Receptors, Serotonin (drug effects)</term><term>Serotonin Agents (pharmacology)</term><term>Serotonin Agents (therapeutic use)</term><term>Synaptic Transmission (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, Serotonin</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Anoxia</term><term>Heart Arrest</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Behavior, Animal</term><term>Brain Stem</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Myoclonus</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Myoclonus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Serotonin Agents</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain Stem</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Serotonin Agents</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Male Sprague-Dawley rats underwent cardiac arrest and resuscitation, subsequently exhibiting posthypoxic myoclonus. The audiogenic posthypoxic myoclonus in these animals could be attenuated with the following drugs: 5-hydroxytryptophan (5-HTP, serotonin [5-HT] precursor), N-(3-trifluoro-methylphenyl)piperazine hydrochloride (TFMPP, 5-HT1B/1C/2 agonist), (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrobromide (DOI, 5-HT2 agonist), and 1-(m-chlorophenyl)-biguanide hydrochloride (m-CPBG, 5-HT3 agonist). In contrast, the following drugs were ineffective: (+/-)-8-hydroxy-dipropylaminotetralin hydrobromide (8-OH-DPAT, 5-HT1A agonist), buspirone hydrochloride (5-HT1A agonist), 7-trifluoromethyl-4(4-methyl-l-piperazinyl)-pyrrolo[1,2- a]quinoxaline maleate (CGS 12066B, 5-HT1B agonist), ketanserin tartrate (5-HT2 antagonist), methysergide maleate (5-HT2 antagonist), fluoxetine (5-HT uptake blocker), and saline (vehicle). The data suggest that enhancement of serotonergic activity, particularly through 5-HT2 and 5-HT3 receptors, have therapeutic potential for the treatment of posthypoxic myoclonus.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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