Movement Disorders (revue)

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Effects of selective serotonergic ligands on posthypoxic audiogenic myoclonus

Identifieur interne : 005909 ( Main/Exploration ); précédent : 005908; suivant : 005910

Effects of selective serotonergic ligands on posthypoxic audiogenic myoclonus

Auteurs : Rae R. Matsumoto [États-Unis] ; Matthew J. Hussong [États-Unis] ; Truong [États-Unis]

Source :

RBID : ISTEX:A1CB08F7F73025563A23660028278804CE82EBCD

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English descriptors

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‐trifluoromethylphenyl) piperazine hydrochloride (TFMPP, 5‐HT1B/1C/2 agonist), (±)‐2,5‐dimethoxy‐4‐iodoamphetamine hydrobromide (DOI, 5‐HT2 agonist), and l‐(m‐chlorophenyl)‐biguanide hydrochloride (m‐CPBG, 5‐HT3 agonist). In contrast, the following drugs were ineffective: (±)‐8‐hydroxy‐dipropylaminottetralin hydrobromide (8‐OH‐DPAT, 5‐HT1A agonist), buspirone hydrochoride (5‐HT1A agonist), 7‐trifluoromethyl‐4(4‐methyl‐1‐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.

Url:
DOI: 10.1002/mds.870100514


Affiliations:


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<term>Animals</term>
<term>Anoxia (complications)</term>
<term>Behavior, Animal (drug effects)</term>
<term>Brain Stem (drug effects)</term>
<term>Brain Stem (physiopathology)</term>
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<term>Myoclonus (etiology)</term>
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<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‐trifluoromethylphenyl) piperazine hydrochloride (TFMPP, 5‐HT1B/1C/2 agonist), (±)‐2,5‐dimethoxy‐4‐iodoamphetamine hydrobromide (DOI, 5‐HT2 agonist), and l‐(m‐chlorophenyl)‐biguanide hydrochloride (m‐CPBG, 5‐HT3 agonist). In contrast, the following drugs were ineffective: (±)‐8‐hydroxy‐dipropylaminottetralin hydrobromide (8‐OH‐DPAT, 5‐HT1A agonist), buspirone hydrochoride (5‐HT1A agonist), 7‐trifluoromethyl‐4(4‐methyl‐1‐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>
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