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Keywords:

  • Myoclonus;
  • Hypoxia;
  • Ischemia;
  • Serotonin;
  • (±)-2,5-Dimethoxy-4-iodoamphetamine hydrobromide;
  • l-(m-Chlorophenyl)-biguanide hydrochloride

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.