Matsumoto R R, Hussong M J, Truong D D
Parkinson and Movement Disorders Program, Department of Neurology, University of California-Irvine 92717, USA.
Mov Disord. 1995 Sep;10(5):615-21. doi: 10.1002/mds.870100514.
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.
