Male Sprague-Dawley rats underwent cardiac arrest and resuscitation, s
ubsequently exhibiting posthypoxic myoclonus. The audiogenic posthypox
ic myoclonus in these animals could be attenuated with the following d
rugs: 5-hydroxytryptophan (5-HTP, serotonin [5-HT] precursor), N-(3-tr
ifluoromethylphenyl)piperazine hydrochloride (TFMPP, 5-HT1B/1C/2 agoni
st), (+/-)-2,5-dimethoxy-4-iodoamphetamine hydrobromide (DOI, 5-HT2 ag
onist), and 1-(m-chlorophenyl)-biguanide hydrochloride (m-CPBG, 5-HT3
agonist). In contrast, the following drugs were ineffective: (+/-)-8-h
ydroxy-dipropylaminotetralin hydrobromide (8-OH-DPAT, 5-HT1A agonist),
buspirone hydrochloride (5-HT1A agonist), 4(4-methyl-1-piperazinyl)py
rrolo[1,2-a]quinoxaline maleate (CGS 12066B, 5-HT1B agonist), ketanser
in tartrate (5-HT2 antagonist), methysergide maleate (5-HT2 antagonist
), fluoxetine (5-HT uptake blocker), and saline (vehicle). The data su
ggest that enhancement of serotonergic activity, particularly through
5-HT2 and 5-HT3 receptors, have therapeutic potential for the treatmen
t of posthypoxic myoclonus.