The effect of (R)-HA966 or ACEA 1021 on dexfenfluramine or (S)-MDMA-induced changes in temperature, activity, and neurotoxicity

The glycine site-specific N-methyl-D-aspartate (NMDA) antagonist 5-nitro-6, 7-dichloro-2,3-quinoxalinedione (ACEA 1021, 4 x 30 mg/ kg, ip) given 30 min before dexfenfluramine (4 x 15 mg/kg, ip, every 2 h) was unable to prevent dexfenfluramine-induced depletion of 5-hydroxytryptamine (5-HT), 5-hydroxy indoleacetic acid (5-HIAA) content, and 5-HT transporter (5-HTT) density. a nother glycine site-specific NMDA antagonist, R(+)-3-aminohydroxypyrrolidin -2-one [(R)-HA 966] (2 x 30 mg/kg, ip), given 30 min before dexfenfluramine (2 x 10 mg/kg, ip, 2 hourly) was also unable to prevent regional depletion of 5-HT, 5-HIAA, and 5-HTT density. However, ACEA 1021 (4 x 30 mg/kg, ip) given 30 min before (S)-3,4-methylenedioxymethamphetamine (MDMA, 4 x 10 mg/ kg, 2 hourly, ip) attenuated the regional depletion of dopamine (DA), dihyd roxyphenylacetic acid (DOPAC), 5-HT, 5-HIAA content, and 5-HTT density. ACE A 1021 combined with (S)-MDMA also prevented (S)-MDMA-induced hyperthermia without causing hypothermia or preventing an (S)-MDMA- induced increase in locomotor activity. (C) 2001 Elsevier Science Inc. All rights reserved.