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Series HG, Cowen PJ, Sharp T. 
“p-Chloroamphetamine (PCA), 3,4-methylenedioxy-methamphetamine (MDMA) and d-fenfluramine pretreatment attenuates d-fenfluramine-evoked release of 5-HT in vivo”. 
Psychopharmacology (Berl). 1994;116(4):508-14.
Previous work has suggested that repeated treatment with substituted amphetamines including PCA,MDMA and d-fenfluramine produces a persistent neur-odegeneration which is relatively selective for the fine serotoninergic terminals arising from the dorsal raphecol-nucleus. The aim of the present study was to investigate whether the acute releasing effect of d-fenfluramine might also be sensitive to lesions produced by PCA, MDMA and d-fenfiuramine itself. Basal and 5-HT release evoked by d-fenfluramine or 100 mM KCI was measured by microdialysis in frontal or parietal cortex of rats 2 weeks after they had been treated with a neurodegenerative regime of PCA, MDMA, d-fenfluramine, or vehicle. In frontal cortex of vehicle controls, d-fenfluramine (10 rog/kg IP) and KCI (100 mM via microdialysis probe)evoked an increase ill 5-HT of 1740% and 779% of basal, respectively. PCA pretreatment reduced d-fenfiuranfine-evoked 5-HT release by 90.9% while potassium-evoked release was reduced by only 66.8%. Sinlihu' results were obtained in parietal cortex. MDMA (20 mg/kg x 81 and d-fenfluramine (12.5 ing/kgx 8) pretreatment reduced d-fenfiuramine~evoked release of 5-HT in fi'ontal cortex by 45.2% and 72.0_,, respectively. Overall, the present data are consistent with tile hypothesis that tile acute release of 5-HT evoked by d-fenfiuramine occurs via those terminals destroyed by pretreatment with PCA, MDMA and d-glven one 40 rog/kg fenlluranlinc, while KCI evokes release from both PCA-sensitive and PCA-insensitivc terminals. Thc signilicance of these results for thc interpretation of ncuroendocrme data from d-fenfiuramine challcngc tests is discussed.
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