Correlation between 5-HT content and uptake site density following (S)-MDMA and dexfenfluramine-induced depletion, and with neuroprotection by the glycine site-specific NMDA antagonist ACEA 1021
by
Russell BR, Laverty R
Department of Pharmacology,
School of Medical Sciences,
University of Otago,
Dunedin, New Zealand.
Ann N Y Acad Sci 2000; 914:208-14

ABSTRACT

3,4-Methylenedioxymethamphetamine (MDMA) and fenfluramine are amphetamine analogues that both cause long-term depletion of serotonin (5-HT) and 5-HT uptake sites in brain tissue. Depletion caused by these amphetamines is commonly measured by labeling 5-HT uptake sites using 3H-paroxetine combined with autoradiography or, alternatively measuring the concentration of 5-HT in tissue using high-performance liquid chromatography (HPLC). A close correlation between the 5-HT concentration measured in micropunch samples and the density of 3H-paroxetine-labeled 5-HT uptake sites measured in corresponding 20 micron coronal slices was determined (R2 = 0.92). These methods combined demonstrated that the glycine-site specific NMDA antagonist ACEA 1021 (4 x 30 mg/kg, i.p., 2 hourly) given 30 minutes before (S)-MDMA (4 x 10 mg/kg, i.p., 2 hourly) was able to prevent the depletion of both 5-HT content and uptake site density but unable to prevent the depletion of 5-HT content and uptake site density caused dexfenfluramine (4 x 15 mg/kg, i.p., 2 hourly).

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