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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
Author(s) -
RUSSELL B. R.,
LAVERTY R.
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb05197.x
Subject(s) - chemistry , mdma , dexfenfluramine , serotonin , antagonist , fenfluramine , 5 ht receptor , paroxetine , pharmacology , endocrinology , biochemistry , receptor , biology
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 3 H‐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 3 H‐paroxetine‐labeled 5‐HT uptake sites measured in corresponding 20 μm coronal slices was determined (R 2 = 0.92). These methods combined demonstrated that the glycine‐site specific NMDA antagonist ACEA 1021 (4 × 30 mg/kg, i.p., 2 hourly) given 30 minutes before ( S )‐MDMA (4 × 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 × 15 mg/kg, i.p., 2 hourly).