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Miller DB, O'Callaghan JP. 
“The interactions of MK-801 with the amphetamine analogues D-methamphetamine (D-METH), 3,4-methylenedioxymethamphetamine (D-MDMA) or D-fenfluramine (D-FEN): neural damage and neural protection”. 
Ann N Y Acad Sci. 1993;679:321-4.
Recently there has been intense speculation concerning the neurotoxicity of certain of the amphetamine analogues, including MDMA and FEN (Ricaurte et al.). Although depletion of a particular neurotransmitter may signify damage of that brain area (e.g., Sonsolla et al.) it is not always synonymous with CNS injury (see O'Callaghan et al.). Many investigators utilize loss of neurotransmitter level and/ or enzyme activity in a particular brain area as evidence for damage or degeneration in that area. Both MDMA and FEN can produce long-lasting neurotransmitter depletions in rodents, hence the conclusion they induce injury. Gliosis, however. is typically associated with the CNS injury induced by a variety of means (see O'Callaghan this volume for further discussion). Because injury to the mammalian nervous system provokes hypertrophy of astrocytes at the sites of damage the enhanced expression of the astrocyte-localized protein, glial fibrillaryacidic protein (GFAP) can be used to define and explore chemically induced neurotoxicity (e.g., O'Callaghan et al.). Thus, in this work we used the level of G FAP in specific brain areas to determine the comparative neurotoxicity of the D isomers of METH, MDMA and FEN in the cortex, striatum and hippocampus of mice.
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