The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Methylenedioxyamphetamine (MDA) and methylenedioxymethamphetamine (MDMA) cause selective ablation of serotonergic axon terminals in forebrain: immunocytochemical evidence for neurotoxicity
Open accessAbstract
The psychotropic amphetamine derivatives 3,4-methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA) have been used for recreational and therapeutic purposes in man. In rats, these drugs cause large reductions in brain levels of serotonin (5-HT). This study employs immunocytochemistry to characterize the neurotoxic effects of these compounds upon monoaminergic neurons in the rat brain. Two weeks after systemic administration of MDA or MDMA (20 mg/kg, s.c., twice daily for 4 d), there is profound loss of serotonergic (5-HT) axons throughout the forebrain; catecholamine axons are completely spared. Regional differences in drug toxicity are exemplified by partial sparing of 5-HT axons in hippocampus, lateral hypothalamus, basal forebrain, and in some areas of neocortex. The terminals of 5-HT axons are selectively ablated, while axons of passage and raphe cell bodies are spared. Thickened preterminal fibers exhibit increased staining due to damming-up of neurotransmitter and other axonal constituents. Fine 5- HT axon terminals are extremely vulnerable to these drugs, whereas terminal-like axons with large varicosities survive, raising the possibility that some 5-HT axons may be resistant to the neurotoxic effects. At short survivals, visualization of greatly swollen, fragmented 5-HT axons provides anatomic evidence for degeneration of 5- HT projections. The results establish that MDA and MDMA produce structural damage to 5-HT axon terminals followed by lasting denervation of the forebrain. Both drugs have similar effects, but MDA produces a greater reduction of 5-HT axons than does MDMA at the same dosage. The selective degeneration of 5-HT axons indicates that these drugs may serve as experimental tools to analyze the organization and function of 5-HT projections. Caution should be exercised until further studies determine whether these compounds may be hazardous in man.
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Cites
Evidence for 5-HT2 involvement in the mechanism of action of hallucinogenic agents
Glennon, R. A., Titeler, M., & McKenney, J. D. (1984) · Life Sciences · doi:10.1016/0024-3205(84)90436-3 · Cited by 631
Nichols, D. E. (1986) · Journal of Psychoactive Drugs · doi:10.1080/02791072.1986.10472362 · Cited by 563
Gerfen, C. R. (1985) · Journal of Comparative Neurology · doi:10.1002/cne.902360404 · Cited by 559
Steinbusch, H. W. M., Verhofstad, A. A. J., & Joosten, H. W. J. (1978) · Neuroscience · doi:10.1016/0306-4522(78)90033-7 · Cited by 540
Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine.
Schmidt, C. J. (1987) · The Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(25)22673-8 · Cited by 529
Dopamine nerve terminal degeneration produced by high doses of methylamphetamine in the rat brain
Ricaurte, G. A., Guillery, R. W., Seiden, L. S., Schuster, C. R., & Moore, R. Y. (1982) · Brain Research · doi:10.1016/0006-8993(82)90198-6 · Cited by 479
The serotonin innervation of the cerebral cortex in the rat—an immunohistochemical analysis
Lidov, H. G. W., Grzanna, R., & Molliver, M. E. (1980) · Neuroscience · doi:10.1016/0306-4522(80)90099-8 · Cited by 417
Self-citationSubjective Reports of the Effects of MDMA in a Clinical Setting
Greer, G., & Tolbert, R. (1986) · Journal of Psychoactive Drugs · doi:10.1080/02791072.1986.10472364 · Cited by 413
Kosofsky, B. E., & Molliver, M. E. (1987) · Synapse · doi:10.1002/syn.890010204 · Cited by 412
Self-citationLysergic acid diethylamide: Sensitive neuronal units in the midbrain raphe
Aghajanian, G. K., Foote, W. E., & Sheard, M. H. (1968) · Science · doi:10.1126/science.161.3842.706 · Cited by 404
Cited by
Role of Quinones in Toxicology
Bolton, J. L., Trush, M. A., Penning, T. M., Dryhurst, G., & Monks, T. J. (2000) · Chemical Research in Toxicology · doi:10.1021/tx9902082 · Cited by 1,703
The Pharmacology and Clinical Pharmacology of 3,4-Methylenedioxymethamphetamine (MDMA, “Ecstasy”)
Green, A. R., Mechan, A. O., Elliott, J. M., O’Shea, E., & Colado, M. I. (2003) · Pharmacological Reviews · doi:10.1124/pr.55.3.3 · Cited by 1,272
A PHA-L analysis of ascending projections of the dorsal raphe nucleus in the rat
Vertes, R. P. (1991) · Journal of Comparative Neurology · doi:10.1002/cne.903130409 · Cited by 842
The human raphe nuclei and the serotonergic system
Hornung, J.-P. (2003) · Journal of Chemical Neuroanatomy · doi:10.1016/j.jchemneu.2003.10.002 · Cited by 742
Toxicity and deaths from 3,4-methylenedioxymethamphetamine ("ecstasy")
Henry, J. A., Jeffreys, K. J., & Dawling, S. (1992) · The Lancet · doi:10.1016/0140-6736(92)91469-o · Cited by 729
Metadata
- Authors
- O'Hearn, E., Battaglia, G., De Souza, E., Kuhar, M., & Molliver, M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1988-08-01
- Volume
- 8
- Issue
- 8
- Pages
- 2788-2803
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1693348571
- Cited by
- 542
- References
- 36
- FWCI
- 9.71
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- O'Hearn, E., Battaglia, G., De Souza, E., Kuhar, M., & Molliver, M. (1988). Methylenedioxyamphetamine (MDA) and methylenedioxymethamphetamine (MDMA) cause selective ablation of serotonergic axon terminals in forebrain: immunocytochemical evidence for neurotoxicity. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.08-08-02788.1988
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