Neurotoxic indoleamines and monoamine neurons.
In 1968 Thoenen & Tranzer (1) discovered that the long-lasting depletion of NA in sympathetically innervated organs by 6-OH-DA is due to degeneration of NA terminals. This provided the basis for the development of a new concept in neurobiological research: the method of selective chemical neurodegeneration. The successful application of this method to produce degeneration of DA and NA neurons in brain (2,3) stimulated a search for compounds with comparable effects on central 5-HT neurons. In studies with a restricted number of 5-HT analogs, we were able to show that certain dihydroxylated tryptamines caused toxic damage to serotonin terminals. The recent findings by Björklund, Baumgarten & Rensch (4) and Gerson & Baldessarini (5) that DMI treatment prior to intraventricular 5,7-DHT injection prevents the damaging effect of the latter drug on NA but not on 5-HT neurons indicate that powerful and probably rather selective destruction of central indoleamine-containing axons and terminals can be achieved.
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D001665:Binding Sites; D001679:Biogenic Amines / Q000096:biosynthesis / Q000378:metabolism / Q000502:physiology*; D002490:Central Nervous System / Q000187:drug effects; D004702:Endocrine Glands / Q000187:drug effects; D005260:Female; D007211:Indoles / Q000633:toxicity*; D008297:Male; D009416:Nerve Regeneration; D009474:Neurons / Q000502:physiology*; D010525:Peripheral Nerves / Q000187:drug effects; D051381:Rats
D001679:Biogenic Amines; D007211:Indoles