Neurotoxicity induced by prenatal exposure to MPTP on the monoaminergic and peptidergic systems of the marmoset brain

• Published in: Experimental neurology 1995, Vol.131 (1), p.108-113
• Main Authors: Pérez-Otaño, Isabel, Luquin, M.Rosario, Oset, Carmen, Herrero, M.Trinidad, Kupsch, Andreas, Oertel, Wolfgang, Obeso, JoséAngel, Del Río, Joaquín
• Format: Article
• Language: English
• Subjects: 3,4-Dihydroxyphenylacetic Acid - metabolism; Animals; Biological and medical sciences; Brain - drug effects; Brain - metabolism; Callithrix; Dopamine - metabolism; Embryology: invertebrates and vertebrates. Teratology; Enkephalin, Methionine - metabolism; Female; Fetus - drug effects; Fundamental and applied biological sciences. Psychology; Homovanillic Acid - metabolism; Hydroxyindoleacetic Acid - metabolism; MPTP Poisoning; Pregnancy; Prenatal Exposure Delayed Effects; Teratology. Teratogens
• ISSN: 0014-4886; 1090-2430
• DOI: 10.1016/0014-4886(95)90012-8

The neurotoxicity induced by incidental prenatal exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was studied in three marmosets. The baby marmosets exposed in utero to MPTP looked normal in the first few weeks of life but around 8 to 10 weeks of life they started to behave abnormally and were sacrificed when they were 20 weeks old. A marked reduction in DA levels was found in the baby marmosets prenatally exposed to MPTP as compared to the corresponding age-matched controls and this was highly significant in the caudate nucleus, putamen, and nucleus accumbens. Serotonin content was normal in the caudate and putamen and was only significantly reduced in the nucleus accumbens, hypothalamus, and cingulate cortex. Met-enkephalin levels were reduced in the caudate nucleus, putamen, and globus pallidus. Substance P content tended to be lower in all regions examined; however, the decrease was only statistically significant in the substantia nigra. These results indicate that prenatal exposure to MPTP induces a marked and long-lasting alteration in monoaminergic and peptidergic systems of the primate brain. This observation may provide a new insight into the role of toxins in the etiology of Parkinson's disease.