Impaired brain development in the rat following prenatal exposure to methylazoxymethanol acetate at gestational day 17 and neurotrophin distribution.
Several neuropsychiatric disorders, including schizophrenia, are the consequence of a disrupted development of the CNS. Accordingly, intrauterine exposure to toxins may increase the risk for psychopathology. We investigated whether prenatal exposure of rats to the neurotoxin methylazoxymethanol acetate led to long-term changes in cerebral neurotrophin levels. We measured the brain levels of nerve growth factor and brain derived neurotrophic factor in young adult and adult rats. Decreased nerve growth factor or brain derived neurotrophic factor were found in the parietal cortex accompanied by altered neurotrophin content in the hippocampus and entorhinal cortex. The present study is the first to show long-lasting effects of a single prenatal exposure to a neurotoxin on adult levels of neurotrophins in brain regions implicated in neuropsychiatric disorders.
Fiore
Marco
M
Department of Biological Psychiatry, University of Groningen, Hanzeplein 1, 9713 EZ Groningen, The Netherlands. mfiore@in.rm.cnr.it
Grace
Anthony A
AA
Korf
Jakob
J
Stampachiacchiere
Barbara
B
Aloe
Luigi
L
D000367:Age Factors; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism*; D005260:Female; D005865:Gestational Age; D008297:Male; D008746:Methylazoxymethanol Acetate / Q000633:toxicity*; D009414:Nerve Growth Factors / Q000378:metabolism*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011916:Rats, Inbred F344; D013997:Time Factors
D009414:Nerve Growth Factors; D008746:Methylazoxymethanol Acetate