We recently demonstrated that perinatal exposure
to the glutamate-related herbicide, glufosinate ammonium,
has deleterious effects on neural stem cell (NSC) homeostasis
within the sub-ventricular zone (SVZ), probably leading to
ASD-like symptoms in offspring later in life. In the present
study, we aimed to investigate whether perinatal exposure to
another glutamate-related toxicant, the cyanobacterial amino
acid β-N-methylamino- L -alanine (BMAA), might also trigger
neurodevelopmental disturbances. With this aim, female mice
were intranasally exposed to low doses of BMAA, 50 mg kg −1
three times a week from embryonic days 7–10 to postnatal day
21. Behavioral analyses were performed during the offspring’s
early life and during adulthood. Developmental analyses

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• Perinatal Exposure to the Cyanotoxin β-N-Méthylamino- L -Alanine (BMAA) Results in Long-Lasting Behavioral Changes in Offspring—Potential Involvement of DNA Damage and Oxidative Stress