Biochemical correlates for behavioral deficits induced by secalonic acid D in developing mice.

Humoral signals (neurotransmitters and hormones) control cell division, migration, and differentiation processes which define the organization of brain pathways. Alterations in maternal, fetal, and neonatal biochemistry during critical periods of neurogenesis may irreparably alter the circuitry and, thus, postnatal behavior of young animals. Secalonic acid D (SAD), an ergochrome mycotoxin, causes behavioral and neurochemical deficits in developing mice following prenatal (transplacental) or early postnatal (transmammary) exposure. SAD-induced functional abnormalities include delays in reflex behaviors, integrated neuromuscular activity and strength, stress adaptation responses, and sensory discrimination. These behavioral changes are associated with reductions of brain monoamine neurotransmitter levels in both fetuses and neonates. SAD also alters concentrations of maternal plasma corticosteroids and fetal cyclic nucleotides during midgestation. SAD thus modulates several chemicals in pregnant mice and their fetuses which contribute to brain development, suggesting that this mycotoxin may pose a neuroteratogenic hazard to other immature mammals, including human infants.