Fetal domoic acid exposure affects lateral amygdala neurons, diminishes social investigation and alters sensory-motor gating
•In utero DA exposure diminishes social investigation and alters sensorimotor gating.•This is more pronounced in males than females.•This is associated with alterations in the parvalbumin-positive subtype of GABAergic neurons. Domoic acid (DA) is an algal neurotoxin that accumulates in marine fish a...
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Veröffentlicht in: | Neurotoxicology (Park Forest South) 2016-03, Vol.53, p.132-140 |
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Sprache: | eng |
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Zusammenfassung: | •In utero DA exposure diminishes social investigation and alters sensorimotor gating.•This is more pronounced in males than females.•This is associated with alterations in the parvalbumin-positive subtype of GABAergic neurons.
Domoic acid (DA) is an algal neurotoxin that accumulates in marine fish and shellfish. DA can move across the placenta and concentrate in amniotic fluid, which can be swallowed during late gestation. DA also transfers to infants via milk. Preclinical studies to determine effects of developmental DA expose have primarily involved DA exposure during the postnatal period and little is known about late CNS effects following prenatal DA. In the present study, we tested the hypothesis that prenatal exposure of FVB mice to low levels of DA would result in diminished social interaction and sensory motor gating associated with alterations in parvalbumin immunoreactivity in relevant brain regions undergoing development during and following DA exposure. In addition to parvalbumin, we stained with NeuN for a neuronal specific nuclear protein to determine if neuronal loss followed prenatal DA exposure. A single moderate dose of DA administered during gestation produces diminishes social investigation and alters sensorimotor gating, behavioral effects more pronounced in males than females. These behavioral changes were associated with discrete alterations in the parvalbumin-positive subtype of GABAergic neurons in the dentate gyrus and lateral amygdala. |
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ISSN: | 0161-813X 1872-9711 |
DOI: | 10.1016/j.neuro.2016.01.007 |