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Advisor(s)
Abstract(s)
Pesticide exposure during brain development could represent an important risk factor for the onset of
neurodegenerative diseases. Previous studies investigated the effect of permethrin (PERM) administered
at 34 mg/kg, a dose close to the no observable adverse effect level (NOAEL) from post natal day (PND)
6 to PND 21 in rats. Despite the PERM dose did not elicited overt signs of toxicity (i.e. normal body
weight gain curve), it was able to induce striatal neurodegeneration (dopamine and Nurr1 reduction, and
lipid peroxidation increase). The present study was designed to characterize the cognitive deficits in the
current animal model. When during late adulthood PERM treated rats were tested for spatial working
memory performances in a T-maze-rewarded alternation task they took longer to choose for the correct
arm in comparison to age matched controls. No differences between groups were found in anxiety-like
state, locomotor activity, feeding behavior and spatial orientation task. Our findings showing a selective
effect of PERM treatment on the T-maze task point to an involvement of frontal cortico-striatal circuitry
rather than to a role for the hippocampus. The predominant disturbances concern the dopamine (DA)
depletion in the striatum and, the serotonin (5-HT) and noradrenaline (NE) unbalance together with a
hypometabolic state in the medial prefrontal cortex area. In the hippocampus, an increase of NE and a
decrease of DA were observed in PERM treated rats as compared to controls. The concentration of the
most representative marker for pyrethroid exposure (3-phenoxybenzoic acid) measured in the urine of
rodents 12 h after the last treatment was 41.50 µ/L and it was completely eliminated after 96 h.
Description
Keywords
Rat Permethrin Early life exposure 3-Phenoxybenzoic acid Spatial working memory T-maze Monoamines