The objective of this application is to distinguish the neurochemical and behavioral effects of gestational-lactational exposure to atrazine. The following central hypothesis will be tested: Developmental exposure to atrazine will alter neurochemical parameters in the brain resulting in behavioral deficits that will persist into adulthood. The rationale for the proposed research is to understand the neurotoxicity induced by developmental exposure to atrazine in order to better protect the nervous system development of our children. We propose to test the following specific aims: 1) to determine the effects of gestational-lactational exposure to atrazine on neurotransmitter levels (yaminobutyric acid, norepinephrine, and dopamine) and neurochemical markers of development for the GABAergic, catecholaminergic, and cholinergic neurotransmitter systems. Working Hypothesis: Atrazine's action on the GABA receptors in the brain during development will induce inappropriate signals resulting in decreased neurotransmitter levels and delayed neurotransmitter system development as indicated by decreased neurochemical markers. 2) to determine the effects of gestational-lactational exposure Io atrazine on memory and learning in the Morris water maze and radial arm maze. Working Hypothesis: The alteration of the development of the neurotransmitter systems will be manifested as long term deficits in working and reference memory. Correlations between neurochemical alterations and behavioral deficits will help to identify the mechanism(s) responsible for behavioral deficits. This research will be innovative because it will determine if the frequently used herbicide atrazine has the potential to put our children at greater risk of neurotoxicity. The research is novel in that it will determine if environmentally relevant levels of exposure (based on the No Observed Adverse Effect Level or NOAEL) would be sufficient to result in transient or permanent effects on behavior including cognition. It is our expectation that by assessing neurochemical effects on several neurotransmitter systems and comparing those effects with behavioral outcomes, some of the critical mechanisms responsible for the neurodevelopmental effects of atrazine can be elucidated. The results will be significant because they will fill data gaps on the responses of young animals to a chemical that has a high volume of use but has only recently been demonstrated to be neuroactive.
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