Date of Award

8-2008

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Legacy Department

Environmental Toxicology

Advisor

Klaine, Stephen J

Committee Member

Lee , Cindy M

Committee Member

Little , Edward E

Committee Member

Roberts , Aaron P

Committee Member

Schwedler , Thomas

Abstract

Biochemical endpoints are useful when determining contaminant exposure in aquatic organisms. However, behaviors can also be impaired by environmental contaminants. Links between changes in brain biochemistry and behavior have been made, and understanding these relationships could increase the utility of these endpoints in ecological risk assessments. The overall goal of this research was to determine relationships between an ecologically relevant fish behavior and brain biochemistry. To accomplish this goal, I developed a behavioral bioassay that quantified the time it took exposed hybrid striped bass (Morone saxatilis x M. chrysops) to capture unexposed prey, fathead minnows (Pimephales promelas). Chemically targeted brain neurotransmitters were also monitored, and the relationship with behavior was determined. Six-day acute exposures to (1) a pesticide (diazinon) targeting acetylcholinesterase (AChE) and (2) a pharmaceutical (fluoxetine) targeting serotonin were conducted with a 6-day recovery periods. Brain biochemistry and behaviors were plotted against each other. Our results indicated that there was a threshold response between AChE activity and feeding behavior following diazinon exposure concentrations of 19.1 ± 0.7, 64.0 ± 2.0, and 101.9 ± 1.4 µg/l. By day 6, AChE activity was significantly inhibited in the low, medium, and high treatment groups by 66.3, 82.2, 86.4%, respectively. However, there were no signs of behavioral impairment in the lowest treatment group. During the 6-day recovery period, there were concentration- and duration-dependent changes in feeding behavior and AChE activity, in which time to capture prey decreased more rapidly than AChE activity increased. Following fluoxetine exposures (23.2 ± 6.6, 51.4 ± 10.9, and 100.9 ± 18.6 µg/l), a linear response between decreased serotonin activity and increased feeding behavior was observed. However, maximum serotonin depression in the low, medium, and high treatment groups occurred on day 9 (day 3 of the recovery period) with concentrations at 23.7, 28.0, and 49.1% of controls, respectively. Our results also indicated that during the recovery period, there was a concentration- and duration-dependent increase in serotonin activity accompanied by a decrease in time to capture prey.
A 27-day chronic exposure to fluoxetine was also conducted at lower exposure concentrations (0.08 ± 0.02, 0.87 ± 0.12, 9.44 ± 0.82 µg/l) than the acute exposure. It was concluded that although fluoxetine can cause impaired serotonin levels and feeding behavior, this was not observed at more environmentally relevant concentrations over the 27 days.

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