Unraveling the biochemical mechanisms of neurobehavioral injury from environmental chemical exposures in fish



Dr. Evan P. Gallagher; University of Washington

April 6 at 12:20pm in the Fralin Auditorium, Fralin Hall room 102

Hosted by Dr. J. Gohlke



Fish rely on olfaction to maintain essential neurobehaviors such as predator detection and avoidance, prey selection, social behavior, imprinting, and habitat location. Salmonids, in particular, have a well developed sensory system that relies on olfactory detection of chemical cues in the environment for these behaviors as well as for outmigration and homing to natal streams. However, exposure to environmental neurotoxicants, including certain trace metals and pesticides, can disrupt these behaviors leading to a loss of survivorship. Ten years of study in our laboratory using two species of fish (coho salmon and zebrafish) have shed light on the molecular mechanisms, adaptive responses, and physiological outcomes associated with chemical inhibition of olfactory function. Specifically, environmental neurotoxicants can cause early changes in the redox status of the olfactory system associated with oxidative stress. By contrast, the fish olfactory system has a robust NrF2-mediated antioxidant protective pathway that can mobilize protective gene responses to respond to adverse changes in oxidative stress. Analysis of salmon promoter flanking sequences for several genes important in mitigating metal injury to olfactory sensory neurons have informed our Nrf2 studies and have facilitated biomarker development. Other early events in olfactory injury include modulation of G-protein coupled receptor signaling, followed by alteration of olfactory sensory neuron populations and induction of cellular apoptosis in the olfactory rosettes.  Whereas rapid recovery from copper-mediated olfactory injury can occur in salmon and zebrafish,  exposure to cadmium can cause long-lasting deficits in neurobehavior. Collectively, our studies as well as those from other laboratories have provided linkages among early initiating events, cellular and physiological responses, and whole animal phenotypic changes associated with loss of survivorship that provide the conceptual basis for olfactory-mediated neurobehavioral injury to as a relevant adverse outcome pathway for regulatory decisions that support protection of aquatic species. Supported by NIEHS Superfund P42-04696.

Keywords: Coho salmon, zebrafish, Nrf2, adverse outcome pathway, olfaction, metals pesticides

Wang et al. 2016.pdf Olfactory Transcriptional Analysis of Salmon Exposed to Mixtures of Chlorpyrifos and Malathion Reveal Novel Molecular Pathways of Neurobehavioral Injury
Williams et al. 2016.pdf Cadmium Exposure Differentially Alters Odorant-Driven Behaviors and Expression of Olfactory Receptors in Juvenile Coho Salmon (Oncorhynchus kisutch)

This seminar will NOT be livestreamed or recorded.