Brief exposure to copper induces apoptosis and alters mediators of olfactory signal transduction in coho salmon

Abstract

Pacific salmon are particularly susceptible to copper (Cu)-induced olfactory injuries that can ultimately inhibit neurobehaviors critical to survival. However, the molecular mechanisms underlying Cu-mediated olfactory impairment remain poorly understood. In the present study, we conducted a short-term Cu exposure at levels relevant to urban runoff (5, 25 and 50 ppb) , and investigated the roles of impaired olfactory signal transduction and induced apoptosis as underlying mechanisms of olfactory injury. Increased cell death in the olfactory epithelium was evident in coho receiving 4h exposures to 25 and 50 ppb Cu. Expression of olfactory marker protein (omp), a marker of mature olfactory sensory neurons, also decreased at 50 ppb Cu. Immunohistochemical analysis of coho olfactory epithelium demonstrated a loss of type 3 adenylate cyclase (ACIII) in the apical olfactory epithelium cilia at all levels of Cu exposure, suggesting an inhibitory effect of Cu in olfactory signaling. Accompanying the loss of ACIII in Cu-exposed coho were reduced intracellular cyclic guanosine monophosphate (cGMP) levels in the olfactory rosettes. Collectively, these results support a linkage among the initial steps of olfactory signaling in Cu-induced salmon olfactory injury, and suggesting that monitoring olfactory cGMP levels may aid in the assessment of salmon olfactory injury.

Keywords: ACIII; Apoptosis; CNG channel; Coho salmon; Copper; EOG; ORN; OST; Olfactory injury; Olfactory signal transduction; cAMP; cGMP; cyclic adenosine monophosphate; cyclic guanosine monophosphate; cyclic nucleotide-gated channel; electroolfactorygram; olfactory marker protein; olfactory receptor neuron; olfactory signal transduction; omp; type III adenylate cyclase.