Regular Article
Neurochemical Effects of Consumption of Great Lakes Salmon by Rats

https://doi.org/10.1006/rtph.1997.1192Get rights and content

Abstract

This study, part of a larger project to determine the health consequences of both perinatal and adult exposure to contaminated salmon from the Great Lakes, determined the neurochemical effects of exposure of rats to chow adulterated with lyophilized salmon fillets. Concentrations of biogenic amines, their metabolites, and choline acetyltransferase (ChAT) were determined in the frontal cortex (FC), nucleus accumbens, caudate nucleus (CN), hippocampus (HC), and substantia nigra (SN) of adult rats who had been exposed, both perinatally and as adults, to standard rat chow adulterated with either 5 or 20% (w/w) lyophilized fillets from either Lake Huron (LH) or Lake Ontario (LO) salmon. Dopamine (DA) concentrations in the FC were significantly decreased following exposure to both 20% fish diets. CN DA concentrations were significantly reduced in rats exposed to all diets, while SN DA was decreased only in the LO20-fed animals. SN norepinephrine concentrations were reduced in all groups except for the LO5-fed rats. 3,4-Dihydroxyphenylacetic acid (DOPAC) concentrations in the FC were significantly increased in the LH20 and LO5 groups, while CN DOPAC concentrations were reduced in LH20, LO5, and LO20 animals. 5-Hydroxyindoleacetic acid concentrations were reduced in the FC and CN of all animals exposed to diets adulterated with Great Lakes salmon. ChAT concentrations were unaffected in rats exposed to any of the adulterated diets. The significant reductions in DA, particularly in the FC and CN, suggest that either fish-borne contaminants or consumption of fish, per se, may affect behaviors that require inhibition of normal responding. We conclude that consumption of contaminated fish from the Great Lakes may result in sufficient reductions in biogenic amine function to result in significant deficits in important behavioral functions in the rat and, by inference, in the perinatally exposed human.

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  • Cited by (0)

    H. M. BoltB. HellmanL. Dencker

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