Abstract
To assess whether the brain's monoaminergic and/or corticotropin-releasing factor (CRF) systems may be involved in mediating the appetite-suppressing effects of high environmental ammonia levels, we exposed rainbow trout to one of four NH4Cl treatments (0, 500, 750, 1000 micromol l(-1)) for 24 or 96 h and monitored changes in food intake, brain serotonin (5-HT) and dopamine (DA) activity, CRF and urotensin I (UI) mRNA levels, and plasma cortisol levels. Food intake decreased in a dose-dependent manner after 24 h of ammonia exposure and partially recovered in all groups after 96 h. Ammonia also elicited dose-dependent increases in serotonergic activity in the hypothalamus (HYP), telencephalon (TEL) and posterior brain (PB). Whereas the increase in serotonergic activity was timed with the 24 h food intake inhibition, TEL and PB serotonergic activity increased after 96 h. In the PB, exogenous ammonia also elicited dose-dependent increases in dopaminergic activity after both 24 and 96 h of exposure. Transient increases in TEL CRF and UI mRNA levels, HYP UI mRNA levels, and plasma cortisol concentrations were evidence that the hypothalamic-pituitary-interrenal (HPI) stress axis was primarily stimulated in the first 24 h of ammonia exposure when food intake was depressed. Overall, the transient nature of the appetite suppression during chronic ammonia exposure, and the time-dependent changes in brain monoaminergic and CRF systems, implicate 5-HT, DA, CRF and UI as potential mediators of the appetite-suppressing effects of ammonia. Among these anorexigenic signals, our results specifically identify hypothalamic 5-HT as a potentially key neurobiological substrate for the regulation of food intake during exposure to high external ammonia concentrations.
Highlights
Most fish, including rainbow trout Oncorhynchus mykiss, excrete the majority of their metabolic nitrogenous waste as ammonia through the gills (Wright, 1995; Kajimura et al, 2004)
MRNA levels, HYP urotensin I (UI) mRNA levels, and plasma cortisol concentrations were evidence that the hypothalamic–pituitary–interrenal (HPI) stress axis was primarily stimulated in the first 24·h of ammonia exposure when food intake was depressed
While fish have evolved several strategies to cope with ammonia toxicity (Randall and Tsui, 2002), exposure to high ammonia levels causes a variety of negative physiological effects including a reduction in growth and food intake (e.g. Alderson, 1979; Lang et al, 1987; Beamish and Tandler, 1990; Atwood et al, 2000; Wicks and Randall, 2002a)
Summary
Most fish, including rainbow trout Oncorhynchus mykiss, excrete the majority of their metabolic nitrogenous waste as ammonia through the gills (Wright, 1995; Kajimura et al, 2004). In these animals, nitrogen excretion is an essential process that counteracts the relative toxicity of ammonia accumulation and under low exogenous ammonia conditions it is readily achieved through passive diffusion (Wilkie, 2002). While fish have evolved several strategies to cope with ammonia toxicity (Randall and Tsui, 2002), exposure to high ammonia levels causes a variety of negative physiological effects including a reduction in growth and food intake In several species, including rainbow trout, there is an inverse relationship within dominance-based hierarchies between brain serotonergic activity and food intake where low-feeding fish have higher serotonergic activity
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