Appetite-suppressing effects of ammonia exposure in rainbow trout associated with regional and temporal activation of brain monoaminergic and CRF systems.
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.
Ortega
Van A
VA
Department of Integrative Biology, University of Guelph, Guelph, ON, Canada, N1G 2W1.
Renner
Kenneth J
KJ
Bernier
Nicholas J
NJ
D000641:Ammonia / Q000633:toxicity*; D000704:Analysis of Variance; D000818:Animals; D001066:Appetite / Q000187:drug effects*; D015306:Biogenic Monoamines / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism*; D017931:DNA Primers; D004298:Dopamine / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004435:Eating; D006854:Hydrocortisone / Q000097:blood; D017686:Oncorhynchus mykiss / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012701:Serotonin / Q000378:metabolism; D013997:Time Factors; D014579:Urotensins / Q000235:genetics / Q000378:metabolism
D015306:Biogenic Monoamines; D017931:DNA Primers; D012333:RNA, Messenger; D014579:Urotensins; D012701:Serotonin; D000641:Ammonia; D003346:Corticotropin-Releasing Hormone; C029676:urotensin I; D004298:Dopamine; D006854:Hydrocortisone