Effects of a single exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on macro- and microstructures of feeding and drinking in two differently TCDD-sensitive rat strains.

In rats, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes anorexia that may lead to fatal wasting but has hitherto been poorly characterized. Therefore, we studied in-depth feeding and drinking behaviors of TCDD-sensitive L–E rats for 5 (100μg/kg; lethal dose) or 10 (10μg/kg; sublethal) days and of TCDD-resistant H/W rats for 14 (100 or 1000μg/kg; both sublethal) days postexposure to TCDD. The 1000-fold higher resistance of H/W rats to acute lethality of TCDD results from a mutation in their AH receptor (AHR). We split days into four (morning, daytime, evening, and night) or two (light/dark) circadian periods and took the repeated nature of the data into account. In L–E rats at 100μg/kg, the feed intake dropped precipitously, due to reduced meal sizes. In H/W rats, the hypophagia remained moderate and stemmed from a reduced meal frequency. While the suppression in L–E rats peaked during the morning (at 100μg/kg), the main effects in H/W rats were seen during the constant light or dark phases. Furthermore, chronologic data analysis revealed alterations in consecutive feeding and drinking patterns. Thus, striking differences were found between these strains in the timing and structure of consummatory behaviors, suggesting involvement of the AHR in these behaviors.