The social environment alters neural responses to a lipopolysaccharide challenge.

Sick animals display drastic changes in their behavioral patterns, including decreased activity, decreased food and water intake, and decreased interest in social interactions. These behaviors, collectively called "sickness behaviors", can be socially modulated. For example, when provided with mating opportunities, males of several species show reduced sickness behaviors. While the behavior is known to change, how the social environment affects neural molecular responses to sickness is not known. Here, we used a species, the zebra finch, Taeniopygia guttata, where males have been shown to decrease sickness behaviors when presented with novel females. Using this paradigm, we obtained samples from three brain regions (the hypothalamus, the bed nucleus of the stria terminalis, and the nucleus taeniae) from lipopolysaccharide (LPS) or control treated males housed under four different social environments. Manipulation of the social environment rapidly changed the strength and co-expression patterns of the neural molecular responses to the immune challenge in all brain regions tested, therefore suggesting that the social environment plays a significant role in determining the neural responses to an infection. In particular, brains of males paired with a novel female showed muted immune responses to LPS, as well as altered synaptic signaling. Neural metabolic activity in response to the LPS challenge was also affected by the social environment. Our results provide new insights into the effects of the social environment on brain responses to an infection, thereby improving our understanding of how the social environment can affect health.

Epigenetic regulation of gonadal and brain aromatase expression in a cichlid fish with environmental sex determination.

A fit animal must develop testes or ovaries, with brain and physiology to match. In species with alternative male morphs this coordination of development across tissues operates within sexes as well as between. For Pelvicachromis pulcher, an African cichlid in which early pH exposure influences both sex and alternative male morph, we sequence both copies of aromatase (cyp19a1), a key gene for sex determination. We analyze gene expression and epigenetic state, comparing gonad and brain tissue from females, alternative male morphs, and fry. Relative to brain, we find elevated expression of the A-copy in the ovaries but not testes. Methylation analysis suggests strong epigenetic regulation, with one region specifying sex and another specifying tissue. We find elevated brain expression of the B-copy with no sex or male morph differences. B-copy methylation follows that of the A-copy rather than corresponding to B-copy expression. In 30-day old fry, we see elevated B-copy expression in the head, but we do not see the expected elevated A-copy expression in the trunk that would reflect ovarian development. Interestingly, the A-copy epialleles that distinguish ovaries from testes are among the most explanatory patterns for variation among fry, suggesting epigenetic marking of sex prior to differentiation and thus laying the groundwork for mechanistic studies of epigenetic regulation of sex and morph differentiation.

The intestinal environment as an evolutionary adaptation to mouthbrooding in the Astatotilapia burtoni cichlid.

Many of the various parental care strategies displayed by animals are accompanied by a significant reduction in food intake that imposes a substantial energy trade-off. Mouthbrooding, as seen in several species of fish in which the parent holds the developing eggs and fry in the buccal cavity, represents an extreme example of reduced food intake during parental investment and is accompanied by a range of physiological adaptations. In this study we use 16S sequencing to characterize the gut microbiota of female Astatotilapia burtoni cichlid fish throughout the obligatory phase of self-induced starvation during the brooding cycle in comparison to stage-matched females that have been denied food for the same duration. In addition to a reduction of gut epithelial turnover, we find a dramatic reduction in species diversity in brooding stages that recovers upon release of fry and refeeding that is not seen in females that are simply starved. Based on overall species diversity as well as differential abundance of specific bacterial taxa, we suggest that rather than reflecting a simple deprivation of caloric intake, the gut microbiota is more strongly influenced by physiological changes specific to mouthbrooding including the reduced epithelial turnover and possible production of antimicrobial agents.