1334Appetitive behaviors in school-age and their genetic and environmental predisposition

Background Given the great variability in adiposity and the exposure to obesogenic food environments, it has been suggested that individuals respond in divergent ways to the environment they live in. Our aim was to explore the genetic and environmental contribution of variations on appetitive behaviors in 10-year-old Portuguese children. Methods Participants were twins from the Generation XXI cohort (n = 86 pairs). Appetitive behaviors at 10 years was assessed through the Children Eating Behavior Questionnaire. Intra-class correlations for appetitive behaviors were calculated for monozygotic and dizygotic twins, and structural equation modelling was conducted to estimate genetic (A), shared (C) and non-shared (E) environmental variances. Results Twins were mainly dizygotic (65%), and a third was classified as having excess weight (30.2%). For all appetitive behaviors, with exception to Emotional Undereating, moderate to strong heritability were found and non-shared environmental effects contributed to appetite variability. For Emotional Undereating, environmental effects seem to be more important than genetic effects (C: 0.81; 95%CI 0.71;0.88 and E: 0.19; 95%CI 0.12;0.29). Conclusions There is a significant genetic contribution, followed by non-shared environmental effects, on appetitive behaviors in school-age years. Results indicate that Emotional Undereating was not heritable, being explained by shared and non-shared environmental factors. Key messages Appetitive behaviors among 10-year-olds seem to be genetically determined, with exception to Emotional Undereating, which showed to be explained by environmental factors. Understanding which genes are associated with child appetitive behaviors would give an insight in biological and behavioral influences on child eating and obesity risk.

Prospective relations between maternal emotional eating, feeding to soothe, and infant appetitive behaviors

Background Infant obesogenic appetitive behaviors are associated with greater infant weight and child obesity, yet little is known about maternal influences on infant appetitive behaviors. This study examines the relations between maternal eating behaviors, feeding to soothe, and infant appetitive behaviors in a longitudinal sample of United States mothers. Methods Pregnant women were recruited in the first trimester (< 12 weeks) and followed through 1 year postpartum. Mothers reported their own eating behaviors (eating competence, restrained, emotional, and external eating) in pregnancy; feeding to soothe their infant at 2, 6, and 12 months postpartum; and their infants’ appetitive behaviors (enjoyment of food, food responsiveness, slowness in eating, and satiety responsiveness) at 6 months. Three path models were estimated to examine the direct relations of maternal eating behaviors with infant appetitive behaviors, the indirect relations of maternal eating behaviors with infant appetitive behaviors through feeding to soothe, and the longitudinal relations between feeding to soothe and infant appetitive behaviors. Results Maternal eating behaviors and infant appetitive behaviors were directly and indirectly related in all three models. Greater maternal eating competence was related to greater enjoyment of food but was not related to feeding to soothe. Greater maternal restrained and external eating were not directly related to infant appetitive behaviors but were indirectly related to greater infant responsiveness to food through more frequent feeding to soothe. Additionally, several longitudinal relations between feeding to soothe behaviors and infant appetitive behaviors were present. More frequent feeding to soothe at 2 months was related to greater responsiveness to food at 6 months, which was then related to more frequent feeding to soothe at 6 months. Furthermore, greater satiety responsiveness, faster eating speed, and greater responsiveness to food at 6 months were related to more frequent feeding to soothe at 12 months. Conclusions Maternal eating behaviors were related to infant appetitive behaviors directly and indirectly through feeding to soothe. Additionally, results suggest feeding to soothe and infant appetitive behaviors may be bidirectionally linked. These results underscore the need to examine how parental feeding behaviors are influenced both by parental eating behaviors and child appetitive behaviors throughout infancy. Trial registration Clinicaltrials.gov. Registration ID – NCT02217462. Date of registration – August 13, 2014.

Cellular, circuit and transcriptional framework for modulation of itch in the central amygdala

Itch is an unpleasant sensation that elicits robust scratching and aversive experience. However, the identity of the cells and neural circuits that organize this information remains elusive. Here we show the necessity and sufficiency of chloroquine-activated neurons in the central amygdala (CeA) for both itch sensation and associated aversion. Further, we show that chloroquine-activated CeA neurons play important roles in itch-related comorbidities, including anxiety-like behaviors, but not in some aversive and appetitive behaviors previously ascribed to CeA neurons. RNA-sequencing of chloroquine-activated CeA neurons identified several differentially expressed genes as well as potential key signaling pathways in regulating pruritis. Finally, viral tracing experiments demonstrate that these neurons send projections to the ventral periaqueductal gray that are critical in modulation of itch. These findings reveal a cellular and circuit signature of CeA neurons orchestrating behavioral and affective responses to pruritus in mice.

Rapid appetitive transitions are sculpted by amygdala to accumbens pathways

Foraging, pursuit, and predation rapidly transition into behavioral quiescence during reward capture and consumption. While appetitive-consummatory dissociations are embedded at both psychological and neural levels, the mechanisms controlling switches or transitions between appetitive seeking and consummatory behaviors remain poorly understood. Here we identify the BLA→AcbSh pathway as critical to these transitions by showing that this pathway inhibits the appetitive seeking response in the presence of consummatory demands. Using an appetitive cue-discrimination task in male rats, we show that reward delivery is a significant driver of seeking inhibition and that a BLA→AcbSh pathway mediates this inhibition. This role in suppressing seeking responses during periods of consumption was not due to a general suppression of behavior because responding to other cues during the same test was unaffected. Moreover, it was specific to the BLA→AcbSh pathway, because the contribution of the BLA→AcbC pathway to appetitive switching was distinct and modest. State-dependent silencing of BLA→AcbSh revealed that the modulation of seeking before and after reward delivery are co-dependent. Finally, we found that BLA terminals in AcbSh have functional connectivity to LH-projecting AcbSh neurons, thereby identifying a BLA→AcbSh→LH pathway as a putative route for the rapid regulation of appetitive behaviors. Taken together, these findings suggest that the BLA→AcbSh pathway is a core component of an appetitive switching system, recruited under conditions requiring rapid or dynamic shifts in appetitive behavior, and that this pathway enables these shifts by actively inhibiting seeking.

Cellular, Circuit and Transcriptional Framework for Modulation of Itch in the Central Amygdala

Itch is an unpleasant sensation that elicits robust scratching and active avoidance. However, the identity of the cells and neural circuits that organize this information remains elusive. Here we show the necessity and sufficiency of itch-activated neurons in the central amygdala (CeA) for both itch sensation and active avoidance. Further, we show that itch-activated CeA neurons play important roles in itch-related comorbidities, including anxiety-like behaviors, but not in some aversive and appetitive behaviors previously ascribed to CeA neurons. RNA-sequencing of itch-activated CeA neurons identified several differentially expressed genes as well as potential key signaling pathways in regulating pruritis. Finally, viral tracing experiments demonstrate that these neurons send a critical projection to the periaqueductal gray to mediate modulation of itch. These findings reveal a cellular and circuit signature of CeA neurons orchestrating behavioral and affective responses to pruritus in mice.