Maternal aggressive behaviour, which protects the offspring from harm, is one component of maternal behaviour. Not only maternal aggression, but also maternal care and social behaviour in general, is regulated by the brain oxytocin (OXT) and vasopressin (AVP) systems. In the present study, we quantified the intensity of maternal aggression using the maternal defence test at key time points throughout pregnancy, parturition and lactation. Furthermore, we quantified changes in central OXT and arginine AVP V1a receptor (V1a-R) binding in brain regions known to be important in regulating maternal aggression, aiming to investigate whether central changes coincide with the intensity of this behaviour. The intensity of aggression was found to dramatically change over the peripartum period, with its first appearance on the day before parturition. Aggression intensity fell immediately after parturition, although it increased during days 4-7 of lactation, before almost disappearing at weaning. OXT receptor (OTR) and V1a-R binding also showed changes through the peripartum period. OTR binding was highest at parturition within the bed nucleus of the stria terminalis and medial preoptic area and on days 4-7 of lactation in the lateral septum (LS) compared to any other time point during the peripartum period. OTR binding positively correlated with the peak of maternal aggression, suggesting that OXT may act in the LS to facilitate the expression of aggressive behaviour. At parturition, V1a-R binding was at its highest levels in the paraventricular nucleus and central amygdala (CeA) and, in the LS, V1a-R binding positively correlated with aggressive behaviour. V1a-R mRNA expression was also increased within the CeA at parturition. Taken together, the observed fluctuations in OTR and V1a-R binding in the neural circuitry important for regulating maternal behaviour may ensure that maternal aggression is expressed at the correct time during the peripartum period.

High glucocorticoid levels induced by stress enhance the memory of fearful events and may contribute to the development of anxiety and posttraumatic stress disorder. In contrast, elevated glucocorticoids associated with ageing impair spatial memory. We have previously shown that pharmacological inhibition of the intracellular glucocorticoid-amplifying enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) improves spatial memory in aged mice. However, it is not known whether inhibition of 11β-HSD1 will have any beneficial effects on contextual fear memories in aged mice. Here, we examined the effects of UE2316, a selective 11β-HSD1 inhibitor which accesses the brain, on both spatial and contextual fear memories in aged mice using a vehicle-controlled crossover study design.Short-term UE2316 treatment improved spatial memory in aged mice, an effect which was reversed when UE2316 was substituted with vehicle. In contrast, contextual fear memory induced by foot-shock conditioning was significantly reduced by UE2316 in a non-reversible manner. When the order of treatment was reversed following extinction of the original fear memory, and a second foot-shock conditioning was given in a novel context, UE2316 treated aged mice (previously on vehicle) now showed increased fear memory compared to vehicle-treated aged mice (previously on UE2316). Renewal of the original extinguished fear memory triggered by exposure to a new environmental context may explain these effects. Thus 11β-HSD1 inhibition reverses spatial memory impairments with ageing while reducing the strength and persistence of new contextual fear memories. Potentially this could help prevent anxiety-related disorders in vulnerable elderly individuals.

BackgroundResearch into energy balance and growth has infrequently considered genetic sex, yet there is sexual dimorphism for growth across the animal kingdom. We test the hypothesis that in the chicken, there is a sex difference in arcuate nucleus neuropeptide gene expression, since previous research indicates hypothalamic AGRP expression is correlated with growth potential and that males grow faster than females. Because growth has been heavily selected in some chicken lines, food restriction is necessary to improve reproductive performance and welfare, but this increases hunger. Dietary dilution has been proposed to ameliorate this undesirable effect. We aimed to distinguish the effects of gut fullness from nutritional feedback on hypothalamic gene expression and its interaction with sex.MethodsTwelve-week-old male and female fast-growing chickens were either released from restriction and fed ad libitum or a restricted diet plus 15% w/w ispaghula husk, a non-nutritive bulking agent, for 2 days. A control group remained on quantitative restriction. Hypothalamic arcuate nucleus neuropeptides were measured using real-time PCR. To confirm observed sex differences, the experiment was repeated using only ad libitum and restricted fed fast-growing chickens and in a genetically distinct breed of ad libitum fed male and female chickens. Linear mixed models (Genstat 18) were used for statistical analysis with transformation where appropriate.ResultsThere were pronounced sex differences: expression of the orexigenic genes AGRP (P < 0.001) and NPY (P < 0.002) was higher in males of the fast-growing strain. In genetically distinct chickens, males had higher AGRP mRNA (P = 0.002) expression than females, suggesting sex difference was not restricted to a fast-growing strain. AGRP (P < 0.001) expression was significantly decreased in ad libitum fed birds but was high and indistinguishable between birds on a quantitative versus qualitative restricted diet. Inversely, gene expression of the anorectic genes POMC and CART was significantly higher in ad libitum fed birds but no consistent sex differences were observed.ConclusionExpression of orexigenic peptides in the avian hypothalamus are significantly different between sexes. This could be useful starting point of investigating further if AGRP is an indicator of growth potential. Results also demonstrate that gut fill alone does not reduce orexigenic gene expression.Electronic supplementary materialThe online version of this article (10.1186/s13293-018-0178-6) contains supplementary material, which is available to authorized users.