Abstract
SummaryAggression, a sexually dimorphic behaviour, is prevalent in males and typically absent in virgin females. Following parturition, however, the transient expression of aggression in adult female mice protects pups from predators and infanticide. While maternal hormones are known to elicit nursing, their potential role in maternal aggression remains elusive. Here, we show in mice that a molecularly defined subset of ventral premammillary (PMvDAT) neurons, instrumental for intermale aggression, switch from quiescence to a hyperexcitable state during lactation. We identify that the maternal hormones prolactin and oxytocin excite these cells through actions on T-type Ca2+channels. Optogenetic manipulation or genetic ablation of PMvDATneurons profoundly affects maternal aggression, while activation of these neurons impairs the expression of non-aggression-related maternal behaviours. This work identifies a monomorphic neural substrate that incorporates hormonal cues to enable the transient expression of a dormant behavioural program in adult females.Graphical abstractIn BriefMaternal hormones activate an otherwise quiescent population of hypothalamic neurons, which are required for the transient expression of aggression during the nursing period.HighlightsQuiescent PMvDATneurons in female mice become hyperexcitable in lactating dams.Manipulation of PMvDATcell activity bidirectionally regulates maternal aggression.The maternal hormones prolactin and oxytocin excite PMvDATcells.Activation of PMvDATneurons impairs non-aggression maternal care behaviour.
Publisher
Cold Spring Harbor Laboratory