Summary: Researchers have identified a brain circuit that becomes active in female mice after pregnancy and childbirth, enabling strong defensive aggression that is normally absent in non-pregnant females. The same neural pathway drives aggressive behavior in males but remains dormant in females until it is activated in mothers by the hormones oxytocin and prolactin.
When scientists silenced these specific neurons, mothers no longer launched attacks on cage intruders, demonstrating that activation of this circuit is necessary for maternal defence. The findings illustrate how the brain can transiently unlock behaviors that are crucial for survival during distinct life stages.
Key Facts
- Dormant circuit: A population of aggression-related neurons in female mice is inactive unless triggered by the physiological state of motherhood.
- Hormone activation: Oxytocin and prolactin, hormones associated with lactation and maternal physiology, strongly activate these neurons.
- Brain flexibility: The work suggests a broader principle that the adult brain can access otherwise dormant behaviours temporarily, when required for survival or offspring protection.
Source: Stockholm University
Researchers at Stockholm University and Karolinska Institutet have shown that female mice can gain access to potent defensive aggression through the transient mobilisation of a hormone-sensitive brain circuit. The study explains how females, typically non-aggressive outside the puerperal period, can display intense maternal aggression while nursing.
The investigators found that a defined group of neurons—previously implicated in male aggression—lies silent in non-pregnant females. During lactation these same neurons become highly excitable. Experimentally turning off this cell population abolished maternal attacks on intruders, while activating the cells influenced the expression of social behaviours in a direction consistent with heightened defence.
Electrophysiological experiments revealed that oxytocin and prolactin act on these neurons through both pre- and post-synaptic mechanisms, directly increasing their excitability. These hormonal actions provide a plausible mechanism by which maternal physiology reconfigures neural activity to permit a behaviour that would otherwise be out of the female’s behavioural repertoire.
The researchers emphasize that the work was conducted in laboratory mice and that any extrapolation to humans must be made cautiously. Nevertheless, the principle demonstrated—of a sexually monomorphic neural substrate that can be turned on or off by hormonal signals to grant temporary access to a specific behavioural program—may reflect a general mechanism of brain plasticity relevant across species.
“Surprisingly, the same network of cells that drives aggression in male mice lies dormant in females until the hormonal state of motherhood flips the switch,” says Stefanos Stagkourakis, first author of the study and now head of his research group at SciLifeLab and Karolinska Institutet.
Christian Broberger, Professor of Neurochemistry at Stockholm University and lead of the research, notes: “This research on laboratory mice reveals a way a behaviour normally outside an individual’s repertoire can become available for a limited life stage. The mechanism may hint at general principles of brain flexibility beyond maternal aggression.” The core experiments were carried out at Karolinska Institutet under Professor Broberger’s leadership.
Key Questions Answered
A: They discovered that a population of aggression-related neurons that is normally inactive in female mice becomes active during motherhood, enabling protective and defensive aggression.
A: Oxytocin and prolactin—two hormones central to maternal physiology, including lactation—were shown to strongly excite the aggression-related neurons.
A: It highlights a broader concept of neural plasticity: behaviours that are normally outside an individual’s repertoire can be made available transiently through hormonal and circuit-level changes when survival or offspring protection requires them.
About this maternal aggression and neuroscience research news
Author: Per Larsson
Source: Stockholm University
Contact: Per Larsson – Stockholm University
Image: Image credited to Neuroscience News
Original research: Open access. “Maternal aggression driven by the transient mobilisation of a dormant hormone-sensitive circuit” by Stefanos Stagkourakis et al., published in Nature Communications. The study details how a subset of ventral premammillary (PMvDAT) neurons shifts from quiescence to a hyperexcitable state during female lactation and how hormonal signals modulate this transition.
Abstract (concise summary)
Maternal aggression driven by the transient mobilisation of a dormant hormone-sensitive circuit
Aggression is a sexually dimorphic behaviour in many species. In laboratory mice, males typically display robust aggression while non-puerperal females do not. Yet during the nursing period, females show maternal aggression, a dramatic and transient change in social behaviour.
This adult phenotypic switch provides an opportunity to ask whether sex-biased behaviours rely on distinct neural circuits or on shared circuits that are differently regulated. The study identifies a molecularly defined subset of PMvDAT neurons—already known to contribute to male aggression—that become excitable during female lactation. Prolactin and oxytocin excite these cells through multiple electrophysiological actions. Manipulating PMvDAT neuron activity bidirectionally affected maternal aggression and suppressed competing social behaviours when activated, supporting the idea of a sexually monomorphic neural substrate that integrates hormonal cues to grant transient access to a dormant behavioural program.