Postpartum Psychological Disturbances in Rodent Models

Postpartum psychological disturbances in rodent models encompass a spectrum of behavioural and neurobiological alterations designed to mimic aspects of human postpartum mood disorders. Depressive-like behaviours are commonly quantified by reduced sucrose preference, increased immobility in the forced swim or tail suspension tests and deficits in maternal care. These phenotypes can be precipitated by gestational or prepregnancy stress, abrupt withdrawal of reproductive hormones or immune challenges. At the neural level, researchers have documented impaired hippocampal neurogenesis, structural remodelling of the medial prefrontal cortex and amygdala, and dysregulation of the hypothalamic–pituitary–adrenal axis. Key molecular pathways implicated include Akt–mTOR, Wnt and BDNF-related signalling cascades, which govern synaptic plasticity and cell survival. Neuroinflammatory processes and shifts in GABAergic/glutamatergic balance further contribute to symptom expression. By elucidating the mechanisms underlying maternal mood disturbances, these rodent paradigms offer critical insight into potential therapeutic targets and the long-term impact of early-life adversity on both dams and their offspring.

Research from Nature Portfolio

Recent studies have demonstrated that chronic prepregnancy stress in mouse models precipitates enduring postpartum depressive-like behaviour, mediated by sustained impairments in hippocampal Akt–mTOR signalling and neurogenesis. In this paradigm, stress prior to conception induces transient mood deficits in virgins but leads to persistent anhedonia, behavioural despair and reduced expression of glutamate receptor subunits after parturition. Molecular profiling revealed long-term downregulation of synaptic proteins in the dentate gyrus, coinciding with compromised neural progenitor proliferation. Notably, a single administration of ketamine rapidly reinstated Akt–mTOR activity, restored synaptic integrity and ameliorated depressive-like behaviours, in stark contrast to conventional antidepressant regimens. These findings underscore the crucial role of mTOR-dependent synaptic plasticity in both the pathophysiology and rapid treatment of postpartum depressive-like states.

Postpartum Psychological Disturbances in Rodent Models publication trend

The graph below shows the total number of articles in postpartum psychological disturbances in rodent models across all publications each year (not limited to Nature Index journals).

Technical terms

Postpartum depression (PPD): Mood disorder occurring after childbirth, characterised in rodents by persistent low mood, anhedonia and maternal care deficits.

Anhedonia: Inability to experience pleasure, operationally defined in rodents by reduced consumption of palatable solutions.

Akt–mTOR signalling: Intracellular pathway regulating protein synthesis and synaptic plasticity, essential for mood and cognitive function.

Wnt signalling: Conserved family of pathways that control neuronal development and synaptic regulation; its dysregulation can lead to affective abnormalities.

Hippocampal neurogenesis: Process by which new neurons are generated in the dentate gyrus, often diminished by peripartum stress and linked to depressive-like phenotypes.

References

1. Restoring Wnt signaling in a hormone-simulated postpartum depression model remediated imbalanced neurotransmission and depressive-like behaviors. Molecular Medicine (2023).
2. Chronic stress prior to pregnancy potentiated long-lasting postpartum depressive-like behavior, regulated by Akt-mTOR signaling in the hippocampus. Scientific Reports (2016).
3. The BDNF-FoxO1 Axis in the medial prefrontal cortex modulates depressive-like behaviors induced by chronic unpredictable stress in postpartum female mice. Molecular Brain (2020).
4. Chronic psychosocial stress during pregnancy affects maternal behavior and neuroendocrine function and modulates hypothalamic CRH and nuclear steroid receptor expression. Translational Psychiatry (2020).