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Updated: Feb 1, 2026
Author Spotlight: Exploring Microglial Interactions with Stress-Response Circuitry Using the Limited Bedding and Nesting Model
Published on: July 12, 2024
Effect of Limited Bedding and Nesting in Early Ontogenesis on Gene Expression in the Hippocampus and Frontal Cortex
Angelina K Deryabina1, Alexey A Kvichanskiy1, Mikhail V Onufriev1
1Institute of Higher Nervous Activity and Neurophysiology, Moscow, Russian Federation.
Insights
Early life stress from limited bedding and nesting material increases Fos gene expression in adolescent rats
Area of Science:
- Neuroscience
- Developmental Psychology
- Stress Research
Background:
- Early-life stress can increase susceptibility to affective disorders later in life.
- Disrupting maternal care during early development alters stress responses.
- Limited bedding and nesting material (LBN) is a model for early-life adversity.
Purpose of the Study:
- To investigate the effects of LBN on gene expression in the hippocampus and frontal cortex of adolescent rats.
- To examine gene expression changes under baseline and acute restraint stress conditions.
- To identify specific genes and brain regions affected by early-life stress.
Main Methods:
- Rats exposed to LBN from postnatal days 2-9.
- Gene expression analysis (RT-PCR) in hippocampus and frontal cortex at 1 month of age.
- Assessed genes related to glucocorticoids, immune activation, and neuronal networks under stress.
Main Results:
- LBN exposure significantly increased baseline Fos gene expression in the amygdala.
- LBN altered expression of other genes (Nr3c1, Cx3cl1, Ier2, Ncf1) post-restraint stress.
- LBN attenuated the hyperglycemic response to restraint stress; corticosterone levels were comparable to controls.
- Amygdala and ventral hippocampus showed highest sensitivity to experimental manipulations.
Conclusions:
- Early-life stress via LBN induces sustained Fos expression in the amygdala and alters adolescent metabolic stress response.
- Amygdala and ventral hippocampus are critical regions where early adversity and acute stress interact to modulate gene expression.
- Amygdalar circuits may play a role in altered stress reactivity following early-life adversity.
Introduction:
According to literature, early stress may lead to a higher susceptibility to the action of various stressors later in life, thus largely contributing to the development of a wide range of affective disorders. Disrupting maternal care is one way to destabilize the environment for pups, which may result in the formation of an altered reaction to acute or moderate stress.
Methods:
In this study, we analyzed the effects of limited bedding and nesting material (LBN) in PND2-PND9 on baseline gene expression in the hippocampus and frontal cortex of 1-month-old rats and the expression of the same genes under conditions of 60-min restraint. Among the analyzed genes, some were associated with glucocorticoids (Nr3c1 and Nr3c2), others with the activation of the immune system (Nfkbia, Ccl2, Il1b, Il6, Tnfα, Cx3cl1, Cx3cr1, and Ncf1), and yet others with the activation of neuronal networks under stress (Cfos, Ier-2). Gene expression was assessed using real-time PCR.
Results:
Exposure to LBN during early postnatal life significantly increased baseline expression of the Fos gene in the amygdala of adolescent rats. LBN exposure more slightly affected the expression of other analyzed genes (Nr3c1, Cx3cl1, Ier2, Ncf1) or evoked alterations of their expression in this group only after exposure to acute restraint stress. The hyperglycemic response to acute restraint was attenuated in LBN-exposed animals, while corticosterone levels were comparable to controls. Among the studied genes, the expression of Nfkbia, Il6, and Tnf was primarily influenced by acute restraint stress, independently of LBN history. The amygdala and ventral hippocampus were the brain regions where the expression of the analyzed genes appeared most sensitive to the experimental manipulations.
Conclusion:
These data indicate that early-life stress induced by LBN leads to a sustained increase in baseline Fos expression in the amygdala and alters the metabolic response to acute stress in adolescence. The findings further suggest that the amygdala and ventral hippocampus are key regions where the expression of a limited set of stress-related genes is modulated by the interplay of early-life adversity and acute stress. These points to a potential role for amygdalar circuits in the altered stress reactivity observed following adverse early-life conditions.
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