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Prenatal stress impairs memory function in the early development of male-offspring associated with the gaba function
Yingchun Shang1, Runwen Chen1, Fangjuan Li1
1College of Life Sciences and Key Laboratory of Bioactive Materials Ministry of Education, Nankai University, 300071 Tianjin, China.
Insights
Prenatal stress (PS) impairs offspring memory and hippocampal function during development. These deficits, linked to GABAergic system disturbances, resolve by adulthood, suggesting a critical developmental window for intervention.
Area of Science:
- Neuroscience
- Developmental Biology
- Psychology
Background:
- Prenatal stress (PS) is known to disrupt offspring development, leading to cognitive and behavioral issues.
- GABAergic systems are crucial for brain development, and their dysregulation is implicated in various neurological disorders.
- While PS increases GABAA receptor expression in young offspring, the long-term impact on GABAergic function throughout development remains unclear.
Purpose of the Study:
- To investigate the long-lasting effects of prenatal stress on memory function and hippocampal synaptic plasticity.
- To determine the association between prenatal stress-induced deficits and GABAergic system function during offspring development.
Main Methods:
- Establishment of a rat model of prenatal stress using daily restraint stress during late gestation.
- Assessment of memory function, long-term potentiation (LTP), depotentiation, and hippocampal spine density in offspring at different developmental stages.
- Analysis of the balance between excitatory and inhibitory receptors and parvalbumin levels in the hippocampus.
Main Results:
- Prenatal stress offspring exhibited memory deficits and impaired LTP/depotentiation in young and pubertal stages, which resolved in adulthood.
- Hippocampal spine density was reduced in prenatal stress offspring.
- A significant disturbance in the balance of excitatory and inhibitory receptors and increased parvalbumin levels were observed in the prenatal stress group.
Conclusions:
- Prenatal stress induces transient memory and hippocampal synaptic plasticity deficits during early development.
- These effects are associated with disruptions in GABAergic function and excitatory/inhibitory balance.
- The findings highlight a critical developmental window where prenatal stress impacts neurodevelopment, offering potential targets for future interventions.
Abstract:
Prenatal stress (PS) induces cognitive deficits, abnormal behavior patterns and physical impairments in offspring, which disturbs the developmental process. GABA systems play a key role in the brain development. The developmental trajectories are less understood although PS increases the expression of GABAAR in young offspring. In the present study, we aimed to examine if the long-lasting effects on memory function and hippocampal synaptic plasticity induced by PS were associated with the GABA function throughout developmental process. Thus, a PS rat model was established by using restraint stress three 45-min periods per day from gestational day 15 until delivery. PS-exposed offspring exhibited the memory function deficits, LTP and depotentiation inhibitions in young and puberty offspring, but the disorder resolved at adult offspring. Meanwhile, the hippocampal spine density was decreased by PS in offspring. Additionally, we found that the balance of excitatory and inhibitory receptors was significantly disturbed after PS. The immunostaining of parvalbumin level was increased in the PS group. Overall, these all results suggest that the PS induces negative effects in memory and hippocampal synaptic plasticity in the early developmental stage, which could be an underlying mechanism of the disturbed GABA function.
