Prenatal sleep restriction altered learning ability and memory behaviour by decreasing hippocampal synaptic plasticity in offspring mice
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Published on: October 11, 2018
Natasha Chitakwa1, Na Chen2, Chuan Chen1
1The Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, 211166, China; State Key Laboratory of Reproductive Medicine, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing 211166, China.
Insights
Prenatal sleep restriction (SR) impairs offspring learning and memory by affecting hippocampal neural plasticity. Even short sleep restriction during pregnancy significantly impacts fetal neurodevelopment and cognitive function in offspring.
Area of Science:
- Neuroscience
- Developmental Biology
- Reproductive Medicine
Background:
- Inadequate sleep during pregnancy negatively impacts offspring neurodevelopment, particularly learning and memory.
- Prenatal sleep restriction (SR) is a potential risk factor for cognitive deficits in offspring.
Purpose of the Study:
- To investigate the effects of prenatal sleep restriction on offspring learning, memory, and hippocampal neural plasticity.
- To determine the molecular mechanisms underlying SR-induced neurodevelopmental impairments.
Main Methods:
- Pregnant mice were subjected to varying durations of sleep restriction (4h, 10h, 18h) from gestation day 8.
- Offspring cognitive functions were assessed using behavioral tests (Morris water maze, passive avoidance, open field).
- Hippocampal synapse structure, and levels of synapse-synthesis proteins (BDNF, Syt7) were analyzed in fetal and adult offspring.
Main Results:
- All SR groups showed significant declines in spatial learning and memory.
- SR led to reduced hippocampal synapse numbers and altered synaptic structures in offspring.
- Decreased expression of BDNF and Syt7 was observed in the hippocampus of SR offspring, with reduced BDNF also in fetal hippocampi.
- Short SR induced more pronounced cognitive impairments than long SR.
Conclusions:
- Prenatal sleep restriction disrupts fetal neurodevelopment and hippocampal synaptic plasticity.
- These disruptions lead to significant learning and memory impairments in offspring.
- Findings highlight the critical role of maternal sleep in fetal cognitive development and suggest targets for early intervention.
Abstract:
Inadequate sleep during pregnancy can have profound effects on offspring neurodevelopment, particularly on learning and memory abilities. This study explored whether prenatal sleep restriction (SR) induces learning and memory impairment in offspring by affecting neural plasticity in the hippocampus using four groups of pregnant mice: short-sleep-restriction (S-SR, 4 h), mid-sleep-restriction (M-SR, 10 h), long-sleep-restriction (L-SR, 18 h), and a control group without SR. SR was implemented from gestation day 8 until delivery. Changes in adult offspring and fetal hippocampal synapse structures were observed and synapse-synthesis-related protein (BDNF and Syt7) levels were measured to establish changes indicative of neurodevelopmental impairment. Offspring learning and memory abilities were further evaluated using Morris water maze test, passive avoidance test, and open field test from postnatal day 35. The findings revealed significant declines in spatial learning and memory across all SR groups. Additionally, adult offspring exhibited reduced hippocampal synapse numbers, thinner postsynaptic densities in S-SR and M-SR groups, and widened synaptic clefts in the L-SR group. Synapse-synthesis-related proteins, including brain-derived neurotrophic factor (BDNF) and synaptotagmin-7 (Syt7), showed decreased expression in the hippocampus of offspring mice in all SR groups, with BDNF expression also reduced in fetal hippocampi. Moreover, BDNF methylation levels indicated significant decreases in BDNF_3 and increases in BDNF_5 specifically in the S-SR group. Notably, prenatal S-SR induced more pronounced impairments in offspring learning and memory compared to L-SR. These findings underscore how prenatal SR disrupts fetal neurodevelopment, emphasizing hippocampal synaptic plasticity as a critical mechanism contributing to impaired cognitive function in offspring. This can help with risk identification and early intervention.
