Abstract
Advanced maternal age (AMA) has become more common in the last decade and is associated with poor neurodevelopmental outcomes in offspring. Neurocognitive and emotional development is associated with synaptic structural and functional plasticity. In the present study, we investigated the relationship between AMA and synapse plasticity in the offspring. We examined the synaptic ultrastructure, synapse-related proteins and long-term potentiation (LTP) in the offspring of Sprague–Dawley female rats aged 12 months (AMA group) and 3 months (Control group) on postnatal (P) days 7, 14, 28 and 60. Immunofluorescence analysis revealed decreases in the expression of neurofilament 200 (NF200) and axon length in the AMA group compared with the control group at P14. Western blot analysis showed that the expression of postsynaptic density-95 (PSD-95) and synaptophysin (SYP) was reduced in the immature offspring of the AMA group at P7. Transmission electron microscopy showed decreased thickness of the PSD and increased length of the active zone (AZ) in the offspring of the AMA group. Electrophysiological recordings in hippocampal slices revealed impaired LTP in the AMA offspring. Our data suggest that AMA impairs the synaptic plasticity of offspring, which may underlie the mechanism of neurodevelopmental disorders.
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