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Background and Objective   Chronic unexpected mild stress (CUMS) destroys synaptic plasticity of hippocampal regenerated neurons that may be involved in the occurrence of poststroke depression. Astrocytes uptake glutamate at the synapse and provide metabolic support for neighboring neurons. Currently, we aim to investigate whether CUMS inhibits synaptic formation of regenerated neurons through a glutamate transporter, GLT-1, of astrocytes in the ischemic stroke rats.Method   We exposed the ischemic stroke rats to ceftriaxone, during the CUMS intervention period to determine the effects of GLT-1 on glutamate circulation by immunofluorescence and mass spectrometry and its influences to synaptic plasticity by western blot and transmission electron microscopy.Result   CUMS evidently reduced the level of astroglial GLT-1 in the hippocampus of the ischemic rats ( p  < 0.05), resulting in smaller amount of glutamate being transported into astrocytes surrounding synapses ( p  < 0.05), and then expression of synaptophysin was suppressed ( p  < 0.05) in hippocampal dentate gyrus. The ultrastructures of synapses in dentate gyrus were adversely influenced including decreased proportion of smile synapses, shortened thickness of postsynaptic density, reduced number of vesicles, and widened average distance of the synaptic cleft (all  p  < 0.05). Moreover, ceftriaxone can promote glutamate circulation and synaptic plasticity (all  p  < 0.05) by raising astroglial GLT-1 ( p  < 0.05) and then improve depressive behaviors of the CUMS-induced model rats ( p  < 0.05).Conclusion   Our study shows that CUMS destroys synaptic plasticity of regenerated neurons in the hippocampus through a glutamate transporter, GLT-1, of astrocytes in the ischemic stroke rats. This may indicate one potential pathogenesis of poststroke depression.

neural plasticity

Chronic Unexpected Mild Stress Destroys Synaptic Plasticity of Neurons through a Glutamate Transporter, GLT-1, of Astrocytes in the Ischemic Stroke Rat