Dexmedetomidine Alleviates Hypoxia-Induced Synaptic Loss and Cognitive Impairment via Inhibition of Microglial NOX2 Activation in the Hippocampus of Neonatal Rats

Figure 2

Dexmedetomidine attenuated hypoxia-induced synaptic loss in the hippocampus. Neonatal rats were treated with dexmedetomidine 30 min before or immediately after hypoxia exposure, and (a–e) synaptic ultrastructure changes in the hippocampal CA1 region were observed under TEM 28 days following hypoxia. (a) Representative photomicrograph (9700x) showing the differences in the number of synapses per slice among the four groups (the red arrows indicate the synapses). (b) Representative high-magnification photomicrograph (37000x) showing the differences in the thickness of PSD and the width of the synaptic cleft among the four groups (the red arrows indicate the synaptic linkage). (c–e) Quantification of synapse density, PSD thickness and synaptic cleft width from at least 20 sections among the four groups. The protein expression of PSD95 and synaptophysin was measured in the hippocampus 24 h (f) and 28 days (g) after hypoxic insult by Western blot analysis. The levels of PSD-95 and synaptophysin expression are presented as the percentages of those in the Control group. The data are expressed as the , . vs. the Control group, ^# vs. the Hypoxia group, ^& vs. the Hypo+Pre-Dex group. Hypo: hypoxia; Pre-Dex: dexmedetomidine pretreatment; Post-Dex: dexmedetomidine posttreatment.

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