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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Hippocampal microglial activation triggers a neurotoxic-specific astrocyte response and mediates etomidate-induced long-term synaptic inhibition

Fig. 5

LPS treatment before etomidate sedative injection impairs cognitive, neuronal, and glial function in the late pathological stage (3 weeks post etomidate sedative injection and 4 weeks post LPS injection). a Graphic illustration of experimental procedure. Flow cytometry were applied to analyze the efficiency of microglial activation and qPCR was applied to evaluate the selected transcripts associated with microglial polarization (microglial phenotype of M1, M2a, and M2b,2c) in hippocampus after LPS treatment at the early stage (1 week post etomidate sedative injection and 2 weeks post LPS injection; b and c) and late stage (3 weeks post etomidate sedative injection and 4 weeks post LPS injection; d and e). During MWM test (3 weeks post etomidate sedative injection and 4 weeks post LPS injection), we recorded (f) swim path and (g) analyzed swim speed and latency to find platform during visible and hidden platform training; (h) swim path and (i) time spent in each quadrant was investigated. j During NOR test, total time spent on object recognition and discrimination index were analyzed. Neuronal activities were detected by (k and l) sIPSC, sEPSC, (m and n) mIPSC, and mEPSC recording and analyzing (scale bar: 200 ms, 25 pA). Selected transcripts on regulation astrocyte activation (Pan-reactive, A1-specific, and A2-specific phenotype; o and p) were detected by qPCR. (n = 12 per group for behavioral and electrophysiological assay; n = 3 for qPCR assay; *p < 0.05, **p < 0.01, ***p < 0.001 compared with saline injected mice)

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