. Author manuscript; available in PMC: 2016 May 1.

Published in final edited form as: Brain Behav Immun. 2015 Feb 18;46:212–220. doi: 10.1016/j.bbi.2015.01.016

Table 3.

RSD increased reactivity of microglia 24 days after stress cessation. Imipramine treatment blocked microglia activation. Male C57BL/6 mice were subjected to six cycles of RSD and treated with imipramine i.p. injections as described in Fig. 1A. Brains were collected at 24 days after RSD. Enriched microglia were collected and cultured ex vivo. Cells were incubated with LPS (0.1 μM) and IL-1β, IL-6, and TNF-α relative gene expression was determined from these cells collected 18 h later. Means represent the relative fold change increase over vehicle controls in media ± SEM.

Gene	Microglia mean relative gene expression after LPS stimulation (normalized to VCON media) 24 days after RSD

	Vehicle		Imipramine

	VCON	VRSD	ICON	IRSD
IL-1β	18.05 ± 3.49^a	67.32 ± 14.86^b	7.60±4.27^a	17.06 ±6.69^a
IL-6	6.84 ± 1.56^a	30.53 ±9.87^b	4.73 ± 1.61^a	6.04 ± 0.95^a
TNF-α	12.72 ± 0.38^a	106.21 ±39.04^b	20.11 ± 8.34^a	21.87 ± 7.93^a

Means with different letters (a, b) are significantly different from each other (p < 0.05). CON = home caged controls; RSD = repeated social defeat; VCON = vehicle controls; ICON = imipramine controls; VRSD = vehicle repeated social defeat; IRSD = imipramine repeated social defeat.