Fig. 11

Microglial repopulation normalizes persistent proinflammatory responses to chronic binge ethanol. Primary ex vivo organotypic hippocampal slice cultures (OHSCs) underwent a model of chronic binge ethanol. OHSCs at 4DIV were exposed to ethanol (100 mM) for 3 cycles of 2 days on/ 2 days without ethanol. At the end of binge ethanol exposure (total duration 12 days), slices received either PLX3397 or vehicle for 10 days (leading to microglial depletion) followed by microglial repopulation for 14 days without PLX3397 or ethanol. Naïve control groups remained in culture without PLX3397 or ethanol for the same duration. a Chronic binge ethanol (4DIV-16DIV) caused a persistent increase in expression of TNFα (3.7-fold) and IL-1β (4.5-fold) out to 40DIV. Microglial repopulation normalized proinflammatory gene expression. Slices that underwent chronic ethanol followed by microglial repopulation showed expression of TNFα (107% of control) and IL-1β (61% of control) near age-matched control levels (naïve 40DIV slices). b–e Effects of microglial repopulation on neuronal b ARC, c NR2A and d PSD-95 and the astrocyte marker e GFAP