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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: Ethanol-activated microglial exosomes induce MCP1 signaling mediated death of stress-regulatory proopiomelanocortin neurons in the developing hypothalamus

Fig. 7

Schematic representing mechanisms by which microglial extravesicular MCP1 induces postnatal alcohol-activated apoptosis in β-endorphin neurons. Postnatal alcohol exposure (PAE) causes hypothalamic microglia to release exosomes containing MCP1 (also known as CCL2). MCP1 by activating it’s receptor CCR2 increases the transcriptional factor MCPIP1 which elevate the levels of apoptotic and inflammatory genes leading to β-endorphin neuronal death. CCR2 antagonist RS504393 prevents β-endorphin neuronal death and improve stress response and anxiety-like behavior in PAE offspring

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Journal of Neuroinflammation

ISSN: 1742-2094