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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: Mu-opioid receptor and delta-opioid receptor differentially regulate microglial inflammatory response to control proopiomelanocortin neuronal apoptosis in the hypothalamus: effects of neonatal alcohol

Fig. 7

Schematic diagram illustrating the proposed mechanism by which ethanol interacts with opioid receptors to control POMC neuronal apoptosis in the hypothalamus. Ethanol activation of MOR induces microglial polarization towards the M1 phenotype to produce overabundance of inflammatory cytokines and inflammation. Chronic inflammation and overproduction of TNF-α and IL-6 cytokines are cytotoxic to POMC producing neurons. DOR activation increases production of anti-inflammatory cytokines and helps microglial polarization towards the M2 phenotypes. Elevated productions of IL-4 and IL-13 cytokines from M2 microglia reduce ethanol’s ability to increase POMC neuronal apoptosis. DOR agonist may have therapeutic potential to prevent ethanol neurotoxic action

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