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J Neuroimmunol. 2013 Jan 15;254(1-2):161-4. doi: 10.1016/j.jneuroim.2012.08.007. Epub 2012 Sep 1.

Beta-adrenergic receptor activation primes microglia cytokine production.

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Kent State University, Biological Sciences Department, Kent, OH 44242, United States.


Exaggerated pro-inflammatory cytokine production by primed microglia is thought to mediate pathology during stress, aging, and neurodegeneration. Recently, it was demonstrated that beta-adrenergic receptor (β-AR) antagonism prevents priming of microglia in mice exposed to chronic stress. To determine if β-AR stimulation is sufficient to prime microglia, rats were intra-cerebroventricularly administered isoproterenol (β-AR agonist) or vehicle and 24 h later hippocampal microglia were placed in culture with media or LPS. Prior isoproterenol treatment significantly enhanced IL-1β and IL-6, but not TNF-α production following LPS stimulation. These data suggest that central β-AR stimulation is sufficient to prime microglia cytokine responses.

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