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Updated: May 19, 2026

Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Beta-adrenergic receptor activation primes microglia cytokine production
John D Johnson1, Zachary R Zimomra, Luke T Stewart
1Kent State University, Biological Sciences Department, Kent, OH 44242, United States. jjohns72@kent.edu
Abstract:
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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