The danger-associated molecular pattern HMGB1 mediates the neuroinflammatory effects of methamphetamine

Highlights • Methamphetamine (METH) induced a neuroinflammatory response in brain reward-related structures. • METH failed to directly induce cytokines in isolated microglia. • METH induced the danger-associated molecular pattern HMGB1 in striatum. • HMGB1 mediated, in part, the METH-induced neuroin...

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Bibliographic Details
Published in:Brain, behavior, and immunity behavior, and immunity, 2016-01, Vol.51, p.99-108
Main Authors: Frank, Matthew G, Adhikary, Sweta, Sobesky, Julia L, Weber, Michael D, Watkins, Linda R, Maier, Steven F
Format: Article
Language:English
Subjects:
Allergy and Immunology
Animals
Brain - drug effects
Brain - metabolism
Corpus Striatum - drug effects
Corpus Striatum - metabolism
DAMP
Encephalitis - chemically induced
Encephalitis - metabolism
HMGB1
HMGB1 Protein - metabolism
Inflammation Mediators - metabolism
Male
Methamphetamine
Methamphetamine - administration & dosage
Microglia
Microglia - drug effects
Microglia - metabolism
Neuroinflammation
Neurotoxicity
Nucleus Accumbens - drug effects
Nucleus Accumbens - metabolism
Prefrontal Cortex - drug effects
Prefrontal Cortex - metabolism
Psychiatry
Rats
Rats, Sprague-Dawley
Ventral Tegmental Area - drug effects
Ventral Tegmental Area - metabolism
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Summary:Highlights • Methamphetamine (METH) induced a neuroinflammatory response in brain reward-related structures. • METH failed to directly induce cytokines in isolated microglia. • METH induced the danger-associated molecular pattern HMGB1 in striatum. • HMGB1 mediated, in part, the METH-induced neuroinflammatory response.
ISSN:0889-1591
1090-2139
DOI:10.1016/j.bbi.2015.08.001