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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Veröffentlicht in:	Brain, behavior, and immunity behavior, and immunity, 2016-01, Vol.51, p.99-108
Hauptverfasser:	Frank, Matthew G, Adhikary, Sweta, Sobesky, Julia L, Weber, Michael D, Watkins, Linda R, Maier, Steven F
Format:	Artikel
Sprache:	eng
Schlagworte:	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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Zusammenfassung:	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