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Verfasst von:Ta, Thuy-Truc [VerfasserIn]   i
 Dikmen, Hasan Onur [VerfasserIn]   i
 Chausse de Freitas, Bruno [VerfasserIn]   i
 Lewen, Andrea [VerfasserIn]   i
 Hollnagel, Jan-Oliver [VerfasserIn]   i
 Kann, Oliver [VerfasserIn]   i
Titel:Priming of microglia with IFN-γ slows neuronal gamma oscillations in situ
Verf.angabe:Thuy-Truc Ta, Hasan Onur Dikmen, Simone Schilling, Bruno Chausse, Andrea Lewen, Jan-Oliver Hollnagel, and Oliver Kann
E-Jahr:2019
Jahr:February 19, 2019
Umfang:6 S.
Fussnoten:Gesehen am 29.05.2019
Titel Quelle:Enthalten in: National Academy of Sciences (Washington, DC)Proceedings of the National Academy of Sciences of the United States of America
Ort Quelle:Washington, DC : National Acad. of Sciences, 1915
Jahr Quelle:2019
Band/Heft Quelle:116(2019), 10, Seite 4637-4642
ISSN Quelle:1091-6490
Abstract:Type II IFN (IFN-γ) is a proinflammatory T lymphocyte cytokine that serves in priming of microglia—resident CNS macrophages—during the complex microglial activation process under pathological conditions. Priming generally permits an exaggerated microglial response to a secondary inflammatory stimulus. The impact of primed microglia on physiological neuronal function in intact cortical tissue (in situ) is widely unknown, however. We explored the effects of chronic IFN-γ exposure on microglia in hippocampal slice cultures, i.e., postnatal parenchyma lacking leukocyte infiltration (adaptive immunity). We focused on fast neuronal network waves in the gamma-band (30-70 Hz). Such gamma oscillations are fundamental to higher brain functions, such as perception, attention, and memory, and are exquisitely sensitive to metabolic and oxidative stress. IFN-γ induced substantial morphological changes and cell population expansion in microglia as well as moderate up-regulation of activation markers, MHC-II, CD86, IL-6, and inducible nitric oxide synthase (iNOS), but not TNF-α. Cytoarchitecture and morphology of pyramidal neurons and parvalbumin-positive inhibitory interneurons were well-preserved. Notably, gamma oscillations showed a specific decline in frequency of up to 8 Hz, which was not mimicked by IFN-α or IL-17 exposure. The rhythm disturbance was caused by moderate microglial nitric oxide (NO) release demonstrated by pharmacological microglia depletion and iNOS inhibition. In conclusion, IFN-γ priming induces substantial proliferation and moderate activation of microglia that is capable of slowing neural information processing. This mechanism might contribute to cognitive impairment in chronic brain disease featuring elevated IFN-γ levels, blood-brain barrier leakage, and/or T cell infiltration, well before neurodegeneration occurs.
DOI:doi:10.1073/pnas.1813562116
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1073/pnas.1813562116
 Volltext: https://www.pnas.org/content/116/10/4637
 DOI: https://doi.org/10.1073/pnas.1813562116
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:interferon-gamma
 microglia
 neuroinflammation
 neuronal electrical activity
 nitric oxide synthase
K10plus-PPN:1666492760
Verknüpfungen:→ Zeitschrift

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