Glycolytic concomitant of brain inflammation produced by goldthioglucose

Richard J. Dirocco; Edgar E. Coons

doi:10.1016/0006-8993(85)90658-4

Glycolytic concomitant of brain inflammation produced by goldthioglucose

Richard J. Dirocco, Edgar E. Coons

Psychology

Research output: Contribution to journal › Article › peer-review

Abstract

In order to determine the effect of inflammation on brain glycolysis in the absence of leukocyte infiltration, [¹⁴C]deoxyglucose autoradiography and hematoxylin-eosin (HE) counter-staining were applied to mice at various times after the induction of chemotoxic inflammatory brain lesions by the systemic administration of goldthioglucose. Glycolysis was intensely stimulated in affected circumventricular organs, without cellular infiltration. This result is consistent with the activation of anaerobic glycolysis by inflammatory sequelae that culminate in ischemic hypoxia in the lesion sites.

Original language	English (US)
Pages (from-to)	313-317
Number of pages	5
Journal	Brain Research
Volume	336
Issue number	2
DOIs	https://doi.org/10.1016/0006-8993(85)90658-4
State	Published - Jun 17 1985

Keywords

[C]deoxyglucose autoradiography
anearobic glycolysis
blood
brain barrier
goldthioglucose
inflammation
ischemia
multiple sclerosis
trauma

ASJC Scopus subject areas

General Neuroscience
Molecular Biology
Clinical Neurology
Developmental Biology

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10.1016/0006-8993(85)90658-4

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title = "Glycolytic concomitant of brain inflammation produced by goldthioglucose",

abstract = "In order to determine the effect of inflammation on brain glycolysis in the absence of leukocyte infiltration, [14C]deoxyglucose autoradiography and hematoxylin-eosin (HE) counter-staining were applied to mice at various times after the induction of chemotoxic inflammatory brain lesions by the systemic administration of goldthioglucose. Glycolysis was intensely stimulated in affected circumventricular organs, without cellular infiltration. This result is consistent with the activation of anaerobic glycolysis by inflammatory sequelae that culminate in ischemic hypoxia in the lesion sites.",

keywords = "[C]deoxyglucose autoradiography, anearobic glycolysis, blood, brain barrier, goldthioglucose, inflammation, ischemia, multiple sclerosis, trauma",

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year = "1985",

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AU - Dirocco, Richard J.

AU - Coons, Edgar E.

PY - 1985/6/17

Y1 - 1985/6/17

N2 - In order to determine the effect of inflammation on brain glycolysis in the absence of leukocyte infiltration, [14C]deoxyglucose autoradiography and hematoxylin-eosin (HE) counter-staining were applied to mice at various times after the induction of chemotoxic inflammatory brain lesions by the systemic administration of goldthioglucose. Glycolysis was intensely stimulated in affected circumventricular organs, without cellular infiltration. This result is consistent with the activation of anaerobic glycolysis by inflammatory sequelae that culminate in ischemic hypoxia in the lesion sites.

AB - In order to determine the effect of inflammation on brain glycolysis in the absence of leukocyte infiltration, [14C]deoxyglucose autoradiography and hematoxylin-eosin (HE) counter-staining were applied to mice at various times after the induction of chemotoxic inflammatory brain lesions by the systemic administration of goldthioglucose. Glycolysis was intensely stimulated in affected circumventricular organs, without cellular infiltration. This result is consistent with the activation of anaerobic glycolysis by inflammatory sequelae that culminate in ischemic hypoxia in the lesion sites.

KW - [C]deoxyglucose autoradiography

KW - anearobic glycolysis

KW - blood

KW - brain barrier

KW - goldthioglucose

KW - inflammation

KW - ischemia

KW - multiple sclerosis

KW - trauma

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JO - Brain Research

JF - Brain Research

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ER -

Glycolytic concomitant of brain inflammation produced by goldthioglucose

Abstract

Keywords

ASJC Scopus subject areas

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