Metabolic coupling between glia and neurons

Tsacopoulos, M.; Magistretti, P. J.

doi:10.1523/jneurosci.16-03-00877.1996

Cited by 924 publications

(608 citation statements)

References 34 publications

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“…A clearer understanding is needed of the relationship between occurrence of PIDs and any progressive loss of perfusion that might occur during penumbral recruitment. That dialysate lactate failed to rise progressively after MCAO in these experiments may be because of the progressive decline in glucose, depletion of astrocyte glycogen (Tsacopoulos and Magistretti, 1996), or separate regulation of glucose and lactate (Fray et al, 1996).…”

Section: Selection Of the Marginal Gyrus For Probe Locationmentioning

confidence: 77%

Transient Changes in Cortical Glucose and Lactate Levels Associated with Peri-Infarct Depolarisations, Studied with Rapid-Sampling Microdialysis

Hopwood

Parkin

Bezzina

et al. 2005

J Cereb Blood Flow Metab

116

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Peri-infarct depolarisations (PIDs) contribute to infarct expansion in experimental focal ischaemia; furthermore, depolarisations propagate in the injured human brain. Glucose utilisation is increased under both conditions, and depletion of brain glucose carries a poor prognosis. We studied dynamics of cerebral glucose and lactate in relation to PID patterns in experimental stroke. The middle cerebral artery was occluded for 3 h in 23 cats under terminal chloralose anaesthesia. We used fluorescence imaging to detect occurrence of PIDs, and rapid-sampling online microdialysis (rsMD), coupled to a flow-injection assay, to examine changes in cerebral cortical extracellular glucose and lactate at intervals of 30 sec each. After 30 min' ischaemia, lactate had increased by 43.67s.d. 45.9 lmol/L, and stabilised in that range for 3 h. In contrast, glucose fell only slightly initially (11.979.7 lmol/L), but progressively decreased to a reduction of 56.7747.2 lmol/L at 3 h, with no evidence of stabilisation. There was a highly significant inverse relationship of frequency of PIDs with plasma glucose (Po0.001). The results also characterise a metabolic signature for PIDs for possible application in clinical work, and emphasise potential risks in the use of insulin to control plasma glucose in patients with brain injury.

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Section: Selection Of the Marginal Gyrus For Probe Locationmentioning

confidence: 77%

Transient Changes in Cortical Glucose and Lactate Levels Associated with Peri-Infarct Depolarisations, Studied with Rapid-Sampling Microdialysis

Hopwood

Parkin

Bezzina

et al. 2005

J Cereb Blood Flow Metab

116

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“…19,20 In the murine brain, GFAP staining of astrocytes appears on embryonic day 18 to P0 with a subsequent rise by 2 weeks and later plateau by 1 month. Astrocytes bearing GFAP immunoreactivity serve many functions in health and disease including guidance of neuronal migration, production of extracellular matrix proteins and adhesion molecules, 21,22 production of neurite promoting factors, cerebral angiogenesis, neurotransmission, regulation of pH and ion concentration, phagocytosis, glutathione production and neuroendocrine functions. 17 More recently, astrocytes have been implicated in metabolic roles such as uptake of glucose and glutamate, storage of glycogen and clearance of potassium.…”

Section: Discussionmentioning

confidence: 99%

Human influenza viral infection in utero alters glial fibrillary acidic protein immunoreactivity in the developing brains of neonatal mice

et al. 2002

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Epidemiological reports describe a strong association between prenatal human influenza viral infection and later development of schizophrenia. Postmodern human brain studies, however, indicate a lack of gliosis in schizophrenic brains presumably secondary to absence of glial cells during the second trimester viral infection in utero. We hypothesized that human influenza infection in day 9 pregnant mice would alter the expression of glial fibrillary acidic protein (GFAP, an important marker of gliosis, neuron migration, and reactive injury) in developing brains of postnatal days 0, 14 and 35 mice. Determination of cellular GFAP immunoreactivity (IR) expressed as cell density in cortex and hippocampus of control and experimental brains showed increases in GFAP-positive density in exposed cortical (P = 0.03 day 14 vs control) and hippocampal cells (P = 0.035 day 14, P = 0.034 day 35). Similarly, ependymal cell layer GFAP-IR cell counts showed increases with increasing brain age from day 0, to days 14 and 35 in infected groups (P = 0.037, day 14) vs controls. The GFAP-positive cells in prenatally exposed brains showed 'hypertrophy' and more stellate morphology. These results implicate a significant role of prenatal human influenza viral infection on subsequent gliosis, which persists throughout brain development in mice from birth to adolescence.

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“…Several of these pathways were previously shown to be affected by HA (Felipo and Butterworth, 2002;Marcaggi and Coles, 2001;Rama Rao et al, 2005;Ratnakumari et al, 1994;Tsacopoulos and Magistretti, 1996). They included glycolysis/gluconeogenesis pathways ( Supplementary Fig.…”

Section: Gene Expression Profiling Of Facs-purified Egfp + Astrocytesmentioning

confidence: 99%

Gene expression profiling of astrocytes from hyperammonemic mice reveals altered pathways for water and potassium homeostasis in vivo

Lichter‐Konecki

Mangin

Gordish‐Dressman

et al. 2008

Glia

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Acute hyperammonemia (HA) causes cerebral edema and brain damage in children with urea cycle disorders (UCDs) and in patients in acute liver failure. Chronic HA is associated with developmental delay and mental retardation in children with UCDs, and with neuropsychiatric symptoms in patients with chronic liver failure. Astrocytes are a major cellular target of hyperammonemic encephalopathy, and changes occurring in these cells are thought to be causally related to the brain edema of acute HA. To study the effect of HA on astrocytes in vivo, we crossed the Otc spf mouse, a mouse with the X-linked UCD ornithine transcarbamylase (OTC) deficiency, with the hGFAP-EGFP mouse, a mouse selectively expressing green fluorescent protein in astrocytes. We used FACS to purify astrocytes from the brains of hyperammonemic and healthy Otc spf /GFAP-EGFP mice. RNA isolated from these astrocytes was used in microarray expression analyses and qRT-PCR. When compared with healthy littermates, we observed a significant downregulation of the gap-junction channel connexin 43 (Cx43) the water channel aquaporin 4 (Aqp4) genes, and the astrocytic inward-rectifying potassium channel (Kir) genes Kir4.1 and Kir5.1 in hyperammonemic mice. Aqp4, Cx43, and Kir4.1/ Kir5.1 are co-localized to astrocytic end-feet at the brain vasculature, where they regulate potassium and water transport.Since, ions can permeate water and K + -channels, downregulation of these three channels may be a direct effect of elevated blood ammonia levels. Our results suggest that alterations in astrocyte-mediated water and potassium homeostasis in brain may be key to the development of the brain edema.

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Metabolic coupling between glia and neurons

Cited by 924 publications

References 34 publications

Transient Changes in Cortical Glucose and Lactate Levels Associated with Peri-Infarct Depolarisations, Studied with Rapid-Sampling Microdialysis

Transient Changes in Cortical Glucose and Lactate Levels Associated with Peri-Infarct Depolarisations, Studied with Rapid-Sampling Microdialysis

Human influenza viral infection in utero alters glial fibrillary acidic protein immunoreactivity in the developing brains of neonatal mice

Gene expression profiling of astrocytes from hyperammonemic mice reveals altered pathways for water and potassium homeostasis in vivo

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