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Brain metabolic interactions between neurons

Dringen R, Gutterer JM, Hirrlinger J. 2000. Glutathione metabolism in brain metabolic interaction between astrocytes and neurons in the defense against reactive oxygen species. Eur J Biochem 267 4912-4916. [Pg.305]

Fig. 2. Metabolic interactions between neurons and astrocytes. Glucose enters the brain through the astrocytic end feet that envelop brain capillaries. In the astrocytes some of the glucose is metabolized to lactate which is exported to the extracellular fluid and taken up by neurons. In neurons lactate is converted to pyruvate which is either decarboxyiated to acetyl-CoA or carboxykited to malate to enter the TCA cycle. Glutamate may therefore be formed in neurons from a-ketoglutarate or from glutamine, which is imported from astrocytes. The glutamate that is released is taken up by astrocytes and amidated to glutamine or metabolized via the TCA cycle. The malate thus formed may leave the TCA cycle and become decarboxyiated to pyruvate and lactate. For lack of space, astrocytic pyruvate carboxylation is indicated only by the reversible formation of lactate. Notice that the relative importance of the various pathways in vivo is a matter of debate (see text). Fig. 2. Metabolic interactions between neurons and astrocytes. Glucose enters the brain through the astrocytic end feet that envelop brain capillaries. In the astrocytes some of the glucose is metabolized to lactate which is exported to the extracellular fluid and taken up by neurons. In neurons lactate is converted to pyruvate which is either decarboxyiated to acetyl-CoA or carboxykited to malate to enter the TCA cycle. Glutamate may therefore be formed in neurons from a-ketoglutarate or from glutamine, which is imported from astrocytes. The glutamate that is released is taken up by astrocytes and amidated to glutamine or metabolized via the TCA cycle. The malate thus formed may leave the TCA cycle and become decarboxyiated to pyruvate and lactate. For lack of space, astrocytic pyruvate carboxylation is indicated only by the reversible formation of lactate. Notice that the relative importance of the various pathways in vivo is a matter of debate (see text).
Interaction with metallothionein is the basis for metabolic interactions between these metals. Metallothionein III is found in the human brain and differs from I and II by having six glutamic acid residues near the terminal part of the protein. Metallothionein III is thought to be a growth inhibitory factor, and its expression is not controlled by metals however, it does bind zinc. Another proposed role for metallothionein III is participation in the utilization of zinc as a neuromodulator, since metallothionein III is present in the neurons that store zinc in their terminal vesicles. Metallothionein IV occurs during differentiation of stratified squamous epithelium, but it is known to have a role in the absorption or toxicity of cadmium. [Pg.73]

Adams RD, Foley JM. The neurological disorder associated with liver disease. In Metabolic and Toxic Diseases of the Nervous System. (H.H. Merritt, and C.C. Hare, eds.)Vol. 32. WiUiams and Wilkins, Baltimore, USA, pp. 198-237, 1953 Ahboucha S, Butterworth RF. The neurosteroid system Implication in the pathophysiology of hepatic encephalopathy. Neurochem. Int., 52, 575-587, 2008 Ahboucha S, Pomier-Layrargues G, Mamer O, Butterworth RF. Increased brain concentrations of a neuroinhibitory steroid in human hepatic encephalopathy. Arm. Neurol, 58, 169-170, 2005 Ahboucha S, Coyne L, Hirakawa R, Butterworth RF, Halliwell RF. An interaction between benzodiazepines and neuroactive steroids at GABA receptors in cultured hippocampal neurons. Neurochem. Int., 48, 703-707, 2006... [Pg.173]


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