Mechanisms of glial swelling induced by glutamate

Schneider, G.-H.; Baethmann, A.; Kempski, Oliver

doi:10.1139/y92-280

Cited by 94 publications

(50 citation statements)

References 33 publications

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“…causes swelling (Schneider et al, 1992). On the other hand, glutamine release into the extracellular space would help reduce the osmotic gradient between the astrocyte and the extracellular space, and thus decrease the degree of swelling.…”

Section: Glutamine/glutamatementioning

confidence: 99%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome that typically develops as a result of acute liver failure or chronic liver disease. Brain edema is a common feature associated with HE. In acute liver failure, brain edema contributes to an increase in intracranial pressure, which can fatally lead to brain stem herniation. In chronic liver disease, intracranial hypertension is rarely observed, even though brain edema may be present. This discrepancy in the development of intracranial hypertension in acute liver failure versus chronic liver disease suggests that brain edema plays a different role in relation to the onset of HE. Furthermore, the pathophysiological mechanisms involved in the development of brain edema in acute liver failure and chronic liver disease are dissimilar. This review explores the types of brain edema, the cells, and pathogenic factors involved in its development, while emphasizing the differences in acute liver failure versus chronic liver disease. The implications of brain edema developing as a neuropathological consequence of HE, or as a cause of HE, are also discussed. HighlightsBrain edema is a common feature in ALF and CLD. HE is inconsistently associated with the presence of brain edema. Fibrous and protoplasmic astrocytes are differentially implicated in the pathogenesis of HE. The pathogenesis of HE is multifactorial causing an array of neurological symptoms.

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Section: Glutamine/glutamatementioning

confidence: 99%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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“…Also, astrocytes are found to undergo swelling after stimulation with glutamate [64] as well as during hyperammonemia [65,66] and lactacidosis [67]. Therefore, it is conceivable that ATP release from swollen astrocytes plays some role in such pathological conditions.…”

Section: +mentioning

confidence: 99%

Maxi-anion channel as a candidate pathway for osmosensitive ATP release from mouse astrocytes in primary culture

et al. 2008

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In the present study, we aimed to evaluate the pathways contributing to ATP release from mouse astrocytes during hypoosmotic stress. We first examined the expression of mRNAs for proteins constituting possible ATPreleasing pathways that have been suggested over the past several years. In RT-PCR analysis using both control and osmotically swollen astrocytes, amplification of cDNA fragments of expected size was seen for connexins (Cx32, Cx37, Cx43), pannexin 1 (Px1), the P2X7 receptor, MRP1 and MDR1, but not CFTR. Inhibitors of exocytotic vesicular release, gap junction hemi-channels, CFTR, MRP1, MDR1, the P2X7 receptor, and volume-sensitive outwardly rectifying chloride channels had no significant effects on the massive ATP release from astrocytes. In contrast, the hypotonicity-induced ATP release from astrocytes was most effectively inhibited by gadolinium (50 µM), an inhibitor of the maxi-anion channel, which has recently been shown to serve as a pathway for ATP release from several other cell types. Thus, we propose that the maxi-anion channel constitutes a major pathway for swelling-induced ATP release from cultured mouse astrocytes as well.

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“…Exposure of cultured astrocytes to glutamate leads to significant cell swelling [15]. Finally, it is conceivable that, under certain circumstances, reduction in the capacity for glutamate uptake by astrocytes as a result of decreased GLT-1 expression could impair ammonia removal by brain.…”

Section: Western Blottingmentioning

confidence: 99%

Decreased glutamate transporter (GLT-1) expression in frontal cortex of rats with acute liver failure

Knecht

Michalak

Rose

et al. 1997

Neuroscience Letters

169

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Knecht, K. et al., 1997. Decreased glutamate transporter (GLT-1) expression in frontal cortex of rats with acute liver failure. Neuroscience Letters, 229(3), The final publication is available at http://dx.doi.org/10.1016/S0304-3940 (97) ABSTRACTIt has been suggested that reduced astrocytic uptake of neuronally released glutamate contributes to the pathogenesis of hepatic encephalopathy in acute liver failure. In order to further address this issue, the recently cloned and sequenced astrocytic glutamate transporter GLT-1 was studied in brain preparations from rats with ischemic liver failure induced by portacaval anastomosis followed 24 h later by hepatic artery ligation and from appropriate sham-operated controls. GLT-1 expression was studied using reverse transcriptase-polymerase chain reaction (RT-PCR). Expression of GLT-1 transcript was significantly decreased in frontal cortex at coma stages of acute liver failure. Western blotting using a polyclonal antibody to GLT-1 revealed a concomitant decrease in expression of transporter protein in the brains of rats with acute liver failure. Reduced capacity of astrocytes to reuptake neuronally released glutamate, resulting from a GLT-1 transporter deficit and the consequently compromised neuron-astrocytic trafficking of glutamate could contribute to the pathogenesis of hepatic encephalopathy and brain edema, two major complications of acute liver failure.Keywords GLT-1; hepatic encephalopathy; Astrocytes; Neuron-astrocyte trafficking; Gene expression; RT-PCR; Western blottingAcute liver failure resulting from viral infections or ingestion of toxic substances results in severe neurological impairment progressing through stupor and coma within hours or days. The pathophysiologic mechanisms responsible for hepatic encephalopathy (HE) in acute liver failure are unknown but deficits of neurotransmission rather than primary cerebral energy failure are currently considered to be implicated [1 and 3]. In this regard, there is increasing evidence to suggest that abnormalities of the glutamate neurotransmitter system are involved in the pathogenesis of HE in acute liver failure. Brain concentrations of glutamate are reduced in both human [13]and experimental [7 and 17] acute liver failure and recent studies using in vivo cerebral microdialysis in both rats 2 and 9and rabbits [5]with acute (ischemic) liver failure have consistently revealed increased extracellular brain concentrations of glutamate. It was suggested that the increased extracellular concentrations of glutamate in the brain of these animals was the consequence of decreased astrocytic uptake [9]. The major high affinity astrocytic transporter for glutamate, GLT-1, has recently been cloned and sequenced 12 and 14. In order to directly assess glutamate uptake capacity in the brain in acute liver failure, GLT-1 gene and protein expression were measured in frontal cortex of rats with acute (ischemic) liver failure.Male, Sprague-Dawley rats (175-200 g) were anesthetized with halothane and an end-to-side portacaval ...

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Mechanisms of glial swelling induced by glutamate

Cited by 94 publications

References 33 publications

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Maxi-anion channel as a candidate pathway for osmosensitive ATP release from mouse astrocytes in primary culture

Decreased glutamate transporter (GLT-1) expression in frontal cortex of rats with acute liver failure

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