Cation transport and membrane potential properties of primary astroglial cultures from neonatal rat brains

Kimelberg, Harold K.; Bowman, Charles L.; Biddlecome, S.; Bourke, Robert S.

doi:10.1016/0006-8993(79)90470-0

Cited by 146 publications

(75 citation statements)

References 23 publications

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“…The existence of an uptake process together with a cation is well established in the kid ney and provides the basis for the action of loop diuretics, e.g., furosemide and ethacrynic acid, which block the active reuptake of chloride from renal tubuli and thus the establishment of a hyper tonic environment in the medulla. That this trans port mechanism does exist in astrocytes in primary cultures has been shown by Kimelberg and Biddlecome (1980), who found that furosemide de- creases both the initial uptake rate and the steady state level of 3 6CI. Potassium is not the counterion, since 4 2 K uptake is unaffected by ethacrynic acid (L. Hertz, unpublished experiment).…”

Section: Io N Tra Nsportmentioning

confidence: 78%

Features of Astrocytic Function Apparently Involved in the Response of Central Nervous Tissue to Ischemia-Hypoxia

Hertz

1981

J Cereb Blood Flow Metab

116

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Section: Io N Tra Nsportmentioning

confidence: 78%

Features of Astrocytic Function Apparently Involved in the Response of Central Nervous Tissue to Ischemia-Hypoxia

Hertz

1981

J Cereb Blood Flow Metab

116

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“…2). 17,18,19,20 and they may be important in H + regulation in mammalian neurons as well, The transmembrane Na + gradient sustained by a selective impermeability to Na + across plasma membranes plus the action of energy-requiring Na + pumps are thought to provide sufficient driving force to power both antiport systems 43,50 . Evidence suggests that in some cell types Cl − /HCO 3 − antiport may be an active process that requires ATP 4 .…”

Section: Resultsmentioning

confidence: 99%

“…Studies of ion transport mechanisms by Kimelberg and his colleagues indicate that astroglial cells provide a major source of HCO 3 − in brain 18 and may serve as important regulators of the organ's [H + ] homeostasis 19,20 . We have extended their theoretical model 19 to include neurons (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Hydrogen ion buffering during complete brain ischemia

1985

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“…Marked acidification may also influence neuronal vulnerability indirectly by damaging glial cells. Astrocytes are thought to help protect neurons by inactivating neurotransmitters, internalizing excess K+ and ammonia, and stabilizing tissue pH (Schousboe et al, 1977;Kimelberg et al, 1979; Hertz, 1981;Kaneko et al, 1988;Szerb, 1991). These cells appear to act as proton sinks, becoming preferentially acidotic during ischemia (Kraig and Nicholson, 1987; Kraig and Cheder, 1990).…”

Section: The Traditional Belief In the Acidotic Route Of Ischemic Damagementioning

confidence: 99%

Evolving Concepts About the Role of Acidosis in Ischemic Neuropathology

Tombaugh

Sapolsky

1993

Journal of Neurochemistry

188

109

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Cerebral ischemia is one of the most common neurological insults. Many pathological events are undoubtedly triggered by ischemia, but only recently has it become accepted that ischemic cell injury arises from a complex interaction between multiple biochemical cascades. Tissue acidosis is a well established feature of ischemic brain tissue, but its role in ischemic neuropathology is still not fully understood. Within the last few years, new evidence has challenged the historically negative view of acidosis and suggests that it may play more of a beneficial role than previously thought. This review reintroduces the concept of acidosis to ischemic brain injury and presents some new perspectives on its neuroprotective potential. Key Words: Ischemia-infarction-Lactic acidosis-Excitotoxicity-Hippocampus-Selective neuronal necrosis -Energy metabolism. Experimental work aimed at understanding ischemic brain injury has highlighted numerous biochemical events that may mediate cell damage. Among these, tissue acidosis has received considerable attention. The history of the acidotic concept in ischemia research forms somewhat of an arch. A number of decades ago, cerebral acidosis was shown first to be a correlate of gross ischemic brain damage and was viewed later as a cause. At the height of interest in this topic, acidosis was considered among the principal mechanisms by which ischemic damage occurs (Myers, 1979;Siesjo, 1988~). Even so, it was clear that "cerebral ischemia" was not a single disease but any insult that involved a partial or complete reduction in cerebral blood flow. Various animal models of both focal and global ischemia have been widely used to study ischemic injury, but the question of whether tissue acidosis satisfactorily explains or even contributes to all forms of ischemic brain injury has never been formally addressed.Though acidosis is generally believed to underlie cerebral infarction, mounting evidence has suggested that acidosis does not contribute to the selective neuronal necrosis that occurs after transient ischemia or in the penumbra of developing infarcts. Not surprisingly, the earlier bias toward acidosis as a neurotoxic mechanism has waned. In this review, we briefly examine the evolution of the acidosis concept. We then focus on a recent and surprising series of in vitro observations suggesting that moderate acidosis may actually play a neuroprotective role during ischemia. We then discuss a striking and paradoxical implication of these data regarding the time course and possible mediators of selective neuronal injury following ischemia. THE TRADITIONAL BELIEF IN THE ACIDOTIC ROUTE OF ISCHEMIC DAMAGESupported by varying degrees of experimental evidence, many distinct mechanisms have been proposed to explain ischemic brain injury; of these, the concept of acidotic damage is perhaps the oldest. Early work suggested that metabolic acidosis, caused by continued glycolysis, was responsible for the severe tissue disruption seen in the postmortem brain (Friede and van Houten, 1961). D...

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Cation transport and membrane potential properties of primary astroglial cultures from neonatal rat brains

Cited by 146 publications

References 23 publications

Features of Astrocytic Function Apparently Involved in the Response of Central Nervous Tissue to Ischemia-Hypoxia

Features of Astrocytic Function Apparently Involved in the Response of Central Nervous Tissue to Ischemia-Hypoxia

Hydrogen ion buffering during complete brain ischemia

Evolving Concepts About the Role of Acidosis in Ischemic Neuropathology

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