Reductions of Γ‐Aminobutyric Acid and Glutamate Uptake and (Na<sup>+</sup>+ K<sup>+</sup>)‐ATPase Activity in Brain Slices and Synaptosomes by Arachidonic Acid

Chan, Pak H.; Kerlan, Randi; Fishman, Robert A.

doi:10.1111/j.1471-4159.1983.tb11284.x

Cited by 197 publications

(56 citation statements)

References 39 publications

(29 reference statements)

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“…Although FFA have been shown to inhibit this enzyme (7,63,64), it is not known if the inhibition is due to direct interactions between FFA and enzyme or due to effects of FFA on the membrane matrix. The release of polyunsaturated fatty acids may be involved in producing the capillary endothelial defects that can be observed within 2 min after injury (33,65).…”

Section: Discussionmentioning

confidence: 99%

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Membrane lipid changes in laminectomized and traumatized cat spinal cord.

Demediuk¹,

Saunders²,

Anderson³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

157

105

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Free fatty acid (FFA), diacyiglycerol (acyl2-Gro), icosanoid, phospholipid, and cholesterol levels were measured in samples of cat spinal cord (L2) that were frozen in situ (i) with vertebrae intact, (ii) at various times after laminectomy, and (iu) at various times after laminectomy with compression trauma to the spinal cord. Tissue samples either were grossly dissected into gray and white portions prior to FFA and acyl2Gro analysis or were used whole for the other lipid types. Gray matter total FFA and acyl2Gro values were abnormally high in samples frozen with vertebrae intact and in those frozen 10 min after laminectomy. This indicates that the surgical procedures resulted in some perturbation of spinal cord lipid metabolism. If the experimental animals were allowed to recover for 90 min after laminectomy, the gray matter FFA and acyl2Gro levels were greatly reduced. Compression of the spinal cord with a 170-g weight for 1, 3, or 5mm (following 90 min of recovery after laminectomy) caused significant elevations of total FFA, acyl2Gro, icosanoids, and phosphatidic acid and significant decreases in ethalamine plasmalogens and cholesterol. Among the total FFA, arachidonic acid was found to have the largest relative increase. Comparisons of gray and white matter demonstrate that, in general, changes in white matter FFA and acyl2Gro were similar to those seen in gray matter. However, the increases in white matter levels of FFA and acyl2Gro were delayed, occurring after the elevations in gray matter. For some FFA (e.g., arachidonate), the rise in white matter occurred as gray matter levels were decreasing. This suggests that the initial alteration in spinal cord lipid metabolism after trauma was in gray matter but, with time, spread radially into white matter.

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Section: Discussionmentioning

confidence: 99%

“…Within the FFA fraction, liberated arachidonic acid may act as a substrate for metabolism to biologically active prostaglandins, thromboxanes, and leukotrienes (icosanoids) (10). Arachidonic acid has also been implicated in the edema production and swelling seen after brain injury (11,12).…”

mentioning

confidence: 99%

Membrane lipid changes in laminectomized and traumatized cat spinal cord.

Demediuk¹,

Saunders²,

Anderson³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

157

105

View full text Add to dashboard Cite

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“…Determination of Na +,K + -ATPase activity Na + ,K + -ATPase activity was assayed as described previously (Chan et al , 1983b). The protein content of each homogenate was determined by the method of Lowry et a1.…”

Section: Measurement Of Total Brain Water and Na+/k+ Contentmentioning

confidence: 99%

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na⁺,K⁺ -ATPase Activity

Mintorovitch

Yang

Shimizu

et al. 1994

J Cereb Blood Flow Metab

191

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Summary: Diffusion-weighted magnetic resonance (MR) images from rats during acute cerebral ischemia induced by middle cerebral artery occlusion were analyzed for correspondence with changes in brain water, cation con centrations , and Na + ,K + -ATPase activity measured in vitro after 30 or 60 min of ischemia. In the ischemic hemi sphere, signal intensity was increased at 30 min (p < 0.05 vs contralateral hemisphere) and further increased at 60 min. Na + ,K + -ATPase activity was 34% lower in isch emic cortex and 40% lower in ischemic basal ganglia after 30 min (p < 0.05), but water content and Na + and K + concentrations were not significantly different between Diffusion-weighted magnetic resonance (MR) im aging can detect less severe and potentially revers ible cerebral ischemia much earlier than conven tional T2-weighted MR imaging (Moseley et aI., 1990; Mintorovitch et aI., 1991; Minematsu et aI., 1992; van Bruggen et aI., 1992 Abbreviations used: ADC, apparent diffusion coefficient; ANOV A, analysis of variance; MCA, middle cerebral artery; MR, magnetic resonance; TE, echo time; TR, repetition time. 332hemispheres. After 60 min , water content and Na + con centration were increased , and both Na + ,K + -ATPase activity and K + concentration were decreased in the ischemic hemisphere (p < 0.05). These findings are con sistent with the hypothesis that the early onset of signal hyperintensity in diffusion-weighted MR images may re flect cellular edema associated with impaired membrane pump function. Early in vivo detection and localization of potentially reversible ischemic cerebral edema may have important research and clinical applications.

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“…Moreover, elevated levels of arachidonic acid are observed after cerebral ischaemia and hypoglycaemia both in vivo (Bazan, 1970) and in vitro (Lazarewicz et al, 1992;Williams et al, 1995). Arachidonic acid potently inhibits Na + -dependent glutamate uptake into synaptosomes and astrocytes (Chan et al, 1983;Barbour et al, 1989;Volterra et al, 1994) and, thereby, potentially induces neuronal damage via an overactivation of glutamate receptors. Thus, factors that are involved in the modulation of glutamate-evoked arachidonic acid release may potentially affect both the physiology and the pathophysiology of the CNS.…”

mentioning

confidence: 99%

Hydrogen Peroxide Enhances Signal‐Responsive Arachidonic Acid Release from Neurons: Role of Mitogen‐Activated Protein Kinase

Samanta

Perkinton

Morgan

et al. 1998

Journal of Neurochemistry

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Abstract:Hydrogen peroxide (H 202) is a potent stimulator of signal-responsive phospholipase A2 (PLA2) in vascular smooth muscle and cultured endothelial cells. We investigated whether H202 plays a similar regulatory role in neurons. H202 did not stimulate a release of arachidonic acid from cultured neurons when applied alone but strongly enhanced the liberation of arachidonic acid evoked by maximally effective concentrations of either glutamate, the glutamate receptor agonist N-methyl-Daspartate (NMDA), the muscarinic receptor agonist carbachol, the Na + -channel opener veratridine, or the Ca 2-ionophore ionomycin. The potentiating effects of H 202 were strongly inhibited in the presence of the PLA2 inhibitor mepacrine, suggesting that the site of action was within the signal responsive arachidonic acid cascade. The enhancing effect of H202 was not reversed by protein kinase C inhibitors (chelerythrine chloride or GF 1 09203X) nor was it mimicked by phorbol ester treatment. H202 alone strongly enhanced the levels of immunodetectable activated mitogen-activated protein kinase (activated MAP kinases ERK1 and ERK2) in a Ca 2~-dependent manner and this effect was additive with increases in the levels of activated MAP kinase evoked by glutamate. The enhanced release of arachidonic acid, however, was not clearly reversed by the MAP kinase kinase (MEK) inhibitor PD 98059, although this treatment effectively abolished H 202 activation of MAP kinase. Thus, MAP kinase activation and Ca 2~-dependent arachidonic acid release are regulated by oxidative stress in cultured striatal neurons.

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Reductions of Γ‐Aminobutyric Acid and Glutamate Uptake and (Na⁺+ K⁺)‐ATPase Activity in Brain Slices and Synaptosomes by Arachidonic Acid

Cited by 197 publications

References 39 publications

Membrane lipid changes in laminectomized and traumatized cat spinal cord.

Membrane lipid changes in laminectomized and traumatized cat spinal cord.

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na⁺,K⁺ -ATPase Activity

Hydrogen Peroxide Enhances Signal‐Responsive Arachidonic Acid Release from Neurons: Role of Mitogen‐Activated Protein Kinase

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Reductions of Γ‐Aminobutyric Acid and Glutamate Uptake and (Na++ K+)‐ATPase Activity in Brain Slices and Synaptosomes by Arachidonic Acid

Cited by 197 publications

References 39 publications

Membrane lipid changes in laminectomized and traumatized cat spinal cord.

Membrane lipid changes in laminectomized and traumatized cat spinal cord.

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na+,K+ -ATPase Activity

Hydrogen Peroxide Enhances Signal‐Responsive Arachidonic Acid Release from Neurons: Role of Mitogen‐Activated Protein Kinase

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Product

Resources

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Reductions of Γ‐Aminobutyric Acid and Glutamate Uptake and (Na⁺+ K⁺)‐ATPase Activity in Brain Slices and Synaptosomes by Arachidonic Acid

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na⁺,K⁺ -ATPase Activity