Metabolism and Role of Phosphatidylinositol in Acetylcholinestimulated Membrane Function

Hokin-Neaverson, Mabel

doi:10.1007/978-1-4684-3276-3_40

Cited by 62 publications

(16 citation statements)

References 36 publications

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“…Of the major FFAs, arachidonic and stearic acids arise primarily from membrane lipids, which is consistent with the reduction in the brain phospholipids during hypoxia (25) and ischemia (26). Membrane phos pholipids are strongly implicated in synaptic transmission (27,28) and phospholipid metabolism dysfunction could impair synaptic transmission (29,30). In addition, it has been reported that fatty acids inhibit oxidative phosphorylation of in vitro mito chondrial preparations (31 ), and arachidonic acid has been shown to be capable of inducing brain edema in vitro (32) and in vivo (33).…”

Section: Discussionsupporting

confidence: 61%

Effects of idebenone (CV-2619) on the concentrations of acetylcholine and choline in various brain regions of rats with cerebral ischemia.

1984

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Abstract-The concentrations of acetylcholine (Ach) and choline in various brain regions of rats with and without cerebral ischemia and the effects of 6-(10-hydroxy decyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone, CV-2619) on the levels of these parameters were investigated.Cerebral ischemia was induced by a 200-sec occlusion of both common carotid arteries in animals in which both vertebral arteries had been permanently cauterized.The concentrations of Ach and choline in the brain were determined by means of pyrolysis gas chromato graphy.In normal rats, CV-2619 (10, 30 and 100 mg/kg, i.p.) did not alter the concentrations of Ach and choline in the brain regions examined. In the ischemic rats, a significant decrease in Ach and a marked increase in choline were observed in the cerebral cortex, hippocampus, striatum, and diencephalon. A slight increase in the concentration of choline was also observed in the cerebellum and brain stem. Pretreatment with CV-261 9 (10 mg/kg, i.p.) inhibited the decrease in Ach and the increase in choline in the forebrain regions.Moreover, the same dose of CV-261 9 inhibited the increment of lactate content and tended to inhibit the decrement of ATP content in the cerebral cortex. These results indicate that CV-261 9 inhibits alterations of the concentrations of Ach and choline in the brain of the ischemic rats; this inhibition may be due to the ameliorating effect of CV-261 9 on the dis turbance of cerebral energy metabolism under ischemic conditions.

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Section: Discussionsupporting

confidence: 61%

Effects of idebenone (CV-2619) on the concentrations of acetylcholine and choline in various brain regions of rats with cerebral ischemia.

1984

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“…The release of FFA from diacyl-GPI and from other phosphoglycerides is attributed largely to the action of phospholipase Az; however, the possibility that a portion of the labeled FFA may have been derived from phospholipase AJysophospholipase action or from the DG lipase action cannot be excluded (Cabot and Gatt, 1976;1977;. The presence of phospholipase A, alone would have yielded 2-[ 14C]arachidonoyl-GPI, but this product was not detected in our chromatographic system.…”

Section: Discussionmentioning

confidence: 76%

“…Although diacyl-GPI is regarded as a minor phospholipid in brain, previous studies in vivo have demonstrated that it is metabolically more active than other membrane phosphoglycerides, especially in the synaptosomal fraction Hawthorne and Pickard, 1979; Sun and Su, 1979). Other studies, in vitro, have also indicated that the breakdown of diacyl-GPI is an important cellular process, possibly associated with cell surface receptor functions as well as other types of membrane transport processes (for reviews, see Michell, 1975;Hokin-Neaverson, 1977; Hawthorne and Pickard, 1979).…”

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confidence: 99%

Degradation of Arachidonoyl‐Labeled Phosphatidylinositols by Brain Synaptosomes

Der

Sun

1981

Journal of Neurochemistry

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Incubation of synaptosomes together with 1-acyl-2-[14C]arachidonoyl-sn-glycerophosphoinositols (GPI) and sodium deoxycholate yielded diacylglycerols and free arachidonic acid. Diacylglycerol formation is attributed to hydrolysis by the diacyl-GPI-specific phospholipase C (EC 3.1.4.10), and this reaction requires sodium deoxycholate for optimal activity. The free arachidonic acid formed is attributed to hydrolysis of diacyl-GPI by phospholipase A (EC 3.1.1.5). Free fatty acid release was observed during incubation, even in the absence of bile salts, but this process was preferentially stimulated by sodium taurocholate. The release of fatty acids was not specific for diacyl-GPI, as similar release was obtained during incubation with other phosphoglycerides. In the presence of deoxycholate (2 mg/ml), the release of diacylglycerols was maximal at a diacyl-GPI concentration around 1.0 mM. However, the free fatty acid release was linear with respect to the substrate at least up to 1.4 mM. The rate of diacylglycerol release from diacyl-GPI was more rapid in the initial 30 min, whereas the free fatty acid release was linear with time up to 2 h. Under this incubation condition, calcium was found to stimulate both types of hydrolytic action, although the concentration needed to achieve this stimulation was rather high. This type of labeled precursor is potentially useful for studies of the different modes of diacyl-GPI degradation by enzymes in brain subcellular membranes.

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“…pineal cells (Eichberg et al, 1973;Smith and Hauser, 19811, and subcellular fractions or tissue slices of rat or guinea pig brain (Abdel-Latif et al, 1974;Miller and Leung, 1979;Schacht and Agranoff, 1972). Stimulusenhanced hydrolysis of PI has been quantitated in terms of reductions in PI content in pancreas and parotid gland (Hokin-Neaverson, 1976;Jones and Michell, 1976) and/or as loss of radioactivity from PI prelabeled with [3H]inositol or "'Pi in preparations of rat or guinea pig brain (Durell andGarland, 1969: Lunt andPickard, 1975).…”

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confidence: 99%

Light Enhances the Turnover of Phosphatidylinositol in Rat Retinas

Schmidt

1983

Journal of Neurochemistry

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Light stimulation of isolated rat retinas is shown to enhance the turnover of phosphatidylinositol (PI) as demonstrated by a light-dependent increase in [3H]inositol incorporation and concurrent hydrolysis of existing PI. Studies with rat retinas incubated with [3H]inositol and then microdissected at the level of the outer plexiform layer into photoreceptor cell and inner retina layers indicated that the light-enhanced incorporation of [3H]inositol was associated with the photoreceptor cell layer. The rate of PI hydrolysis in retinas prelabeled in vivo with [3H]inositol was higher in light than in dark incubations and was higher in the photoreceptor cell layer than within the inner retina. Within the photoreceptor cell layer. PI turnover involved 2%/min of the total PI content in dark and 6-8%/min in light. In contrast to what has been reported for stimulus-enhanced turnover of PI in some tissues, this light-enhanced turnover of PI in the retina was not associated with detectable reductions in PI content. Parallel studies of sodium (22Na) uptake demonstrated that the photoreceptor cells remained functional during these incubations as they retained the capacity to restrict the entry of 22Na in light but not in dark.

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Metabolism and Role of Phosphatidylinositol in Acetylcholinestimulated Membrane Function

Cited by 62 publications

References 36 publications

Effects of idebenone (CV-2619) on the concentrations of acetylcholine and choline in various brain regions of rats with cerebral ischemia.

Effects of idebenone (CV-2619) on the concentrations of acetylcholine and choline in various brain regions of rats with cerebral ischemia.

Degradation of Arachidonoyl‐Labeled Phosphatidylinositols by Brain Synaptosomes

Light Enhances the Turnover of Phosphatidylinositol in Rat Retinas

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