Direct assay for calcium in brain homogenates and synaptosomal pellets

Schmidt, William K.; Way, E. Leong

doi:10.1111/j.1471-4159.1979.tb04599.x

Cited by 16 publications

(9 citation statements)

References 21 publications

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“…The values are not corrected for recovery, which was virtually 100% for the TCA method, but lower than 70%, and more variable, for the wet-ashing method. Apparently, the extraction of the various cations is virtually complete using the TCA extraction procedure, which is in agreement with a report of Schmidt and Way (1979). Higher and more variable blanks were obtained after solubilization.…”

Section: Resultssupporting

confidence: 92%

Regional Calcium Accumulation and Cation Shifts in Rat Brain by Kainate

Korf¹,

Postema²

1984

Journal of Neurochemistry

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Following local application of kainic acid, changes in the contents of Na+, K+, Ca2+, and Mg2+ of the striatum, cerebellum, and hippocampus of the rat were observed at various times after surgery. Within 1 h the levels of K+ decreased 20% whereas the levels of Na+ and Ca2+ increased at least 50% and 20%, respectively. These changes persisted for more than 8 weeks. Ca2+ levels rose further, to more than 10-fold during 8 weeks. The Mg2+ levels were slightly and only transiently decreased. Unilateral injections of kainate into the striatum affected the contents of these cations not only in this area, but also in the overlying cerebral cortex, the olfactory tubercle, and the ipsilateral substantia nigra. The Ca2+ increases were less when rats were kept on a diet deficient in Ca2+ and vitamin D. 45Ca2+, intravenously administered, accumulated significantly more in the kainate-lesioned striatum and substantia nigra than in the homotopic contralateral areas. Electron microscopic examination of the localization of Ca2+ with the oxalate-pyroantimonate technique showed the appearance of extracellularly located deposits and the accumulation of Ca2+ in (possibly degenerating) myelinated axons in kainate-lesioned striata. This study provides evidence that calcification of cerebral tissue is closely associated with neurodegenerative processes and shows that kainate may serve as a tool to elucidate the mechanism of brain calcification. The results are discussed in relation to idiopathic calcinosis (striopallidodentate calcinosis, Fahr's disease).

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Section: Resultssupporting

confidence: 92%

Regional Calcium Accumulation and Cation Shifts in Rat Brain by Kainate

Korf¹,

Postema²

1984

Journal of Neurochemistry

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“…In some of these studies, whole nervous tissue homogenates were used (Schmidt and Way, 1979). In addition, our results illustrate the unique compartmentalization of water in nerve cells and axons.…”

Section: Discussionmentioning

confidence: 69%

Distribution of Elements in Rat Peripheral Axons and Nerve Cell Bodies Determined by X‐Ray Microprobe Analysis

LoPachin¹,

Lowery

Eichberg

et al. 1988

Journal of Neurochemistry

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X-ray microprobe analysis was used to determine concentrations (millimoles of element per kilogram dry weight) of Na, P, Cl, K, and Ca in cellular compartments of frozen, unfixed sections of rat sciatic and tibial nerves and dorsal root ganglion (DRG). Five compartments were examined in peripheral nerve (axoplasm, mitochondria, myelin, extraaxonal space, and Schwann cell cytoplasm), and four were analyzed in DRG nerve cell bodies (cytoplasm, mitochondria, nucleus, and nucleolus). Each morphological compartment exhibited characteristic concentrations of elements. The extraaxonal space contained high concentrations of Na, Cl, and Ca, whereas intraaxonal compartments exhibited lower concentrations of these elements but relatively high K contents. Nerve axoplasm and axonal mitochondria had similar elemental profiles, and both compartments displayed proximodistal gradients of decreasing levels of K, Cl, and, to some extent, Na. Myelin had a selectively high P concentration with low levels of other elements. The elemental concentrations of Schwann cell cytoplasm and DRG were similar, but both were different from that of axoplasm, in that K and Cl were markedly lower whereas P was higher. DRG cell nuclei contained substantially higher K levels than cytoplasm. The subcellular distribution of elements was clearly shown by color-coded images generated by computer-directed digital x-ray imaging. The results of this study demonstrate characteristic elemental distributions for each anatomical compartment, which doubtless reflect nerve cell structure and function.

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“…As expected from our earlier study, 9 tion spectrometry, as previously described. 9, 26 Liver was hothere was a threefold increase in total hepatic calcium mogenized in 5% lanthanum chloride and 25% HCl, and procontent in livers removed 19 hours after halothane extein was precipitated by 5% trichloroacetic acid; the posure compared with nonexposed guinea pigs (Table supernatant was used for calcium determination. The protein 3).…”

Section: Methodsmentioning

confidence: 99%

Impaired bile flow and disordered hepatic calcium homeostasis are early features of halothane-induced liver injury in guinea pigs

et al. 1996

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To characterize the early events in liver injury produced by halothane, experiments were performed in genetically susceptible guinea pigs 19 hours after halothane exposure. Serum bile acid concentrations were fourfold increased in halothane-exposed animals compared with controls. In isolated perfused liver experiments, livers from halothane-exposed animals did not differ in hepatic oxygen uptake or in perfusion pressure at the end of experiments, but bile flow and biliary bile salt concentrations were reduced. Hepatic calcium content was increased in halothane-exposed guinea pigs compared with controls, and further experiments were performed to explore the reason for this. As determined by infusion of 45Ca to steady-state perfusate concentrations, hepatic calcium clearance was increased in halothane-exposed guinea pigs compared with controls (0.37 +/- 0.06 vs. 0.28 +/- 0.02 mL/min, P < .01). Decreased biliary excretion of calcium was also noted and was entirely attributable to reduced bile flow. However, although decreased excretion contributed to hepatic accumulation of calcium, it was quantitatively less important than enhanced hepatic uptake. As indicated by passage of a bolus of horseradish peroxidase from perfusate into bile, hepatic tight junction permeability was increased five-fold after halothane exposure. It is concluded that cholestasis, as exemplified by reduced bile flow, is an early feature of the liver injury produced by halothane in guinea pigs and is associated with increased tight junction permeability. Although the decrease in bile flow contributes to an early increase in hepatic calcium content, entry of calcium from the perfusion compartment is quantitatively more important.

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Direct assay for calcium in brain homogenates and synaptosomal pellets

Cited by 16 publications

References 21 publications

Regional Calcium Accumulation and Cation Shifts in Rat Brain by Kainate

Regional Calcium Accumulation and Cation Shifts in Rat Brain by Kainate

Distribution of Elements in Rat Peripheral Axons and Nerve Cell Bodies Determined by X‐Ray Microprobe Analysis

Impaired bile flow and disordered hepatic calcium homeostasis are early features of halothane-induced liver injury in guinea pigs

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