FORMATION OF PHOSPHATIDES FROM C14-LABELLED PRECURSORS IN RAT BRAIN SLICES. EFFECT OF CHLORPROMAZINE

1963 ◽  
Vol 41 (1) ◽  
pp. 341-345 ◽  
Author(s):  
E. T. Pritchard ◽  
R. J. Rossiter
Keyword(s):  
Guinea Pig ◽  
Phosphatidic Acid ◽  
Rat Brain ◽  
Phosphatidyl Ethanolamine ◽  
Brain Slices ◽  
Phosphatidyl Inositol ◽  
Phosphatidyl Serine ◽  
Inorganic P ◽  
The Individual ◽  
Guinea Pig Brain

The addition of chlorpromazine (0.1 mM) to slices of rat brain respiring in a suitable medium caused an increase in the incorporation of radioactivity from glycerol-1-C14, glycine-2-C14, and serine-3-C14 into the phospholipids of the slices. There was no increase in the incorporation of radioactivity from choline-1,2-C14 or ethanolamine-1,2-C14. Examination of the individual phosphatides showed an increase in the incorporation of radioactivity from glycerol-1-C14 into phosphatidc acid and phosphatidyl serine, with no change for lecithin and phosphatidyl ethanolamine. Higher concentrations of chlorpromazine (1.0 mM) either inhibited (glycerol-1-C14, choline-1,2-C14), did not significantly alter (glycine-2-C14, ethanolamine-1,2-C14), or stimulated (serine-3-C14) the incorporation of radioactivity into phospholipids. These results are discussed in relation to previous experiments, in which it was found that the addition of chlorpromazine (0.1 mM) to slices of guinea pig brain caused an increase in the incorporation of inorganic P32 into phosphatidic acid, phosphatidyl inositol, phosphatidyl serine, but not into lecithin or phosphatidyl ethanolamine.

FORMATION OF PHOSPHATIDES FROM C14-LABELLED PRECURSORS IN RAT BRAIN SLICES. EFFECT OF CHLORPROMAZINE

1963 ◽  
Vol 41 (2) ◽  
pp. 341-345 ◽  
Author(s):  
E. T. Pritchard ◽  
R. J. Rossiter
Keyword(s):  
Guinea Pig ◽  
Phosphatidic Acid ◽  
Rat Brain ◽  
Phosphatidyl Ethanolamine ◽  
Brain Slices ◽  
Phosphatidyl Inositol ◽  
Phosphatidyl Serine ◽  
Inorganic P ◽  
The Individual ◽  
Guinea Pig Brain

The addition of chlorpromazine (0.1 mM) to slices of rat brain respiring in a suitable medium caused an increase in the incorporation of radioactivity from glycerol-1-C14, glycine-2-C14, and serine-3-C14 into the phospholipids of the slices. There was no increase in the incorporation of radioactivity from choline-1,2-C14 or ethanolamine-1,2-C14. Examination of the individual phosphatides showed an increase in the incorporation of radioactivity from glycerol-1-C14 into phosphatidc acid and phosphatidyl serine, with no change for lecithin and phosphatidyl ethanolamine. Higher concentrations of chlorpromazine (1.0 mM) either inhibited (glycerol-1-C14, choline-1,2-C14), did not significantly alter (glycine-2-C14, ethanolamine-1,2-C14), or stimulated (serine-3-C14) the incorporation of radioactivity into phospholipids. These results are discussed in relation to previous experiments, in which it was found that the addition of chlorpromazine (0.1 mM) to slices of guinea pig brain caused an increase in the incorporation of inorganic P32 into phosphatidic acid, phosphatidyl inositol, phosphatidyl serine, but not into lecithin or phosphatidyl ethanolamine.

INCORPORATION OF INORGANIC P32INTO PHOSPHOLIPIDS OF BRAIN SLICES: EFFECT OF CERTAIN TRANQUILLIZING DRUGS

1963 ◽  
Vol 41 (1) ◽  
pp. 1155-1162 ◽  
Author(s):  
W. L. Magee ◽  
R. J. Rossiter
Keyword(s):  
Methylene Blue ◽  
Guinea Pig ◽  
Aerobic Glycolysis ◽  
Brain Slices ◽  
Inorganic P ◽  
Pig Brain ◽  
Low Concentrations ◽  
High Concentrations ◽  
Derivatives Of ◽  
Guinea Pig Brain

Promazine, promethazine, tetrameprazine, and WY 1172, four tranquillizing drugs that are derivatives of phenothiazine, resembled chlorpromazine in that when they were added in a concentration of 0.1 mM to slices of guinea pig brain respiring in a suitable medium they stimulated the incorporation of inorganic P32into the phospholipids of the slices. With one of the drugs, promethazine, this concentration of 0.1 mM was found to cause no significant increase in respiration, in aerobic glycolysis, or in the concentration of phosphocreatine. In higher concentrations (1.0 mM), all of the compounds inhibited the labelling of phospholipid. Promethazine caused a reduction in respiration and in the concentration of phosphocreatine, accompanied by an increase in aerobic glycolysis. Methylene blue, a derivative of phenothiazine with no reported tranquillizing properties, did not stimulate the labelling of phospholipid in brain slices. Azacyclonol, pipradrol, and mepazine, drugs that are derivatives of piperidine, also stimulated phospholipid labelling in low concentrations and inhibited the labelling at higher concentrations. Piperidine and benzhydrol, the two components from which azacyclonol is derived, did not stimulate phospholipid labelling at the concentration which was most effective for azacyclonol. Low concentrations of benzhydrol, however, caused a slight stimulation. Meprobamate and phenaglycodol, two other compounds with reputed tranquillizing action, had either little or no effect. Most of the substances tested inhibited phospholipid labelling when they were added in sufficiently high concentrations.

PHOSPHOLIPIDS OF EHRLICH ASCITES TUMOR

1964 ◽  
Vol 42 (3) ◽  
pp. 299-308 ◽  
Author(s):  
H. David ◽  
R. J. Rossiter
Keyword(s):  
Phosphatidic Acid ◽  
Microsomal Fraction ◽  
Phosphatidyl Ethanolamine ◽  
Specific Radioactivity ◽  
Phosphatidyl Inositol ◽  
Ehrlich Ascites Carcinoma ◽  
Inorganic P ◽  
High Specific Radioactivity ◽  
Ehrlich Ascites ◽  
Ethanolamine Plasmalogen

The following phosphatides (in approximate order of concentration) were studied in cells of the Ehrlich ascites carcinoma incubated in a medium containing inorganic P32: lecithin > sphingomyelin > phosphatidyl ethanolamine = phosphatidyl inositol = phosphatidic acid > choline plasmalogen = phosphatidyl serine > ethanolamine plasmalogen. The specific radioactivity of the diacyl-glycerophosphatide fraction exceeded that of both the plasmalogen and the sphingomyelin – glycerol ether phosphatide fraction, the specific radioactivity of the individual phosphatides being as follows: phosphatidic acid > phosphatidyl inositol > ethanolamine plasmalogen > phosphatidyl ethanolamine = choline plasmalogen = lecithin > sphingomyelin. The microsomal fraction contained more phospholipid, followed by the mitochondrial and nuclear fractions, in that order. The specific radioactivities of the phospholipids of the microsomes and nuclei were greater than that of the mitochondria, chiefly because of the high specific radioactivity of the diacylglycerophosphatide fraction. The high specific radioactivity of the diacylglycerophosphatides was largely the result of a very active incorporation of inorganic P32into phosphatidic acid, particularly in the microsomal fraction. The significance of these findings is discussed.

INCORPORATION OF INORGANIC P32INTO PHOSPHOLIPIDS OF BRAIN SLICES: EFFECT OF CERTAIN TRANQUILLIZING DRUGS

1963 ◽  
Vol 41 (5) ◽  
pp. 1155-1162 ◽  
Author(s):  
W. L. Magee ◽  
R. J. Rossiter
Keyword(s):  
Methylene Blue ◽  
Guinea Pig ◽  
Aerobic Glycolysis ◽  
Brain Slices ◽  
Inorganic P ◽  
Pig Brain ◽  
Low Concentrations ◽  
High Concentrations ◽  
Derivatives Of ◽  
Guinea Pig Brain

Promazine, promethazine, tetrameprazine, and WY 1172, four tranquillizing drugs that are derivatives of phenothiazine, resembled chlorpromazine in that when they were added in a concentration of 0.1 mM to slices of guinea pig brain respiring in a suitable medium they stimulated the incorporation of inorganic P32into the phospholipids of the slices. With one of the drugs, promethazine, this concentration of 0.1 mM was found to cause no significant increase in respiration, in aerobic glycolysis, or in the concentration of phosphocreatine. In higher concentrations (1.0 mM), all of the compounds inhibited the labelling of phospholipid. Promethazine caused a reduction in respiration and in the concentration of phosphocreatine, accompanied by an increase in aerobic glycolysis. Methylene blue, a derivative of phenothiazine with no reported tranquillizing properties, did not stimulate the labelling of phospholipid in brain slices. Azacyclonol, pipradrol, and mepazine, drugs that are derivatives of piperidine, also stimulated phospholipid labelling in low concentrations and inhibited the labelling at higher concentrations. Piperidine and benzhydrol, the two components from which azacyclonol is derived, did not stimulate phospholipid labelling at the concentration which was most effective for azacyclonol. Low concentrations of benzhydrol, however, caused a slight stimulation. Meprobamate and phenaglycodol, two other compounds with reputed tranquillizing action, had either little or no effect. Most of the substances tested inhibited phospholipid labelling when they were added in sufficiently high concentrations.

scholarly journals Platelet Phospholipid Changes in Atherosclerosis

1977 ◽  
Author(s):  
A. Z. Aktulga ◽  
O. N. Ulutin
Keyword(s):  
Fibrinolytic Activity ◽  
Phosphatidyl Ethanolamine ◽  
Total Phospholipid ◽  
Phosphatidyl Inositol ◽  
Phosphatidyl Serine ◽  
Platelet Phospholipid ◽  
Lipid Contents ◽  
Coagulation Mechanism ◽  
The Individual ◽  
Platelet Functions

The platelet phospholipids content and their per cent distribution in atherosclerotic cases and in thromboembolic cases related to atherosclerosis was investigated with respect to normals. In normals the total phospholipid phosphorus value was found to be 10.88±0.24μg/109 platelets whereas this value changed to 14.29±0.39μg/109 platelets in atherosclerosis. The individual phospholipids follow the decreasing order of phosphatidyl choline, phosphatidyl ethanolamine, sphingomyeline, phosphatidyl serine, phosphatidyl inositol. In atherosclerotic cases although no difference was observed in this order, there was an increase in the quantity of certain phospholipids. In these cases the coagulation mechanism, the fibrinolytic activity, the platelet functions, and the serum lipid contents were also investigated in comparison to the above findings.

scholarly journals The glial antioxidant network and neuronal ascorbate: protective yet permissive for H2O2 signaling

2004 ◽  
Vol 1 (4) ◽  
pp. 365-376 ◽  
Author(s):  
MARAT V. AVSHALUMOV ◽  
DUNCAN G. MACGREGOR ◽  
LILLY M. SEHGAL ◽  
MARGARET E. RICE
Keyword(s):  
Guinea Pig ◽  
Rat Brain ◽  
Brain Tissue ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Brain Slices ◽  
Edema Formation ◽  
Pig Brain ◽  
The Brain ◽  
Guinea Pig Brain

Increasing evidence implicates reactive oxygen species, particularly hydrogen peroxide (H2O2), as intracellular and intercellular messengers in the brain. This raises the question of how the antioxidant network in the brain can be sufficiently permissive to allow messages to be conveyed yet, at the same time, provide adequate protection against oxidative damage. Here we present evidence that this is accomplished in part by differential antioxidant compartmentalization between glia and neurons. Based on the rationale that the glia-to-neuron ratio is higher in guinea-pig brain than in rat brain, we examined the neuroprotective role of the glial antioxidant network by comparing the consequences of H2O2 elevation in slices of guinea-pig and rat brain. The effects of exogenously applied H2O2 on evoked population spikes in hippocampal slices and on edema formation in forebrain slices were assessed. In contrast to the epileptiform activity observed in rat hippocampal slices after H2O2 exposure, no pathophysiology was seen in guinea-pig hippocampal slices. Similarly, elevated H2O2 caused edema in rat brain slices but not in guinea-pig brain tissue. The resistance of guinea-pig brain tissue to H2O2 challenge was lost, however, when glutathione (GSH) synthesis was inhibited (by buthionine sulfoximine), GSH peroxidase activity was inhibited (by mercaptosuccinate) or catalase was inhibited (by 3-amino-1, 2, 4, -triazole). Strikingly, exogenously applied ascorbate, a predominantly neuronal antioxidant, could compensate for the loss of any other single component of the antioxidant network. Together, these data imply significant roles for glial antioxidants and neuronal ascorbate in the prevention of pathophysiological consequences of the endogenous neuromodulator H2O2.

scholarly journals The Effects of Acetylcholine on the Turnover of Phosphatidic Acid and Phosphoinositide in Sympathetic Ganglia, and in Various Parts of the Central Nervous System in Vitro

1960 ◽  
Vol 44 (2) ◽  
pp. 217-226 ◽  
Author(s):  
Mabel R. Hokin ◽  
Lowell E. Hokin ◽  
Weldon D. Shelp
Keyword(s):  
Nervous System ◽  
Phosphatidic Acid ◽  
Phosphatidyl Ethanolamine ◽  
Cholinergic Neurons ◽  
Postsynaptic Membrane ◽  
Sympathetic Ganglia ◽  
The Central Nervous System ◽  
The Individual ◽  
Guinea Pig Brain

The effect of acetylcholine on the incorporation of P32 into the individual phosphatides in slices of various structures of the nervous system has been studied. There was a marked stimulation of P32 incorporation into phosphoinositide and phosphatidic acid, but not into phosphatidyl choline and phosphatidyl ethanolamine, in the cat stellate and celiac ganglia in vitro. Acetylcholine stimulated P32 incorporation into certain phosphatides, primarily phosphoinositide and phosphatidic acid, in several structures of the cat and guinea pig brain; there was little or no effect of acetylcholine on phosphatide turnover in the inferior corpora quadrigsemina and cerebellar cortex. The suggestion is made that the phospholipid effect can best be explained as being concerned with the active transport of sodium ions out of the cell across the postsynaptic membrane of cholinergic neurons in response to acetylcholine.

Sign in / Sign up

Export Citation Format

Share Document