ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01535.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01536.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01537.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY

摘要:

Abstract—The fraction that sediments between 2 × 105g‐min and 6 × 106g‐min from dilute dispersions of rat brain in 0.32m‐sucrose is a microsomal fraction with very little contamination by myelin. A crude microsomal fraction prepared in the same way from rat spinal cord contains more myelin than microsomes. Centrifugation of the crude microsomal fraction in 0.85m‐sucrose gave a floating fraction, an infranatant fraction (purified microsomes) and a small pellet. The purified microsomes contained very little myelin as judged by electron microscopy and polyacrylamide gel electrophoresis. The lipid composition resembled that of spinal cord myelin except that the purified microsomes contained relatively less cholesterol and ethanolamine plasmalogens. The content of galactolipids was much greater in spinal cord microsomes than in brain microsomes. The spinal cord CDP‐ethanol‐amine:diglyceride ethanolaminephosphotransferase activity (EC 2.7.8.1) was concentrated in the purified microsomes.A spinal cord myelin fraction isolated from the 2 × 105g‐min pellet was quite pure as judged by electron microscopy, enzyme activities and polyacrylamide gel electrophoresis. No NADPH‐cyto‐chromecreductase activity (EC 1.6.2.3) could be detected in the purified myelin. The ethanolaminephosphotransferase specific activity was about 5% of that found in the purified microsomal fraction. The protein content was 25% by weight for spinal cord myelin and 31% for brain myelin. Of the total spinal cord 2′,3′‐cyclic nucleotide‐3′‐phosphohydrolase activity, 16% was lost from the crude myelin during purification, 21% was recovered in the purified myelin, and 11% was found in the floating fraction from the crude microsomes. The purified myelin and microsomal fractions from spinal cord were relatively pure. Additional myelin was recovered in the floating

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01538.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY

摘要:

Abstract—Vanillylmandelic acid (VMA) and 3‐methoxy‐4‐ hydroxyphenylglycol (MHPG) were measured in rat brain by a mass fragmentographic procedure. The concentration of VMA and MHPG in whole brain is 11 and 533 pmol/g, respectively. Both compounds were found in all areas of brain studied with VMA, as a percentage of both metabolites, ranging between about 1 and 8%. From the decline of the compounds after pargyline. 75 mg/kg i.p., we calculated that the rate of formation of VMA is 15 and for MHPG 202 pmol/g per h. The fractional rate of elimination of VMA and MHPG is 1.4 and 0.38 h−1, respectively. The rapid rate of loss of VMA suggests that it is transported from brain. However, we were unable to block the elimination of VMA from brain by treatment with probenecid. In contrast, the elimination of MHPG could be blocked by treatment with probenecid. Our study adds support to the notion that MHPG is a major whereas VMA is a minor product of norepinephrine metabolism

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01539.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY

摘要:

Abstract—Lowering the concentration of oxygen or of glucose to which mouse and rat brains were exposed impaired the synthesis of acetylcholine from labelled precursorsin vivo.Histotoxic hypoxia induced with KCN or anemic hypoxia induced with NaNO2(to oxidize hemoglobin to methemoglobin) reduced incorporation of [2H4]choline into acetylcholine. This change in acetylcholine metabolism occurred with doses of KCN or NaNO2which did not alter the concentrations of ATP or ADP or the adenylate energy charge. Hypoglycemia induced by large doses of insulin also reduced the incorporation of [2H4]choline into acetylcholine. Both hypoxia and hypoglycemia increased the concentration of choline in the brain. The specific activity of choline did not decrease in hypoxia; it did not decrease enough in hypoglycemia to explain the reduced incorporation of [2H4]choline into acetylcholine.Pretreatment with the cholinesterase inhibitor physostigmine delayed the onset of both seizures and death in mice after induction of hypoxia by large doses of NaNO2. Pretreatment with physostigmine also decreased the number of mice dying within 3 h after the induction of hypoglycemia with large doses of insulin. These observations suggest that the effects of hypoxia and hypoglycemia interfere with the synthesis of a critical pool of acetylcholine.The incorporation of labelled precursors into acetylcholine related linearly to both the cytoplasmic redox state (NAD/NADH ratio) and to the NAD/NADH potential across the mitochondrial membrane. The redox potential of NAD/NADH in the cytoplasm was calculated from the [pyruvate]/[lactate]equilibrium and the redox potential of NAD/NADH in the mitochondria from the [NH4][2‐oxoglutar‐ate]/[glutamate] equilibrium. The potential across the mitochondrial membrane was calculated from the difference.These observations indicate that carbohydrate oxidation is one of the factors on which the synthesis of the neurotransmitter acetylcholine depends closely in mouse and rat

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01540.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY

摘要:

Abstract—Pre‐treatment of rat brain slices with organic mercurials prevents the increased acetylcholine release induced by tityustoxin. This inhibition is reversed by dithiothreitol.N‐Ethylmaleimide blocks the tityustoxin effect irreversibly. Simultaneous incubation with mercurials and toxin reveals a competition of both ligands for a membrane sulfhydryl group apparently required for tityustoxin act

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01541.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY

摘要:

Abstract—α‐Bungarotoxin (α‐BuTX) has been used as a marker for studying the acetylcholine receptors (AChRs) in the superior cervical ganglion (SCG) of the adult rat. Binding of [125I]α‐BuTX to detergent‐solubilized AChRs from rat SCG is a saturable and practically irreversible process. The rate constant of association of the toxin‐receptor complex is 1.66 × 105M−1S−1. The receptor is of nicotinic type. One SCG of adult rat binds about 57 fmol of [125I]α‐BuTX corresponding to 9.2 × 105AChRs per sympathetic neuron. Light microscope autoradiography shows that AChRs are mainly localized along neuronal processes (probably dendrites). The perikarya exhibit a weak radioactive reaction, while the nerve fibres are devoid of AChRs. Following preganglionic denervation the number of AChRs never increases and their spatial distribut

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01542.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY

摘要:

Abstract—A partially purified rat brain preparation, enriched in cerebroside β‐galactosidase activity, was found to catalyze the synthesis of labelled galactosyl‐ceramide from [14C]oleoyl‐sphingosine as acceptor and several β ‐galactosides as donor. The following compounds in the order of their effectiveness served as galactose donors for this reaction: para‐nitrophenyl‐β ‐galactoside (PNP‐β ‐gal), galactosyl‐ceramide, lactosyl‐sphingosine, lactosyl‐ceramide, 4‐methyl‐umbelliferyl‐β ‐galactoside (4‐MU‐β ‐gal). asialo‐GM1, galactosyl‐sphingosine, GM1and monogalactosyl‐diglyceride. It is believed that this transgalactosylation reaction is probably not a mere reversal of the hydrolytic reaction. Under optimal conditions the quantity of galactosyl‐ceramide formed represented 10% of the amount of donor hydrolysed. These observations in conjunction with those on the hydrolyses provide further support for the possible existence of two β ‐galactosidase isoenzymes involved with the catabolism of GM1and/or lactosyl‐ceramide, and a single form for galactosyl‐ceramide. The activity of one isoenzyme can be ‘se

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01543.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY

摘要:

Abstract—From the third day of pregnancy rats were fed a diet containing either 7% casein (experimental) or 24% casein (control). During lactation the control dams were fed the 24% casein diet and the experimental dams a 12% casein diet. From 25 to 50 days of age the experimental and control progeny were fed diets containing 7 and 24% casein, respectively. Between 50 and 120 days both groups were fed a diet containing 24% crude protein. Several indications of brain maturation in two brain areas were examined at various stages of development. In addition to retardation of brain growth, protein restriction led to myelin of an immature composition at 25 and 50 days of age. The immature composition was indicated by a low plasmalogen content at 25 days and by a high phospholipid and low galactolipid and plasmalogen contents at 50 days of age. The activity of the myelin marker enzyme, 2′3′‐cyclic nucleotide 3′‐phosphohydrolase (CNP), was significantly lower in the brains (excluding the cerebella) of malnourished rats at 21, 30 and 50 days. At all ages except at 50 days the activity of CNP in the cerebellum was higher in protein‐deprived animals than in controls. The activity of glutamic acid decarboxylase (GAD) in the brains (excluding the cerebella) of protein‐deprived rats was significantly lower at 21, 25 and 30 days but not at 50 and 65 days of age. As indicated by brain/body ratios, myelin composition and GAD activity, nutritional rehabilitation led to almost complete recovery of brain maturity, but the activity of CNP remained lower in the experimental group after

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1976.tb01544.x

出版商:Blackwell Publishing Ltd    

年代:1976

数据来源: WILEY