摘要:

Abstract–In the retinas of 1‐day‐old chickens that received an intraocular injection ofN‐[3H]acetylmannosamine the labelling ofN‐acetylneuraminic acid and CMP‐N‐acetylneuraminic acid increased for at least 8 h and that of gangliosides for at least 24 h after injection. In the optic tectum contralateral to the injected eye at 8 h after the intraocular injection, the labelling of gangliosides exceeded the labelling of gangliosides in the ipsilateral tectum by approx 20‐fold. In the contralateral tectum the highest concentration of labelled gangliosides was in subfractions enriched in synaptosomes and synaptic plasma membranes. No significant contralateral ipsilateral differences were found in the acid soluble substances of the tectum. In the optic tectum, labelled gangliosides appeared earlier in the neuronal perikarya than in synaptosomes when the injection was intracranial. Conversely, when the injection was intraocular the labelling appeared earlier in the synaptosomes than in the neuronal perikarya. The radioactivity pattern of the optic tectum gangliosides resembled the pattern of retina gangliosides whenN‐[3H]acetylmannosamine was injected intraocularly, but whenN‐[3H]acetylmannosamine was given intracerebrally the radioactivity pattern resembled that of optic tectum gangliosides. Intraocular injection of colchicine or vinblastine did not affect the labelling of retinal gangliosides fromN‐[3H]acetylmannosamine injected into the same eye but prevented the appearance of labelled gangliosides in the optic tectum.In vitrothe ganglioside glycosylating activity of optic tectum synaptosomes and synaptic plasma membranes was between 6 and 10‐fold lower than that found in the optic tectum neuronal perikarya. These findings support the notion that the main subcellular site of synthesis of neuronal gangliosides is in the neuronal perikarya, from which they are translocat

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09912.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY

摘要:

Abstract–Various aspects of amino acid metabolism were studied in striatum of rats with unilateral, kainic acid‐induced lesions. Tissue slices were prepared from the lesioned and the contralateral, unlesioned, striatum. The preparations were incubated with a mixture ofd‐[2‐14C]glucose and [3H]acetate in a Krebs‐Ringer bicarbonate medium to evaluate oxidative metabolism. Glutamate and aspartate levels were decreased in the slices prepared from the lesioned striata by 35‐40% and that of GABA by 75% compared to the levels found in the slices from the contralateral striata; glutamine levels were not different in the two preparations. Glucose utilization was decreased 60% in the slices from the lesioned striatum; this was caused not only by decreased levels of glutamate, aspartate and GABA but also by a decreased rate of labelling of glutamate and aspartate. On the other hand, the metabolism of [3H]acetate was greatly increased. The specific activities of glutamate and aspartate were 4‐5‐fold higher in the slices from kainic acid‐lesioned striata; those of glutamine and GABA were unchanged. Thus, there was a 6‐7‐fold increase in the ratio of3H to14C in the specific activities of glutamate, aspartate and GABA with no change in this ratio in glutamine. The labelling of glutamine relative to that of glutamate, especially from [3H]acetate, suggested that the compartmentation of the glutamate‐glutamine system was greatly altered in the kainate‐lesioned striatum which now more closely resembled a single compartment system. The activities of lactate dehydrogenase, glutamate dehydrogenase, GABA transaminase and ‘cytoplasmic’ aspartate aminotransferase were decreased in homogenates of lesioned striatum. Succinate dehydrogenase, glutaminase (phosphate‐activated) and ‘mitochondrial’ aspartate aminotransferase activities were unchanged whilst that of glutamine synthetase was increased. The results are consistent with hypotheses concerning the assignment of labelled acetate metabolism to glial cells as well as the distribution of the above enzymes betwe

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09913.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY

摘要:

Abstract–Embryonic sensory neurons have an absolute requirement for the nerve growth factor to survive and grow fibers, at leastin vitro. We have now shown that the inorganic cations, magnesium and potassium are also necessary for the survival of these cells. On the other hand, calcium is not needed for the survival of the sensory neurons, but is needed for the neurons to grow fibers. Therefore, by changing the concentration of calcium ions in the culture medium it is possible to separate the two actions (survival and fiber outgrowth) of the nerve growth factor on sensory neuron

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09914.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY

摘要:

Abstract–The GABA content of the spinal cord and of approx 70 discrete rat brain nuclei is measured with a simple rapid semi‐automated fluorimetric assay, after prevention of post‐mortem effects with 3‐mercaptopropionic acid. We found that microwave irradiation produced decreases in the GABA contents of the microdissected zona reticulata of the substantia nigra, indicating that microwave fixation is not suitable to measure GABA levels in microdissected brain nuclei. In approx 70% of the nuclei in the anterior half of the brain the GABA concentration was found to be between 41 and 90nmol GABA/mg protein. The GABA content varied from 11 to 40 nmol GABA/mg protein in the posterior half of the brain. High GABA levels were found in some hypothalamic nuclei, the globus pallidus and eminentia mediana. An extremely high GABA level was found in the zona reticulata of the substantia nigra. GABA is unevenly distributed in the striatum. The highest concentration was found in the caudal part and in the ventral region at any level of the striatum. In the spinal cord the highest concentration of GABA was in the sacral

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09915.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY

摘要:

Abstract–Experimental rat neural tumors in offspring were induced transplacentally by a single injection of a chemical carcinogen, ethylnitrosourea, 20mg/kg body wt, in the tail vein of the mother. The ganglioside content and pattern in these tumors and the normal tissues from which the tumors originated are described. The ganglioside content in tumors was reduced, on wet tissue weight basis, compared to normal control. However, there was no significant difference of ganglioside content on dry weight or protein basis. Altered ganglioside composition was found in most of the neural tumors. In central nervous system tumors, there was some increase in GM3and GT1b′(nomenclature according to Svennerholm, 1963), a marked decrease in GM1and some decrease in GD1a,but no apparent loss in GD1b.Extreme simplification of ganglioside pattern was seen in tumors originated from peripheral nervous system. Large accumulation of GM3with concomitant loss of all the higher gangliosides was seen. GM3from neurinomas as well as from normal gray matter was isolated and characterized. GM3from neurinomas separated into two bands on thin layer chromatographic plates. Both these GM3bands had identical sphingosine and carbohydrate composition but differed in their fatty acid composition. The fast moving band had 77% of the total fatty acids as C20:0or longer chain while the slow moving band had only 22% of the long chain fatty acids. Normal gray matter GM3had one major band containing 82% of and only 17% of the fatty acids as C20:0or higher. It is suggested that in the tumor cells either the specificity of the enzyme cytidine monophosphate‐N‐acetyl neuraminic acid: ceramide dihexoside sialyltransferase for C18.0fatty acid containing glycolipid was altered or that the compartmentation of precursor pools for the simpler glycolipids present in normal tissue did not exist in transforme

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09916.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY

摘要:

Abstract–The buoyant density, ultrastructure and protein composition of dendrodendritic (DD), axodendritic (AD) and axosomatic (AS) synaptosomes were compared. DD synaptosomes prepared from either bovine superior colliculi or olfactory bulbs sedimented in 0.32m‐sucrose at 1000gwhereas AD and AS synaptosomes from frontal and temporal lobe cortices sedimented at 10.000g. In gradients of Renografin the DD contacts banded at a density of 1.12 whereas AD and AS banded at 1.07. The DD contacts appeared as large clusters of serial contacts, and each individual terminal had a mean surface area of 1.48 μm2; the mean area of AD and AS terminals was less than 0.35 μm2. The protein compositions of DD, AD and AS synaptosomes were quite similar, with minor exceptions. These findings suggest that different synaptosmal types evolved from common membrane constit

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09917.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY

摘要:

Abstract–In a previous publication (Wheeler&Hollingsworth, 1978), a model was presented which accounted for the role of sodium in the high affinity transport of glutamic acid in rat brain synaptosomes. Subsequent studies confirmed a lack of fit of the model to the data at the higher sodium and glutamate concentrations. The model has therefore been reexamined and refined. By removing some of the restrictions placed on the original model, a model emerges which fits the data at all sodium and glutamate concentrations with an average per cent error of only 2.14% per experimental data point. The kinetic constants describing uptake have been redefined and recalculated in accordance with this revised mode

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09918.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY

摘要:

Abstract–The concentration ol niacinamide in plasma and CSF was 0.5 and 0.7 μmrespectively. The, mechanisms by which niacin and niacinamide, which are not synthesized in brain, enter brain, CSF and choroid plexus were investigated by injecting [14C]niacin or [14C]niacinamide intravenously and intraventricularly. [14C]Niacin or [14C]niacinamide, with or without unlabeled niacin or niacinamide, were infused intravenously at a constant rate into conscious rabbits. At 3 h, [14C]niacinamide, but not [14C]niacin, readily entered CSF, choroid plexus and brain. The addition of 4.1 mmol/kg niacinamide to the infusate markedly depressed the relative entry of [14C]niacinamide into choroid plexus and brain but not into CSF. After intraventricular injection, [14C]niacin was rapidly cleared from CSF and readily entered brain and choroid plexus. The addition of unlabeled niacin to the intraventricular injectate decreased the clearance of [14C]niacin from CSF and the entry of [14C]niacin into choroid plexus and brain. Unlike niacin, carrier niacinamide (82 μmol) in the injectate did not depress the extremely rapid clearance of intraventricularly injected [14C]niacinamide from CSF but did decrease the entry of [14C]niacinamide into brain. These results show that the control of entry and exit of niacinamide and niacin is the mechanism, at least in part, by which total niacin and NAD levels in brain cells are regulated. In the case of niacinamide which readily passes between CSF and plasma, the regulation of entry of niacinamide into brain cells by a high affinity accumulation system is an integral part of the homeostatic system. In the case of niacin, penetration into CSF and the extracellular space of brain from plasma as well as regulation of entry into brain cells by a saturable accumulation system are two distinct parts of the homeostatic system.In vivo, niacin that enters the central nervous system is converted to the principal plasma vitamer, niacinamide, in its free or bound forms such as

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09919.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY

摘要:

Abstract–8‐Anilino‐1‐naphthalene sulfonic acid (ANS), a fluorescent probe specific for membrane polar‐apolar interfaces, has been used to investigate differences in corrected excitation, emission and scanned excitation polarization spectra of intact age, sex and passage number matched Huntington's disease (HD) and normal fibroblasts grown in cell culture. At passage number 4, the HD fibroblasts, compared to normals, exhibited a 30‐fold increase in excitation and emission intensity, a 30 nm blue shift of the emission maximum and a 0.18 polarization unit increase. These findings suggest that the ANS molecule experiences either increased binding sites or an increased quantum yield, a more nonpolar environment, and a more restricted motion in HD fibroblasts. Continued subculture at higher passages (10) showed a change of these findings towards normals. These fluorescent studies support the concept that a membrane abnormality is pr

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09920.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY

摘要:

Abstract–Rat serum dopamine‐β‐hydroxylase (DBH) activity decreased 5‐7‐fold between 15 and 60 days of age. Immunoprecipitation performed with homologous antibody (guinea‐pig anti‐rat adrenal DBH) showed that during this time period the quantity of antibody necessary to precipitate 50% of the enzymatic activity (AD50) decreased 5‐fold from 0.25 to 0.05 μl/ml. The biochemical properties of rat serum DBH at 15 and 60 days of age were compared to test the hypothesis that there might be different biochemical forms of the enzyme in the blood of immature and adult rats. Thermal stability, apparentKmfor tyramine, electrophoretic mobility, pH optima and elution profile on gel filtratioh chromatography were all found to be similar for rat serum DBH at both ages. On the basis of homospecific activity and multiple similarities in biochemical characteristics, it appears that differences in serum activity at the two ages reflect differences in the steady‐state levels of enzyme.To determine the turnover of serum DBH in the two age groups, the recovery of enzyme activity was monitored after acute clearance of the circulating pool of DBH by treatment with the homologous antiserum. Immunotitration of DBH activityin vivoindicated that the total pool of serum enzyme was 4‐fold greater in the mature rat than in 4‐day‐olds. After treatment of adult rats with 2μl of homologous antiserum, serum DBH activity was reduced by 85% with a half‐life of recovery of 3.0 ± 0.6 days; the estimated fractional rate of degradation was 0.23 ± 0.06 day−1and the rate of entrance was 2.3 ± 0.2 units/ml/day. After treatment of 4‐day‐old rats with 1 μl of homologous antiserum, serum DBH activity was reduced by 95% with a half‐life of recovery of 3.3 ± 0.5 days: the estimated average fractional rate of degradation was 0.22 ± 0.06 day−1and the average rate of entrance was 10.7 ± 1.6 units/ml/day. Thus, the several‐fold difference in steady‐state levels of serum DBH in rat pups as compared to adult rats appears to be due to greatly increased rat

ISSN:0022-3042    

DOI:10.1111/j.1471-4159.1979.tb09921.x

出版商:Blackwell Publishing Ltd    

年代:1979

数据来源: WILEY