bluuebunny/crossref_metadata_2025_split huggingface dataset:
SUBCELLULAR SITE OF THE PHOSPHATIDYLINOSITOL EFFECT. DISTRIBUTION ON DENSITY GRADIENTS OF LABELLED LIPIDS FROM RESTING AND ACTIVE SYMPATHETIC GANGLIA OF THE RAT1
Authors: Burt D. R. , Larrabee M. G. 
Published: October 2006

AbstractLocalization of the increased [32P]‐labelling of phosphatidylinositol, caused by arrival of presynaptic impulses in a sympathetic ganglion, was investigated by subcellular fractionation of ganglia that had been labelled before homogenization. Paired superior cervical ganglia were excised from adult rats and incubated with 32P1 and [methyl‐14C]choline for 4 h at 37°C. The preganglionic nerve of one ganglion of each pair was stimulated repetitively (10/s) during the last 3 h of incubation. The ganglia were then softened with collagenase, homogenized, and fractionated by density gradient centrifugation. Succinate dehydrogenase served as marker for the distribution of mitochondria on the gradient, and [14C]ACh for synaptosomes. [32P]‐labelling of lipids was measured relative to that of phosphatidylcholine. The average changes in relative labelling that were caused by neuronal activity ranged as follows over the homogenate and the various fractions: phosphatidylinositol (PI), increased 39–75%; phosphatidylethanolamine, decreased 10–20%; diphosphatidylglycerol, not significantly affected. The increase in PI labelling was much greater in the denser fractions, in which synaptosomes and mitochondria were concentrated, than in the less dense fractions. The distribution of the PI effect on the gradient could be reasonably well explained by assuming that synaptosomes and mitochondria both contributed to the increase in PI labelling in proportion to the amount of their respective markers in a fraction. One‐third or more of the total increase could thus be associated with synaptosomes and one‐third or more with mitochondria, although alternative association with other structures could not be excluded. The implications of the inferred association with synaptosomes and mitochondria are discussed, current knowledge of the PI effect caused by impulses entering sympathetic ganglia is summarized, and suggestions concerning its physiological significance are reviewed. It is concluded that PI may have multiple roles in neuronal activity.
SULPHATE ESTER FORMATION FROM CATECHOLAMINE METABOLITES AND PYROGALLOL IN RAT BRAIN IN VIVO
Authors: Eccleston D. , Ritchie I. M. 
Published: October 2006

Abstract—A sulphotransferase enzyme capable of utilizing ethanolic or glycolic catecholamine metabolites and other phenols as substrates was studied in rat brain in vivo following the intraventricular injection of sodium [35S]sulphate and the subsequent isolation and identification of the labelled sulphate esters. A quantitative examination was made possible by the injection of increasing amounts of substrates of the enzyme together with sodium [35S]sulphate and the application of Michaelis‐Menten kinetics. 3‐Methoxy‐4‐hydroxyphenylethyleneglycol and 3,4‐dihydroxyphenylethyleneglycol were shown to be readily esterified as was 3‐methoxy‐4‐hydroxyphenylethanol (‘half‐saturating dose’ of 5‐1, 34 and 18 nmol respectively). Three esters of pyrogallol were isolated after its administration. This compound was also shown to inhibit sulphate ester formation from both substituted glycols, probably by competitive inhibition. The amines 5‐hydroxytryptamine and normetanephrine were not found to be substrates for the sulphotransferase system in brain.
EVIDENCE FOR EXTRANORADRENERGIC DOPAMINE‐β‐HYDROXYLASE ACTIVITY IN RAT SALIVARY GLAND
Authors: Coyle J. T. , Wooten G. F. , Axelrod J. 
Published: October 2006

Abstract—Three days after superior cervical ganglionectomy of adult Sprague‐Dawley rats, the levels of endogenous norepinephrine, the uptake process for [3H]norepinephrine and the activity of tyrosine hydroxylase decreased 99 per cent in the ipsilateral salivary gland. In contrast, the activity of dopamine‐β‐hydroxylase and DOPA decarboxylase fell to 30 per cent of the activity of the contralateral innervated gland. Examination of the cofactor requirements, the characteristics of activation by cupric ion and the immunologic identity of this residual hydroxylase activity indicated that it was authentic dopamine‐β‐hydroxylase. The residual dopamine‐β‐hydroxylase in the denervated gland had the same subcellular distribution as the enzyme in the innervated salivary gland. Procedures that caused atrophy or hypertrophy of the acinar cells did not affect the total content of dopamine‐β‐hydroxylase in the denervated salivary gland. Chemical sympathectomy with 6‐hydroxy‐dopamine caused a 40 per cent decrement in the serum levels of dopamine‐β‐hydroxylase but a 30 per cent increase in its activity in the denervated salivary gland. Although denervation caused a complete loss of endogenous norepinephrine in the salivary gland, it resulted in only a 15 per cent decrement in the levels of endogenous octopamine and β‐phenylethanolamine, two other products of dopamine‐β‐hydroxylase.
MINIMUM DURATION OF TRANS‐SYNAPTIC STIMULATION REQUIRED FOR THE INDUCTION OF TYROSINE HYDROXYLASE BY RESERPINE IN THE RAT SUPERIOR CERVICAL GANGLION
Authors: Zigmond R. E. , Mackay A. V. P. , Iversen L. L. 
Published: October 2006

Abstract—The period during which trans‐synaptic stimulation is required by the rat superior cervical ganglion for induction of tyrosine hydroxylase by reserpine has been studied. Ganglia were decentralized on one side at various times before or after an injection of reserpine. The tyrosine hydroxylase activity of the denervated and control ganglia was assayed 72 h after drug treatment. When decentralization was performed 8 h after an injection of reserpine the increase in tyrosine hydroxylase activity was blocked in the denervated ganglia. Decentralization 12 h after reserpine treatment or later had no effect on the enzyme induction. The actual increase in tyrosine hydroxylase activity occurred between 24 and 48 h after injection of reserpine.
INCORPORATION IN VIVO DE LA l‐[3H]LEUCINE DANS LES PROTEINES DU CERVELET DE JEUNES RATS NORMAUX, SOUS‐ALIMENTES, HYPERTHYROIDIENS ET HYPOTHYROIDIENS. THE INCORPORATION IN VIVO OF l‐[3H]LEUCINE INTO CEREBELLAR PROTEINS, IN THE YOUNG NORMAL, UNDERFED, HYPERTHYROID AND HYPOTHYROID RAT
Authors: Dainat J. 
Published: October 2006

Résumé—L'évolution de l'incorporation in vivo de la l‐[3H]leucine dans les protéines totales du cervelet de jeunes Rats normaux, sous‐alimentés, rendus hypo‐ ou hyperthyroïdiens, met en évidence deux phases dans l'évolution de la radioactivité spécifique des protéines en fonction de l'âge :la première phase se caractérise par une radioactivité spécifique élevée, alors que dans la deuxième phase, la radioactivité spécifique décroît fortement puis se stabilise à une valeur faible. La première phase s'étend sur 2 semaines chez les animaux normaux et sous‐alimentés, sur 1 semaine chez les animaux hyperthyroïdiens, et sur 3 semaines chez les animaux hypothyroïdiens. Il semble qu'à la première phase puisse correspondre la dernière ‘poussée’ de prolifération cellulaire, alors que la seconde phase qui débute à la fin de la période de prolifération cellulaire correspondrait à la prépondérance de la différenciation des cellules, puis au maintien du turnover des protéines. Les variations de la radioactivité spécifique des protéines, pourraient refléter les effets des différents traitements sur la prolifération cellulaire de l'organe.Abstract—The evolution of the incorporation of l‐[3H]leucine into cerebellar proteins in vivo in the normal, the underfed, the hypo‐ and the hyperthyroid young rat shows two phases. The first phase exhibits high specified radioactivity values for protein which decrease markedly in the second phase and stabilize at a low level by the third or fourth postnatal week. The duration of the first phase lasts for 2 weeks in the normal and underfed animals, 1 week in the hyperthyroid animals and 3 weeks in the hypothyroid animals. The first phase thus parallels the last 'surge’ of cellular multiplication and the second phase, which begins when cellular multiplication and migration are about over, reflects preponderantly cellular differentiation. Metabolically the latter phase would thus correspond to the period of slowdown of protein turnover to maintenance levels. The results suggest that the variations in the specific radioactivity values in the different physiological states reflect the effects of hypo‐ and hyper‐thyroidism and of underfeeding on the cellular proliferation and differentiation of the cerebellum.
MEMBRANE PROTEINS OF RAT BRAIN: COMPOSITIONAL CHANGES DURING POSTNATAL DEVELOPMENT
Authors: Waehneldt T. V. , Neuhoff V. 
Published: October 2006

Abstract— Membrane fractions from forebrain of rat were isolated at ages ranging from 5 to 93 days. Among these fractions were total membranes, three fractions isolated by density gradient centrifugation, and three subfractions which consisted of purified myelin and of two supernatant fractions. All membrane fractions showed an increase in protein content during the first postnatal month; however, only the myelin fraction and one of its supernatant fractions showed a prolonged accumulation. Myelin protein increased continually from 0.17 mg/g brain at 15 days to 8.3 mg/g brain at 93 days.All fractions were analysed for protein composition by sodium dodecyl sulphate polyacrylamide gel electrophoresis. Characteristic changes in protein composition were noted during postnatal development, most of which were pronounced up to the age of 20 days. Among others was a decrease in histones as compared to other proteins, with a concomitant shift in preponderance from the slow‐ to the fast‐migrating histone band. In parallel, other proteins of high molecular weight became more prominent. No myelin could be isolated at 5 and 10 days. The deposition of myelin proteins was parallelled by the appearance of the Wolfgram protein which points to a close correlation of the Wolfgram protein to the process of myelination.
IN VIVO INHIBITION OF RAT BRAIN PROTEIN SYNTHESIS BY l‐DOPA
Authors: Roel L. E. , Schwartz S. A. , Weiss B. F. , Munro H. N. , Wurtman R. J. 
Published: October 2006

Abstract— A study has been made of the effect of a single intraperitoneal dose of l‐DOPA on the in vivo metabolism of [14C]leucine and [14C]lysine by the brain, and on their uptake into brain protein. Administration of 500 mg DOPA/kg to 40‐g rats raised the concentrations of several free amino acids; the only amino acid which underwent a statistically significant increment was alanine. Intracisternally‐injected [U‐14C]leucine was rapidly metabolized to other labelled compounds; DOPA administration did not influence significantly the rate of its metabolism. No similar metabolic change was observed after administering [U‐14C]lysine intracisternally.Incorporation of [14C]leucine and [14C]lysine into total brain protein was significantly reduced 45 min after DOPA administration. There was also depression of the uptake of labelled amino acid into a supernatant fraction, obtained by high speed centrifugation of the brain homogenate, and into brain microtubular protein (tubulin). Reduced amino‐acid incorporation into brain proteins observed 45 min after l‐DOPA injection coincided with extensive disaggregation of brain polyribosomes. At 120 min after DOPA treatment, disaggregation was no longer significant and there was a smaller depression in labelled amino aicd incorporation, which disappeared completely 240 min after l‐DOPA injection. It is concluded that disaggregation of brain polysomes following DOPA treatment is an accurate reflection of a change in the intensity of brain protein synthesis in vivo.
THE CHARACTERIZATION OF SPHINGOLIPIDS FROM NEURONS AND ASTROGLIA OF IMMATURE RAT BRAIN1
Authors: Abe T. , Norton W. T. 
Published: October 2006

Abstract— Isolated neuronal cell bodies and astroglia of young (15–20‐day‐old) rat brains were both found to contain small concentrations of a variety of glycosphingolipids, including glucosylceramide, galactosylceramide, sulphatide, dihexosylceramide and gangliosides. These sphingolipids, plus sphingomyelin, were isolated, quantitated and their fatty acid and long chain base patterns determined. These data were compared to similar data obtained on these lipids isolated from whole brain and myelin of rats of the same age range.Glucosylceramide was found in an amount equal to galactosylceramide in neurons, and accounted for 35 per cent of the total monohexosylceramide in astroglia. Dihexosylceramide was present in nearly the same amount as sulphatide in both cell types.The sphingolipids of each cell type had characteristic fatty acid patterns. Generally the whole brain fatty acid patterns resembled those of astroglial lipids rather than neuronal lipids. In no case did the cell sphingolipid fatty acids resemble those of myelin. However, the galactosylceramide and sulphatides of both cells had unsubstituted and α‐hydroxy acids, both of which had appreciable quantities of C24 acids.The ganglioside fatty acids of each cell type were similar and not unusual, but were quite different from those of glucosylceramide and dihexosylceramide; the latter having appreciable quantities of 16:0 and acids longer than 18:0. The ganglioside patterns of these cells were similar and only slightly different from that of whole brain. Long chain bases of sphingolipids were mainly C18‐sphingosine in both cell types, and those of ganglioside and sphingomyelin contained small amounts of C20‐sphingosine.
STIMULATION OF SEROTONIN N‐ACETYLTRANSFERASE IN PINEAL ORGAN CULTURE BY DRUGS
Authors: Holz R. W. , Deguchi T. , Axelrod J. 
Published: October 2006

Abstract— Drugs such as cocaine, procaine, pheniprazine (Catron) and veratridine, which have actions on sympathetic nerves and nerve terminals, were examined for their ability to increase serotonin N‐acetyltransferase (EC 2.3.1.5; NAT) in pineal organ culture. The absence of potassium (0 KCl) was also examined. NAT is known to respond to β‐adrenergic stimulation. It was found that these drugs and 0 KCl increased the enzyme activity 100 to 2000‐fold in innervated pineals but had virtually no effect in denervated pineals. The effects on innervated pineals were blocked by the β‐blocker propranolol but not by the α‐blocker, phentolamine. These drugs and 0 KCl inhibited to varying degrees [3H] 1‐norepinephrine uptake in pineals. It is concluded that these agents activated the β‐adrenergic receptor on pineal cells by causing an accumulation of extraneuronal norepinephrine. The accumulation of norepinephrine is due, at least in part, to the blockade of norepinephrine reuptake by nerve terminals.The ability of veratridine to stimulate NAT and to inhibit norepinephrine uptake was reversed by tetrodotoxin, a blocker of sodium permeability in excitable tissue, thus veratridine acts by increasing sodium permeability in nerve terminals. This adds support to the theory that catecholamine uptake is a process that requires a sodium gradient across the nerve terminal membrane.
EARLY CHANGES IN ACETYLCHOLINE POOLS IN THE HIPPOCAMPUS OF THE RAT BRAIN AFTER SEPTAL LESIONS
Authors: Potempska Anna , Grądkowska Malgorzata , Oderfeld‐Nowak Barbara 
Published: October 2006

Abstract—After placement of lesions in the hippocampus by electrocoagulation, an increase in bound acetylcholine above control levels was shown. There was no concomitant rise in free acetylcholine. The rise in bound acetylcholine was not due to changes in levels of either acetylcholinesterase or choline acetyltransferase and it is suggested that the interruption of septal impulses and/or alterations in uptake or availability of substrates is responsible.
DECREASED METABOLISM IN VIVO OF GLUCOSE INTO AMINO ACIDS OF THE BRAIN OF THIAMINE‐DEFICIENT RATS AFTER TREATMENT WITH PYRITHIAMINE
Authors: Gaitonde M. K. , Fayein N. A. , Johnson A. L. 
Published: October 2006

Abstract— Thiamine deficiency produced by administration of pyrithiamine to rats maintained on a thiamine‐deficient diet resulted in a marked disturbance in amino acid and glucose levels of the brain.In the two pyrithiamine‐treated groups of rats (Expt. A and Expt. B) there was a significant decrease in the levels of glutamate (23%, 9%) and aspartate (42%, 57%), and an increase in the levels of glycine (26%, 27%) in the brain, irrespective of whether the animals showed signs of paralysis (Expt. A) or not (Expt. B). as a result of thiamine deficiency. A significant decrease in the levels of γ‐aminobutyrate (22%) and serine (28%) in the brain was also observed in those pyrithiamine‐treated rats which showed signs of paralysis (Expt. A). Threonine content increased by 57% in Expt. A and 40% in Expt. B in the brain of pyrithiamine‐treated rats, but these changes were not statistically significant.The utilization of [U‐14C]glucose into amino acids decreased and accumulation of glucose and [U‐14C]glucose increased significantly in the brain after injection of [U‐14C]glucose to pyrithiamine‐treated rats which showed abnormal neurological symptoms (Expt. A). The decrease in 14C‐content of amino acids was due to decreased conversion of [U‐14C]glucose into alanine, glutamate, glutamine, aspartate and γ‐aminobutyrate. The flux of [14C]glutamate into glutamine and γ‐aminobutyrate also decreased significantly only in the brain of animals paralysed on treatment with pyrithiamine.The decrease in the labelling of, amino acids was attributed to a decrease in the activities of pyruvate dehydrogenase and α‐oxoglutarate dehydrogenase in the brain of pyrithiamine‐treated rats. The measurement of specific radioactivity of glucose, glucose‐6‐phosphate and lactate also indicated a decrease in the activities of glycolytic enzymes in the brain of pyrithiamine‐treated animals in Expt. A only. It was suggested that an alteration in the rate of oxidation in vivo of pyruvate in the brain of thiamine‐deficient rats is controlled by the glycolytic enzymes, probably at the hexokinase level.The lack of neurotoxic effect and absence of significant decrease in the metabolism of [U‐14C]glucose in the brain of pyrithiamine‐treated animals in Expt. B were probably due to the fact that animals in Expt. B were older and weighed more than those in Expt. A, both at the start and the termination of the experiments.
ORGAN CULTURE OF THE RAT ADRENAL MEDULLA: A MODEL SYSTEM FOR THE STUDY OF TRANS‐SYNAPTIC ENZYME INDUCTION
Authors: Goodman R. , Otten U. , Thoenen H. 
Published: October 2006

Abstract—It was the aim of the present study to develop organ culture conditions for the rat adrenal medulla which are representative for the in vivo situation. This is a prerequisite for studying the complex processes involved in trans‐synaptic enzyme induction. The processes of trans‐synaptic enzyme induction initiated in vivo by injecting 5 mg/kg of reserpine 2 h prior to the removal of the adrenal medulla, continued in this culture system and final levels of tyrosine hydroxylase were comparable to those seen in vivo. That these culture conditions are representative for the in vivo induction is also supported by the fact that transection of the splanchnic fibres supplying the adrenal medulla or administration of actinomycin D prior to reserpine abolished the rise in tyrosine hydroxylase activity not only in vivo, but also in culture.The findings that high concentrations (0·29 mm) of corticosterone in the culture medium inhibited the increase in tyrosine hydroxylase activity caused by reserpine support the hypothesis that glucocorticoids act as modulatory agents in trans‐synaptic enzyme induction. This inhibition was exhibited only when corticosterone was added at the initiation of the culture period. If added 2 or 4 h after the beginning of the culture period there was little or no effect on the subsequent increase of tyrosine hydroxylase.
THE CHLORIDE CONTENT, ANION DEFICIT AND VOLUME OF SYNAPTOSOMES
Authors: Marchbanks R. M. 
Published: October 2006

Abstract—The uptake of 36Cl− into incubated synaptosomes was found to reach a steady state within 30 min enabling estimates of the amount of intra‐synaptosomal chloride to be made. There was an excess in the total charge of sodium and potassium over that of chloride within the synaptosomes. This deficit of permeant anions is balanced within the synaptosome by negatively charged protein and other anions such as aspartate and phosphate. Their combined amount could be estimated from the magnitude of the anion deficit.The net valency of the substances causing the anion deficit was determined by relating the ion content to the intra‐synaptosomal volume when metabolic activity was blocked. It was found to be similar to that of cerebral cortex tissue in vivo. The intra‐synaptosomal volume was found to change so that the osmolarity of the synaptosomal contents equalled the osmolarity of the incubation medium. A method of determining the intra‐synaptosomal volume by measuring the ion content is described. The results from this method are compared with those obtained using conventional space markers.
PURIFICATION AND PROPERTIES OF BRAIN N‐ACETYL‐β‐HEXOSAMINIDASE A
Authors: Aruna Rita M. , Basu Debkumar 
Published: October 2006

Abstract—N‐Acetyl‐β‐hexosaminidase A was purified to homogeneity from human and monkey brains by the conventional procedures followed by concanavalin A–Sepharose affinity chromatography. The optimal activity was observed at pH 4·5 for both enzyme preparations with both the aglycones N‐acetylglucosamine and N‐acetylgalactosamine derivatives. The Km values for hexosaminidase A from monkey brain were 0·26 mm and 0·04 mm respectively for N‐acetylglucosamine and N‐acetylgalactosamine. Km values obtained for glucosamine and galactosamine derivatives for the human brain hexosaminidase A were of the same order. The glycoprotein nature of the enzymes was established by the affinity towards concanavalin A as well as by the presence of sialic acid, galactose, glucose, mannose and hexosamines in the enzyme molecule from monkey brain.
ACETYLCHOLINESTERASE ET BIOSYNTHESE DES PROTEINES DU GANGLION SYMPATHIQUE AU REPOS ET STIMULE1: ACETYLCHOLINESTERASE AND BIOSYNTHESIS OF PROTEINS IN THE RESTING AND STIMULATED SYMPATHETIC GANGLION1
Authors: Gisiger V. , Venkov L. , Gautron J. 
Published: October 2006

Résumé—Des séparations sur gel de polyacrylamide ont permis d'établir la distribution électrophorétique des protéines, de l'incorporation d'acides aminés et de l'acétylcholinestérase (AChE; EC 3.1.1.7) du ganglion sympathique au repos et stimulé. Une étude conjointe d'histochimie ultrastructurale a montré que l'essentiel de l'activité acétylcholinestérasique des neurones sympathiques et des nerfs préganglionnaires est localisée dans le réticulum endoplasmique. Les molécules d'AChE du ganglion ont une faible mobilitéélectrophorétique, elles se répartissent en 3 bandes: une majeure et deux mineures. Le profil de radioactivité obtenu après marquage par la l‐[U‐14C]leucine se caractérise par la présence de 3 pics importants qui sont situés au début, au milieu et à la fin de l'électrophorégramme. Les bandes de protéines et le pic de radioactivité migrant dans le début du gel ainsi que la bande majeure d'AChE ne sont extraites qu'en présence de Triton X‐100. La zone de radioactivité contenant l'activité acétylcholinestérasique perd plus de 50% de sa radioactivité après 5 à 8 h de chasse du précurseur. La stimulation préganglionnaire à 16/s appliquée durant 1 à 4h abaisse d'environ 50% l'incorporation de la l‐[U‐14C]leucine dans les protéines migrant au début et à la fin de l'électrophorégramme. La radioactivité associée à la région des bandes d'AChE est diminuée de moitié par la stimulation.