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J Elbrink

Publications and source records attributed to J Elbrink.

At least 19 recordsLinked to original sources
PubMed1991

Glial fibrillary acidic protein, J1-31 antigen and vimentin in adult hamster brain: an immunohistochemical study.

Different regions of the prosencephalon and mesencephalon of the adult hamster brain displayed differences in the immunofluorescence expression of astrocytic proteins, namely glial fibrillary acidic protein and J1-31 antigen (30 kD protein). Neither of these proteins could be detected in layers II-VI of the cerebral cortex. However, varying degrees of immunostaining were detectable in perivascular glia, stria medullaris thalamus, the basal cerebral peduncle and the dentate molecular layer of the hippocampus. Vimentin was conspicuous in neurons, particularly in the cerebral cortex and hippocampus, and in glial fibrillary acidic protein-positive astrocytes in major fibre tracts. These observations are discussed in relation to interspecies differences in the expression of intermediate filament proteins.

Animals↗
PubMed1990

Reactive astrocytes--a review.

This review provides an historical and current perspective on astrocytes in the CNS, detailing their morphological and biochemical diversity, origins and transformation to reactive astrocytes in experimental lesions and clinical disease states which result in gliosis. Recent studies on reactive astrocytes have been facilitated by the availability of immunocytochemical probes for GFAP and other distinctive cellular components. The effects in vitro of 'growth factors' on astrocytic transformation are briefly considered. An understanding of astrocytic transformation has implications for neural transplantation.

Animals↗
PubMed1989

Characterization of intermediate filament proteins in astroglia of hamster cerebellum.

This investigation was initiated to determine whether the organization of intermediate filament (IF) proteins is affected in the central nervous system of polymyopathic hamsters, as the Duchenne muscular dystrophy gene is normally expressed in the nervous system, in addition to cardiac and skeletal muscle, and changes in cell shape and cytoplasmic organization can serve as the regulators of growth, gene expression and cellular differentiation. The cerebellum of dystrophic hamster (CHF 146) was selected as the model system with the CHF 148 hamster providing the control for normal cerebellum. Using immunofluorescence microscopy for IF proteins, no difference could be detected in the cerebellum of dystrophic and normal hamsters. However, the glial fibrillary acidic protein and an IF-associated protein (J1-31 antigen), are lacking in Bergmann glia of the molecular layer. Moreover, vimentin persists in the cerebellum, its presence being most pronounced in a subset of Purkinje neurons in the adult hamster. These results are in contrast to those obtained in the rat cerebellum which has been extensively studied in respect to the organization of IFs.

Animals↗
PubMed1986

Glucose oxidation in white adipose tissue from BIO 14.6 dystrophic hamsters.

In studies of glucose oxidation in white retroperitoneal adipose tissue of BIO 14.6 dystrophic and F1B normal hamsters aged 55-67 and 368-379 days, no difference was found in the basal state of radiolabelled 14CO2 production using either D-[6-14C]glucose or D-[1-14C]glucose. When C6-labelled glucose was used, insulin induced a slightly greater increase in glucose oxidation in dystrophic adipose tissue at both ages. When C1-labelled glucose was used, insulin enhanced glucose oxidation in dystrophic tissue more than twice normal in tissues from young animals and five times normal in tissues from the old ones. The increase in oxidation with D-[1-14C]glucose likely represents enhanced activity of the pentose phosphate pathway, which has also been observed in certain tissues of other animals with inherited skeletal-muscle degeneration. The change can probably be classified as being compensatory, an attempt by tissues to maintain functional integrity.

Adipose Tissue↗
PubMed1985

The pathogenesis of Duchenne muscular dystrophy: significance of experimental observations.

The pathogenesis of Duchenne muscular dystrophy (DMD) remains elusive, but as this is an inherited condition the primary manifestation of the disease is assumed to be in the regulatory control or biosynthesis of a protein. Current hypotheses attribute the pathological state of skeletal muscle in DMD to a defect in the nerve supply, or in the vasculature, or in the muscle itself. However, various tissues other than skeletal muscle are also affected; thus the current view of DMD requires reevaluation. The following possibilities should be considered: That the primary lesion is expressed in one of the major communication systems (nervous, vascular, or endocrine). That the primary lesion is expressed in a specific tissue: a) if in skeletal muscle, alterations in non-muscular tissues must be due to the release of muscle constituents into extracellular fluid; b) if in a non-muscular tissue, this might produce too much (or too little or none) of a constituent normally secreted into the extracellular fluid, or produce a "toxic" agent. That the primary lesion is expressed in a wide variety of tissues: the effect on a particular tissue will depend entirely upon the degree of requirement of the altered protein for function.

Humans↗
PubMed1985

Electrophysiological observations on diaphragm muscle from normal and dystrophic hamsters.

The cellular electrical activity of diaphragm from F1B normal and BIO 14.6 dystrophic hamsters has been investigated using microelectrodes. Resting membrane potentials and action potentials were recorded from control muscles and from muscles exposed to 2,4-dinitrophenol. The action potentials of normal and dystrophic diaphragms were similar in amplitude and configuration. Treatment with 2,4-dinitrophenol caused the action potential amplitude of both diaphragms to decline by similar amounts. The control resting membrane potential of diaphragm from dystrophic hamsters is not significantly different from that of normal hamsters. Treatment with 2,4-dinitrophenol caused a linear decrease in the resting membrane potentials of both groups of muscles. Dystrophic muscle, however, showed a more rapid decline in excitability when exposed to 2,4-dinitrophenol. This suggests that adenosine triphosphate production in dystrophic muscle is partially inhibited as has been suggested by other workers.

2,4-Dinitrophenol↗
PubMed1984

Facilitated diffusion of monosaccharides in smooth muscle of rat vas deferens in vitro.

The suitability of rat vas deferens for investigating sugar transport in smooth muscle was determined in vitro, with the nonmetabolized glucose analog 3-O-methyl-D-glucose as test sugar. Vas deferens smooth muscle contains a facilitated diffusion system for monosaccharides, as shown by saturation of the transport sites and by competition between 3-O-methyl-D-glucose and D-glucose. The activity of the facilitated diffusion system could be enhanced by hyperosmolarity and by contractile activity, but frequency dependency could not be established. A high concentration of insulin (100 mU/mL) was required to stimulate sugar transport. As smooth muscle is not a primary tissue for the storage of energy reserves, it does not require large numbers of insulin receptors.

Animals↗
PubMed1983

Increased contractility in vascular smooth muscle of dystrophic hamsters.

To investigate the "vascular" hypothesis of muscular dystrophy, the sensitivity and contractility of aortic spiral strips of dystrophic (BIO 14.6) and normal (FIB) hamsters have been determined to various smooth muscle agonists. The results obtained with cumulative dose-response curves show that there is no increase in the sensitivity of the dystrophic compared with the normal aorta to noradrenaline, phenylephrine, isoproterenol, histamine, or 5-hydroxytryptamine. However, there was a significant increase in the force generated by aortic strips of the dystrophic animals to all agonists. Determination of noncollagen and collagen protein showed that there was no difference in the relative proportions of these proteins in the aortas from the two strains. The results show that in this animal model of dystrophy an increased response to vasopressor amines occurs and is in accordance with that expected of the vascular hypothesis.

Animals↗
PubMed1983

Monosaccharide transport and hexokinase activity in leg muscles from cardiomyopathic hamsters.

The facilitated diffusion system for monosaccharides was studied with nonmetabolized 3-O-methyl-D-glucose (3-O-MG) and hexokinase activity was determined with 2-deoxyglucose (2-DG) in extensor digitorum longus (EDL) and soleus muscles from BIO 14.6 (dystrophic) hamsters. Motor activity was recorded at 2 months of age. F1B (normal) hamsters were controls. In EDL (fast-twitch) muscle, sugar transport was unaltered at 6 weeks; at 2 to 5 months the normal decrease in sugar transport with time was reduced, decreasing stimulation of the facilitated diffusion system by anoxia. Phosphorylation in EDL muscles, measured at 2 months, probably was decreased. In soleus (slow-twitch) muscle, 3-O-MG transport was unaltered with age but hexokinase activity, determined at 2 months, was greatly increased in the quiescent state and during stimulation at 2 Hz. Motor activity was less, but not significantly, in the dystrophic hamsters. The results indicate that the alterations in glucose metabolism depend upon both muscle type and age. We interpret the changes in dystrophic fast- and slow-twitch muscles as reflecting compensatory mechanisms to increase the generation of energy.

3-O-Methylglucose↗
PubMed1979

The effect of hyperosmolarity and insulin on resting tension and calcium fluxes in rat soleus muscle.

1. The effect of hyperosmolarity on resting tension and on the fluxes of Na and Ca has been characterized in isolated soleus muscles of the rat. 2. When the osmolarity of the incubation medium was increased by the addition of non-permeant solutes (100-400 m-osmole), the tension showed a rapid dos-dependent rise which could be maintained for up to 60 min. 3. Tension development was unaffected by tubocurarine (2 X 10(-5) M), considerably diminished by the omission of Na or Ca from the incubation medium, and inhibited by tetracaine (10(-4) M). 4. The addition of mannitol or sucrose (200 mM) induced a prompt stimulation of the influx of 22Na and 45Ca. Both in the absence and the presence of extracellular Ca hyperosmolarity stimulated the washout of 45Ca from preloaded muscles. Tetracaine (5 X 10(-4 M) suppressed the effects of hyperosmolarity on both the influx and the efflux of 45Ca, but only gave a modest reduction in the stimulation of 22Na influx. 5. Insulin (5-100 mu./ml.) induced a considerable further rise in the resting tension of muscles exposed to mannitol or sucrose (200 mM). This effect was seen in a glucose-free medium and could be abolished by the addition of insulin antibody. 6. It is concluded that hyperosmolarity leads to a rise in the concentration of free Ca2+ ions in the sarcoplasm, partly due to a mobilization of Ca from intracellular pools, but to a considerable extent supplemented from extracelluar sources. Under these conditions, insulin further augments the Ca2+ ion level in the cytoplasm.

Animals↗
PubMed1979

Defect in regulation of membrane transport of monosaccharides in dystrophic muscle.

The penetration of a nonmetabolized glucose analogue, 3--O-methyl-D-glucose, across the plasma membranes of tissues from dystrophic mice and cardiomyopathic (dystrophic) hamsters has been compared with that of normal controls. Under basal conditions the penetration of test sugar was similar in lens and diaphragm of normal and dystrophic 129/ReJ mice. Stimulation of sugar transport by 2,4-dinitrophenol did occur in normal but not in dystrophic diaphragm. A submaximal concentration of insulin had a more variable effect in dystrophic than in normal muscle while a supramaximal concentration of the hormone increased the uptake of the glucose analogue to an equal extent in the two tissues. In the BIO 14.6 strain of cardiomyopathic hamsters, uncoupling of oxidative phosphorylation did not increase sugar transport in extensor digitorum longus muscles, while the normal effect was observed in dystrophic soleus and in both these muscles of the random bred controls. The absence of an effect by a condition simulating anoxia suggests that in dystrophy, certain muscles are unable to accelerate the entry of glucose when this is required.

Animals↗
PubMed1976

A specific sugar transport mechanism in smooth muscle and its regulation.

The membrane transport of 3-O-methyl-D-glucose was studied in vitro in a smooth muscle, the detrusor of rat urinary bladder. Transport occurred by facilitated diffusion and showed the same chemical specificity and sensitivity to specific inhibitors as skeletal and cardiac muscle but its insulin sensitivity was smaller. Transport was increased by agents inhibiting the Na+pump and was decreased by agents which increased Na+ and K+ gradients by apparently stimulating the Na+pump. In accord with a rate limiting role of transport in glucose utilization, similar stimulating and inhibitory effects were seen when CO2 production from (14C) glucose was measured.

Animals↗
PubMed1975

The relationship between the transport of glucose and cations across cell membranes in isolated tissues. IX. The role of cellular calcium in the activation of the glucose transport system in rat soleus muscle.

1. The role of cellular Ca2+ in the transport of glucose has been investigated by determining the time-course of tension development and the release of 45Ca and 3-0-[14C]methylglucose from preloaded rat soleus muscles. 2. Electrical stimulation, 2,4-dinitrophenol (0.05 mM) and hyperosmolarity (200 mM mannitol) were all found to induce a rapid rise in tension and the rate coefficient of 45Ca release, which coincided with an acceleration of 3-0-[14C]methylglucose efflux. 3. Caffeine (10 mM) or exposure to K+ -substituted buffer induced a rapid increase in tension and the release of 45Ca, but a much later stimulation of 3-0-methylglucose efflux. This delayed response may be related to the fact that both factors induce a pronounced suppression of the effect of various agents known to stimulate sugar transport.4. Following a washout period of 120 min at 0 degreesC, the return to 30 degrees C elicited a prompt transient rise in the rate coefficient for the release of 45Ca and 3-0-[14C]meth ylglucose to levels, respectively, 2.8 and 14.6 times the control levels measured at 30 degrees C. The magnitude of these peaks appeared to be a function of the duration of the exposure to 0 degrees C. Cooling also led to a stimulation of the uptake of 3-0-[14C]methylglucose, and phlorizin suppressed the rise. 5. It was not possible to detect any significant effect of insulin on basal tension or on the influx or efflux of 45Ca. However, in a hyperosmolar environment, insulin (10-100 munits/ml) induced a marked further rise in tension, indicating that the hormone can elicit a redistribution of cellular Ca2+. 6. It is concluded that a rise in the cytoplasmic concentration of free Ca2+ constitutes a part of the mechanism by which the glucose transport system is activated by a variety of stimuli, perhaps also insulin.

Animals↗