scholarly journals The light-induced increase of carbohydrate metabolism in glial cells of the honeybee retina is not mediated by K+ movement nor by cAMP.

1991 ◽  
Vol 98 (3) ◽  
pp. 497-515 ◽  
Author(s):  
V Evêquoz-Mercier ◽  
M Tsacopoulos
Keyword(s):  
Glial Cells ◽  
Extracellular Space ◽  
Glycogen Metabolism ◽  
Significant Rise ◽  
Covalent Modification ◽  
Metabolic Effects ◽  
Light Stimulation ◽  
Glycogen Enzymes ◽  
Photoreceptor Neurons ◽  
Retinal Slices

The retina of the honeybee drone is a nervous tissue in which glial cells and photoreceptor neurons constitute two distinct metabolic compartments. The phosphorylation of glucose and its subsequent incorporation into glycogen occur essentially in glia, whereas O2 consumption occurs in the photoreceptors. After [3H] glucose loading of superfused retinal slices, light stimulation induced a significant rise in [3H] glycogen turnover in the glia. This occurs without a concomitant covalent modification of glycogen enzymes. Probably only an increase or a decrease of the availability of [3H] glycosyls that are incorporated into glycogen is necessary. As only photoreceptors are directly excitable by light, we searched for a signal that stimulates glycogen metabolism in the glia. Although K+ in extracellular space and glia increases after repetitive light stimulation, increasing bath K+ in the dark did not mimic the metabolic effects of light, despite an equivalent increase of K+ in the extracellular space and glia. We subsequently explored the role of cAMP, a universal intracellular second messenger. Exposure of retinal slices to the adenylate-cyclase activator forskolin induced an expected increase in the rate of formation of cAMP, but only partially mimicked the metabolic effects of light. Furthermore, light stimulation failed to induce a rise in the rate of formation of cAMP. We conclude that in this nervous system, without synapses, neither K+ nor cAMP mediates the effect of light stimulation on intraglial glucose metabolism.

scholarly journals Ionic and possible metabolic interactions between sensory neurones and glial cells in the retina of the honeybee drone

1981 ◽  
Vol 95 (1) ◽  
pp. 75-92
Author(s):  
J. A. Coles ◽  
M. Tsacopoulos
Keyword(s):  
Glial Cells ◽  
Review Paper ◽  
Glycogen Metabolism ◽  
Light Stimulation ◽  
Retinal Tissue ◽  
Single Flash ◽  
Metabolic Interactions ◽  
Spatial Buffering ◽  
Honeybee Drone ◽  
Stimulation Of

This is a review paper that includes original calculations and figures. The drone retina is composed of two essentially uniform populations of cells, the photoreceptors and the glial cells. The photoreceptors contain many mitochondria but no glycogen has been detected; the glial cells contain much glycogen and very few mitochondria. The oxygen consumption of the photoreceptors in the dark is 20 microliters min-1 per g of retinal tissue and in response to a single flash of light there is an extra consumption that reaches a maximum of 40 microliters min-1 per g. In addition, light stimulation of the photoreceptors leads to changes in the glycogen metabolism of the glial cells, and to movements of K+. Measurements with intracellular K+-sensitive micro-electrodes showed that during light stimulation with a series of flashes the K+ activity (alpha K) in the photoreceptors fell by an average of 27% while in the glial cells alpha K rose by an amount that is estimated to correspond to most of the quantity of K+ lost by the photoreceptors. The relative contributions to the clearance of extracellular K+ of extracellular diffusion, spatial buffering and possible net K+ uptake by glial cells are discussed.

Epitrochlearis muscle. II. Metabolic effects of contraction and catecholamines

1980 ◽  
Vol 239 (6) ◽  
pp. E461-E467 ◽  
Author(s):  
R. Nesher ◽  
I. E. Karl ◽  
D. M. Kipnis
Keyword(s):  
Isometric Contraction ◽  
Mechanical Performance ◽  
Lactate Production ◽  
Glycogen Metabolism ◽  
Metabolic Effects ◽  
Inotropic Effects ◽  
Muscle Work ◽  
Two Phases ◽  
Fast Twitch

Effects of isometric contraction and catecholamines on glucose and glycogen metabolism in skeletal muscle were investigated with the in vitro rat epitrochlearis preparation. Mechanical performance and glycogenolysis exhibited two phases. During the initial 30 min, muscle work was 30% greater and glycogenolysis 8- to 10-fold faster than the steady-state values in the subsequent 3–4 h of contraction. Glucose uptake was increased by contraction and remained relatively constant during stimulation. Epinephrine (10(-9) to 10(-6) M) and norepinephrine (10(-7) to 10(-5) M) produced inotropic and glycogenolytic effects blocked by propranolol but not phentolamine. Chemical sympathectomy and propranolol blocked the initial glycogenolytic and inotropic effects produced by isometric contraction, suggesting that they were caused by the release of endogenous catecholamines. Net lactate production in resting muscles accounted for > 50% of total glucosyl units utilized. During contraction net lactate production accounted < 10–15% of total glycosyl flux indicating that rat fast-twitch pale muscle is capable of significant rates of aerobic glucose oxidation. Oleate and caprylate did not affect mechanical performance, glycogen, or glucose metabolism in resting or contracting muscles.

Origins of endogenous noradrenaline overflow during reperfusion of the ischaemic rat heart

1988 ◽  
Vol 74 (3) ◽  
pp. 269-274 ◽  
Author(s):  
A. M. Dart ◽  
R. A. Riemersma
Keyword(s):  
Extracellular Space ◽  
Rat Heart ◽  
Fold Increase ◽  
Isolated Rat Heart ◽  
Significant Rise ◽  
Endogenous Noradrenaline ◽  
Substrate Deprivation ◽  
Space Marker ◽  
Isolated Rat ◽  
Ischaemic Episode

1. Reperfusion of the globally ischaemic isolated rat heart is associated with an enhanced overflow of endogenous noradrenaline (NA) after ischaemic periods of 20, 40 or 60 min but not of 10 min. 2. Reperfusion NA overflow, after 40 min of ischaemia, is suppressed by desipramine and increased when ischaemia follows a period of substrate deprivation. 3. Reperfusion after 40 min of ischaemia is associated with a significant rise in NA concentration despite a simultaneous 20-fold increase in flow. This increase in concentration is abolished by treatment with desipramine or if ischaemia follows a period of substrate deprivation. 4. Reperfusion NA overflow correlates with the reperfusion overflow of an extracellular space marker infused before the ischaemic episode. 5. These results suggest that ischaemia is heterogeneous and that NA is released into regions of particularly profound ischaemia from which it is subsequently eluted during reperfusion.

Ultrastructure of region of a low safety factor in inhomogeneous giant axon of the cockroach

1976 ◽  
Vol 39 (4) ◽  
pp. 900-908 ◽  
Author(s):  
M. Castel ◽  
M. E. Spira ◽  
I. Parnas ◽  
Y. Yarom
Keyword(s):  
Electron Microscopy ◽  
Glial Cells ◽  
Extracellular Space ◽  
Light And Electron Microscopy ◽  
Giant Axon ◽  
Serial Sections ◽  
Giant Axons ◽  
Chemical Synapses ◽  
Cytoplasmic Processes ◽  
Periaxonal Space

1. The structure of the ventral giant axons of the cockroach at the level of ganglion T3 was studied by means of light and electron microscopy. 2. From serial sections and cobalt injections, the axons diameter was found to range between 40 and 60 mum at the caudal end of ganglion T3; toward the center of T3 they narrow to 20-40 mum, and again expand to 30-45 mum anteriorly in ganglion T3. 3. Each giant axon sends off several branches, 1-15 mum in diameter, into the neuropil. The giant axons and the bases of their branches are enveloped by cytoplasmic processes of glial cells. The periaxonal space is about 100-200 A. 4. Distally the branches are devoid of glial envelopes and the extracellular space between the branches and other axonal profiles is about 200 A. Terminals with presumptive chemical synapses on the giant axon branches were found. Clear vesicles, 300-400 A in diameter, are seen clustered together. The width of the supposedly synaptic gap is about 100 A. 5. In some areas the branches and other axonal profiles form close appositions.

Effective Use of Amino Acid Dialysate over four Weeks in CAPD Patients

1983 ◽  
Vol 3 (2) ◽  
pp. 66-72 ◽  
Author(s):  
Arie Oren ◽  
George Wu ◽  
G. Harvey Anderson ◽  
Errol Marliss ◽  
Ramesh Khanna ◽  
...  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Acid Solution ◽  
Serum Albumin ◽  
Hdl Cholesterol ◽  
Significant Rise ◽  
Protein Malnutrition ◽  
Metabolic Effects ◽  
Amino Acid Solution ◽  
Total Body

We studied the effectiveness, tolerance to, and beneficial metabolic effects of amino acid dialysate over an intermediate period in six CAPD patients. Two liters of 1% amino acid solution (Amino-Dianeal) were alternated with dialysate containing glucose. After four weeks there were significant increases in BUN (from 64 to 102 mg%), total body nitrogen (from 1333 to 1380 g), serum transferrin (from 175 to 222 mg%) and anion gap (from 15.1 to 17.3). Initially, there was a significant rise in HDL cholesterol, however, this was not sustained. No significant change was detected in total-body potassium, fasting serum albumin, triglyceride, insulin, glucagon, electrolytes, anthropometric measurements and daily ingestion of calories and proteins. During the study individual fasting, plasma amino acid levels showed significant increments in respect to histidine, tryptophan and glycine but alanine decreased. Several essential amino acids continued to show values below normal. Two hours after consumption of breakfast and concurrent infusion of the amino acid solution, the plasma levels of the amino acids in the dialysate peaked at emia, which develops in almost onehalf of the CAPD patients (7), and the significant weight gain observed in some of them. Furthermore, the daily losses of albumin and amino acids in the dialysate may induce protein malnutrition, especially if these losses are not replaced by an adequate daily protein intake. The presence of protein malnutrition in CAPD patients is indicated by the low serum albumin and total protein, and by the decrease in total body nitrogen over one year of CAPD (8).

Müller Cell Ca2+ Waves Evoked by Purinergic Receptor Agonists in Slices of Rat Retina

2001 ◽  
Vol 85 (2) ◽  
pp. 986-994 ◽  
Author(s):  
Yang Li ◽  
Lynne A. Holtzclaw ◽  
James T. Russell
Keyword(s):  
Glial Cells ◽  
Purinergic Receptor ◽  
Rank Order ◽  
Müller Cells ◽  
Uridine Diphosphate ◽  
Muller Cells ◽  
Wave Amplification ◽  
Dye Loading ◽  
Intracellular Ca ◽  
Retinal Slices

We have measured agonist evoked Ca2+ waves in Müller cells in situ within freshly isolated retinal slices. Using an eye cup dye loading procedure we were able to preferentially fill Müller glial cells in retinal slices with calcium green. Fluorescence microscopy revealed that bath perfusion of slices with purinergic agonists elicits Ca2+ waves in Müller cells, which propagate along their processes. These Ca2+ signals were insensitive to tetrodotoxin (TTX, 1.0 μM) pretreatment. Cells were readily identified as Müller cells by their unique morphology and by subsequent immunocytochemical labeling with glial fibrillary acidic protein antibodies. While cells never exhibited spontaneous Ca2+ oscillations, purinoreceptor agonists, ATP, 2 MeSATP, ADP, 2 MeSADP, and adenosine readily elicited Ca2+ waves. These waves persisted in the absence of [Ca2+]o but were abolished by thapsigargin pretreatment, suggesting that the purinergic agonists tested act by releasing Ca2+ from intracellular Ca2+ stores. The rank order of potency of different purines and pyrimidines for inducing Ca2+ signals was 2 MeSATP = 2MeSADP > ADP > ATP ≫ αβmeATP = uridine triphosphate (UTP) > uridine diphosphate (UDP). The Ca2+signals evoked by ATP, ADP, and 2 MeSATP were inhibited by reactive blue (100 μM) and suramin (200 μM), and the adenosine induced signals were abolished only by 3,7-dimethyl-1-propargylxanthine (200 μM) and not by 1,3-dipropyl-8-(2-amino-4-chlorophenyl)-xanthine) or 8-cyclopentyl-1,3-dipropylxanthine at the same concentration. Based on these pharmacological characteristics and the dose-response relationships for ATP, 2 MeSATP, 2 MeSADP, ADP, and adenosine, we concluded that Müller cells express the P1A2 and P2Y1 subtypes of purinoceptors. Analysis of Ca2+ responses showed that, similar to glial cells in culture, wave propagation occurred by regenerative amplification at specialized Ca2+ release sites (wave amplification sites), where the rate of Ca2+ release was significantly enhanced. These data suggest that Müller cells in the retina may participate in signaling, and this may serve as an extra-neuronal signaling pathway.

scholarly journals Epidermal growth factor counteracts the glycogenic effect of insulin in parenchymal hepatocyte cultures

1987 ◽  
Vol 247 (2) ◽  
pp. 307-314 ◽  
Author(s):  
M H Chowdhury ◽  
L Agius
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Cyclic Amp ◽  
Glycogen Metabolism ◽  
Metabolic Effects ◽  
Hepatocyte Cultures ◽  
Glucose Incorporation ◽  
Epidermal Growth ◽  
Parenchymal Hepatocytes

Rat parenchymal hepatocytes in monolayer culture were used to study the metabolic effects of epidermal growth factor (EGF) and insulin on ketogenesis, gluconeogenesis and glycogen metabolism. EGF, unlike insulin, did not inhibit ketogenesis from palmitate or gluconeogenesis from pyruvate in hepatocyte cultures. It also had no effect on these pathways in the presence of insulin. In contrast, EGF potently counteracted the stimulation of [14C]pyruvate incorporation into glycogen by insulin, and also glycogen deposition from both gluconeogenic precursors and glucose. The EGF concentration causing half-maximal effect was about 0.1 nM. The anti-glycogenic effect of EGF was observed after both long-term (24 h) and short-term (1 h) exposure to EGF, and was more marked in the presence of insulin than in its absence. EGF did not displace bound insulin, suggesting that it neither competes for the insulin receptor nor affects the affinity of the receptor for insulin. EGF did not alter cellular cyclic AMP; and inhibition of cyclic AMP phosphodiesterase activity did not prevent the anti-glycogenic effect of EGF. In liver-derived dividing epithelial cells, Hep-G2 cells and fibroblasts, which have no capacity for gluconeogenesis, EGF did not counteract the stimulatory effect of insulin on [14C]glucose incorporation into glycogen, and in the epithelial cells EGF increased [14C]glucose incorporation into glycogen. The counter-effect of EGF on the glycogenic action of insulin in parenchymal hepatocytes may be due to a direct effect on glycogen metabolism or to an interaction with the post-receptor events in insulin action.

scholarly journals Lactate Accumulation during Moderate Hypoxic Hypoxia in Neocortical Rat Brain

1996 ◽  
Vol 16 (6) ◽  
pp. 1345-1352 ◽  
Author(s):  
Jean-François Payen ◽  
Emmanuelle LeBars ◽  
Bernard Wuyam ◽  
Bernard Tropini ◽  
Jean-Louis Pépin ◽  
...  
Keyword(s):  
Control Period ◽  
Relaxation Times ◽  
Significant Rise ◽  
Hypoxic Hypoxia ◽  
Metabolic Effects ◽  
Marked Rise ◽  
Arterial Lactate ◽  
Apparent Decrease ◽  
Lactate Infusion ◽  
Lactate Peak

Neocortical metabolism was studied during moderate hypoxic hypoxia, reoxygenation, and postmortem periods in anesthetized normocapnic rats using 1H nuclear magnetic resonance (NMR) spectroscopic imaging. Rats were prepared with unilateral common carotid occlusion to determine the ipsilateral metabolic effects of inadequate cerebral blood flow (CBF) response to hypoxia. No difference in brain metabolism between the two hemispheres was found during the control period. Hypoxic hypoxia (Pao2 = 54.1 ± 5.8 mm Hg) resulted in a significant rise in neocortical lactate peak in both hemispheres, with an additional marked rise in the clamped side compared to the unclamped side (53 ± 27 vs. 22 ± 13% of postmortem value, p < 0.001). These lactate changes were not reversible within 30 min of reoxygenation in the clamped hemisphere. No changes in neocortical lactate peak were observed while elevating arterial lactate via intravenous lactate infusion without hypoxia. In addition, hypoxic hypoxia resulted in an apparent decrease in neocortical water and N-acetyl aspartate (NAA) signals, which were related to a shortening in T2 relaxation times. It is concluded that neocortical lactate is an early metabolic indicator during moderate hypoxic hypoxia in normocapnic conditions.

Effect of osmotic stress on potassium accumulation around glial cells and extracellular space volume in rat spinal cord slices

2001 ◽  
Vol 65 (2) ◽  
pp. 129-138 ◽  
Author(s):  
Lýdia Vargová ◽  
Alexandr Chvátal ◽  
Miroslava Anděrová ◽  
Šárka Kubinová ◽  
Drahomír Žiak ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Osmotic Stress ◽  
Glial Cells ◽  
Extracellular Space ◽  
Rat Spinal Cord ◽  
Potassium Accumulation ◽  
Space Volume
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