Inhibition of glycogenesis in rat muscles partially depleted of glycogen

1991 ◽  
Vol 261 (2) ◽  
pp. C305-C309 ◽  
Author(s):  
J. Gorski ◽  
I. Krawczuk ◽  
M. Gorska ◽  
J. Rutkiewicz
Keyword(s):  
Sciatic Nerve ◽  
Wistar Rats ◽  
Contractile Activity ◽  
Muscle Group ◽  
Glycogen Depletion ◽  
Stomach Tube ◽  
Plantaris Muscle ◽  
Anesthetized Rats ◽  
Male Wistar Rats ◽  
Stimulation Of

This study aimed to examine the extent to which repletion of glycogen in muscles partially depleted of glycogen may be inhibited by contractions and epinephrine. Four experiments were carried out on untrained male Wistar rats. 1) Animals ran 150 min (1,200 m/h) on a treadmill set at +10 degrees incline. After 60, 90, and 120 min of running, they were given glucose (40% solution, 1 ml/100 g) by a stomach tube. 2) Rats ran on a treadmill set as above for 20 min at 3,200 m/h and then 2 h at 800 m/h. 3) In anesthetized rats, gastrocnemius-plantaris muscle group was made to contract isometrically by means of stimulation of the sciatic nerve. The nerve was stimulated with tetanic pulses (7 V, 0.05-ms duration, delivered in 100-ms trains at 100 Hz): first 15 min, 2 pulses/s, then 2 h, 1 pulse/2 s. 4) Epinephrine (0.5 mg/kg) was administered subcutaneously 10 min before onset of stimulation of the sciatic nerve. The nerve was stimulated 15 min with tetanic pulses (as above), 2 pulses/s. Next, rats were rested for 2 h. Level of glycogen was determined in samples of white and red gastrocnemius, plantaris, and soleus. Initial running or stimulation resulted in pronounced glycogen depletion in each muscle. Thereafter, either considerable or full repletion of glycogen occurred in the muscles despite continued contractile activity or the presence of epinephrine. The degree of repletion depended both on the type of muscle and the type of activation of glycogenolysis (running, stimulation of the nerve, epinephrine).(ABSTRACT TRUNCATED AT 250 WORDS)

Nerve stimulation decreases malonyl-CoA in skeletal muscle

1992 ◽  
Vol 72 (3) ◽  
pp. 901-904 ◽  
Author(s):  
C. Duan ◽  
W. W. Winder
Keyword(s):  
Sciatic Nerve ◽  
Creatine Phosphate ◽  
Muscle Group ◽  
Carnitine Palmitoyl Transferase ◽  
Plantaris Muscle ◽  
Malonyl Coa ◽  
Left And Right ◽  
Muscle Groups ◽  
Stimulation Of

This study was designed to determine the effect of in situ electrical stimulation of the sciatic nerve on malonyl-CoA, an inhibitor of carnitine palmitoyl transferase, in the gastrocnemius/plantaris muscle group of rats. The left sciatic nerve was stimulated at a frequency of 5 Hz with 100-ms trains of impulses (50 Hz) for 1, 3, or 5 min. At the end of stimulation, the left and right (nonstimulated) gastrocnemius/plantaris muscle groups were clamp-frozen and later analyzed for malonyl-CoA and other metabolites. No change was observed in the noncontracting contralateral muscles in malonyl-CoA, ATP, creatine phosphate (CP), or citrate. In the stimulated muscles, malonyl-CoA decreased from 1.7 +/- 0.1 to 1.0 +/- 0.1 nmol/g (P less than 0.05), and CP decreased from 15.8 +/- 0.9 to 12.2 +/- 1.0 mumol/g (P less than 0.05) after 3 min of stimulation. After 5 min of stimulation, malonyl-CoA was 1.0 +/- 0.1 nmol/g and CP was 10.3 +/- 1.3 mumol/g. When muscles were stimulated for 5 min with single impulses (5 Hz), malonyl-CoA was decreased from 1.8 +/- 0.3 to 1.0 +/- 0.1 nmol/g, with no change in CP, ATP, or adenosine 3′,5′-cyclic monophosphate. Thus a decline in malonyl-CoA can be induced by muscle contraction independently of humoral influence.

Tissue distribution and antithrombotic activity of unlabeled or 14C-labeled porcine intestinal mucosal heparin following administration to rats by the oral route

2000 ◽  
Vol 78 (4) ◽  
pp. 307-320 ◽  
Author(s):  
Linda M Hiebert ◽  
Sandra M Wice ◽  
Tilly Ping ◽  
Ronald E Hileman ◽  
Ishan Capila ◽  
...  
Keyword(s):  
Gel Electrophoresis ◽  
Wistar Rats ◽  
Jugular Vein ◽  
Oral Route ◽  
Gut Contents ◽  
Agarose Gel Electrophoresis ◽  
Antithrombotic Effect ◽  
Stomach Tube ◽  
Antithrombotic Activity ◽  
Male Wistar Rats

Distribution and antithrombotic activity of orally administered unfractionated porcine heparin were studied. [14C]Heparin was prepared by de-N-acetylation of porcine mucosal heparin followed by re-N-acetylation, using [14C]acetic anhydride. [14C]Heparin and (or) cold heparin (60 mg/kg) were administered by stomach tube to male Wistar rats. Blood, all levels of gut and gut contents, liver, lung, spleen, kidney, and aortic and vena caval endothelium were collected under deep anesthesia at 3, 6, 15, 30, and 60 min and 4 and 24 h (6 rats/group) after administration. Urine and feces were collected at 24 h, using metabolic cages. In three additional rats, drugs were administered in gelatin capsules. Tissues listed above and tongue, esophagus, trachea, brain, heart, thymus, bile ducts, vena caval and aortic walls, ureters, bladder, samples of muscle, skin, hair, and bone marrow were collected at 24 h. Radioactivity and chemical heparin, measured by agarose gel electrophoresis, were observed in all tissues examined as well as gut washes, plasma, urine, and feces. Radiolabel recovered was confirmed to be heparin by autoradiograms of gradient polyacrylamide electrophoretic gels. [14C]Heparin and chemical heparin in gut tissue suggest a transit time of 4 h. Porcine or bovine heparin (7.5 mg/kg), administered by stomach tube, decreased the incidence of thrombosis induced by applying 10% formalin in 65% methanol to the exposed jugular vein of rats. Heparin isolation from non-gut tissue, endothelium, urine, and plasma and the observed antithrombotic effect are consistent with oral bioavailability.Key words: heparin, [14C]heparin, oral administration, distribution, radiolabel, thrombosis.

Antinociceptive effects of lead acetate in sciatic nerve chronic constriction injury model of peripheral neuropathy in male Wistar rats

2020 ◽  
Vol 394 (1) ◽  
pp. 117-125
Author(s):  
Bamidele Victor Owoyele ◽  
Ahmed Olalekan Bakare ◽  
Maryam Tayo Ayinla ◽  
Kehinde Ahmed Adeshina ◽  
Damilola Onietan ◽  
...  
Keyword(s):  
Peripheral Neuropathy ◽  
Sciatic Nerve ◽  
Lead Acetate ◽  
Wistar Rats ◽  
Chronic Constriction Injury ◽  
Injury Model ◽  
Antinociceptive Effects ◽  
Male Wistar Rats ◽  
Chronic Constriction Injury Model

Exercise and glycogen depletion: effects on ability to activate muscle phosphorylase

1986 ◽  
Vol 60 (5) ◽  
pp. 1518-1523 ◽  
Author(s):  
S. H. Constable ◽  
R. J. Favier ◽  
J. O. Holloszy
Keyword(s):  
Muscle Contraction ◽  
Muscle Glycogen ◽  
Contractile Activity ◽  
Strenuous Exercise ◽  
Glycogen Depletion ◽  
Significant Difference ◽  
Muscle Phosphorylase ◽  
Glycogen Repletion ◽  
Stimulation Of

Phosphorylase activation reverses during prolonged contractile activity. Our first experiment was designed to determine whether this loss of ability to activate phosphorylase by stimulation of muscle contraction persists following exercise. Phosphorylase activation by stimulation of muscle contraction was markedly inhibited in rats 25 min after exhausting exercise. To evaluate the role of glycogen depletion, we accelerated glycogen utilization by nicotinic acid administration. A large difference in muscle glycogen depletion during exercise of the same duration did not influence the blunting of phosphorylase activation. Phosphorylase activation by stimulation of contraction was more severely inhibited following prolonged exercise than after a shorter bout of exercise under conditions that resulted in the same degree of glycogen depletion. A large difference in muscle glycogen repletion during 90 min of recovery was not associated with a significant difference in the ability of muscle stimulation to activate phosphorylase, which was still significantly blunted. Phosphorylase activation by epinephrine was also markedly inhibited in muscle 25 min after strenuous exercise but had recovered completely in glycogen-repleted muscle 90 min after exercise. These results provide evidence that an effect of exercise other than glycogen depletion is involved in causing the inhibition of phosphorylase activation; however, they do not rule out the possibility that glycogen depletion also plays a role in this process.

scholarly journals GABA and glycine receptors in the nucleus ambiguus mediate tachycardia elicited by chemical stimulation of the hypothalamic arcuate nucleus

2015 ◽  
Vol 309 (1) ◽  
pp. H174-H184 ◽  
Author(s):  
Vineet C. Chitravanshi ◽  
Kazumi Kawabe ◽  
Hreday N. Sapru
Keyword(s):  
Paraventricular Nucleus ◽  
Wistar Rats ◽  
Arcuate Nucleus ◽  
Chemical Stimulation ◽  
Nucleus Ambiguus ◽  
Glycine Receptors ◽  
Inhibitory Neurotransmitters ◽  
Hypothalamic Arcuate Nucleus ◽  
Male Wistar Rats ◽  
Stimulation Of

We have previously reported that stimulation of the hypothalamic arcuate nucleus (ARCN) by microinjections of N-methyl-d-aspartic acid (NMDA) elicits tachycardia, which is partially mediated via inhibition of vagal inputs to the heart. The neuronal pools and neurotransmitters in them mediating tachycardia elicited from the ARCN have not been identified. We tested the hypothesis that the tachycardia elicited from the ARCN may be mediated by inhibitory neurotransmitters in the nucleus ambiguus (nAmb). Experiments were done in urethane-anesthetized, artificially ventilated, male Wistar rats. In separate groups of rats, unilateral and bilateral microinjections of muscimol (1 mM), gabazine (0.01 mM), and strychnine (0.5 mM) into the nAmb significantly attenuated tachycardia elicited by unilateral microinjections of NMDA (10 mM) into the ARCN. Histological examination of the brains showed that the microinjections sites were within the targeted nuclei. Retrograde anatomic tracing from the nAmb revealed direct bilateral projections from the ARCN and hypothalamic paraventricular nucleus to the nAmb. The results of the present study suggest that tachycardia elicited by stimulation of the ARCN by microinjections of NMDA is mediated via GABAA and glycine receptors located in the nAmb.

scholarly journals Differential effects of GH and GH-releasing peptide-6 on astrocytes

2013 ◽  
Vol 218 (3) ◽  
pp. 263-274 ◽  
Author(s):  
Eva Baquedano ◽  
Julie A Chowen ◽  
Jesús Argente ◽  
Laura M Frago
Keyword(s):  
Wistar Rats ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Pi3k Inhibitor Ly294002 ◽  
Astrocytoma Cells ◽  
Proliferation And Differentiation ◽  
C6 Astrocytoma ◽  
Male Wistar Rats ◽  
Independent Effects ◽  
Stimulation Of

GH and GH secretagogues (GHSs) are involved in many cellular activities such as stimulation of mitosis, proliferation and differentiation. As astrocytes are involved in developmental and protective functions, our aim was to analyse the effects of GH and GH-releasing hexapeptide on astrocyte proliferation and differentiation in the hypothalamus and hippocampus. Treatment of adult male Wistar rats with GH (i.v., 100 μg/day) for 1 week increased the levels of glial fibrillary acidic protein (GFAP) and decreased the levels of vimentin in the hypothalamus and hippocampus. These changes were not accompanied by increased proliferation. By contrast, GH-releasing hexapeptide (i.v., 150 μg/day) did not affect GFAP levels but increased proliferation in the areas studied. To further study the intracellular mechanisms involved in these effects, we treated C6 astrocytoma cells with GH or GH-releasing hexapeptide and the phosphatidylinositol 3′-kinase (PI3K) inhibitor, LY294002, and observed that the presence of this inhibitor reverted the increase in GFAP levels induced by GH and the proliferation induced by GH-releasing hexapeptide. We conclude that although GH-releasing hexapeptide is a GHS, it may exert GH-independent effects centrally on astrocytes when administered i.v., although the effects of both substances appear to be mediated by the PI3K/Akt pathway.

GABAergic effects on the depressor responses elicited by stimulation of central nucleus of the amygdala

1999 ◽  
Vol 276 (1) ◽  
pp. H242-H247 ◽  
Author(s):  
John Ciriello ◽  
Stefanie Roder
Keyword(s):  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Wistar Rats ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
The Other ◽  
Central Nucleus ◽  
Male Wistar Rats ◽  
The Mean ◽  
Stimulation Of

GABAergic inputs have been demonstrated in the central nucleus of the amygdala (ACe). However, the contribution of these inhibitory inputs to the cardiovascular responses elicited from the ACe is not known. Experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated male Wistar rats to investigate the effects of microinjections of GABA, the selective GABAA-receptor antagonist bicuculline, or the GABAB-receptor antagonist phaclofen, in the ACe on the mean arterial pressure (MAP) and heart rate (HR) responses elicited byl-glutamate (Glu) stimulation of the ACe. Microinjections of Glu in the ACe elicited decreases in MAP (−13.7 ± 1.6 mmHg) and HR (−5.3 ± 1.9 beats/min). The MAP and HR responses elicited by Glu stimulation of the ACe were significantly reduced (89%) by the prior microinjection of GABA in the same ACe site. In addition, at some sites in the ACe at which microinjection of Glu did not elicit depressor responses, Glu injections in the presence of phaclofen elicited decreases in MAP (−9.5 ± 1.0 mmHg) and variable changes in HR. On the other hand, the magnitude of the depressor responses elicited during stimulation of the ACe site in the presence of bicuculline was significantly attenuated (60%), whereas phaclofen had no effect on the magnitude of the depressor responses elicited by Glu stimulation of the ACe. These data suggest that GABAergic mechanisms in the ACe alter the excitability of ACe neurons involved in mediating changes in systemic arterial pressure and HR.

scholarly journals Contractions dynamic of “fast” and “slow” rat muscle under spinal shock and modulators of contraction

2021 ◽  
Vol 102 (3) ◽  
pp. 329-334
Author(s):  
V V Valiullin ◽  
A E Khairullin ◽  
A A Eremeev ◽  
A Yu Teplov ◽  
A R Shaikhutdinova ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Sciatic Nerve ◽  
Femoral Artery ◽  
Contractile Function ◽  
Contractile Activity ◽  
Circulatory System ◽  
Control Group ◽  
Contraction Force ◽  
Spinal Shock ◽  
Stimulation Of

Aim. To study the dynamics of neuromotor regulation of the contractile function of fast and slow muscles in rodents during spinal shock by spinal cord transection at the level Тh11Тh12. Methods. The experiments were carried out on laboratory rats weighing 140180 g. The animals were divided into two groups: Control (8 rats) and Spinal shock (6 rats). The lower leg muscles, m. soleus and m. extensor digitorum longus (m. EDL), were dissected by partially isolating without disrupting the connection with the body's circulatory system. The sciatic nerve was stimulated with single electrical impulses (10 V, 0.5 ms). Contractions of both muscles caused by electrical stimulation of the sciatic nerve before and after the injection of the substances into the femoral artery tubocurarine (1 mM) or norepinephrine (10 mM) were recorded in animals of both groups. After spinalization, muscle contractions were re-recorded during electrical stimulation of the sciatic nerve before and 10 minutes after the injection of tubocurarine or noradrenaline into the femoral artery in the same concentrations. Results. After spinalization of the animal, the contraction force of the muscle m. EDL fibers increased to 0.430.03 g (p=0.040), but the temporal parameters remained unchanged. M. soleus, on the contrary, showed a decrease in the contraction time to 0.0530.005 s (p=0.045), and no change in the contraction force was observed under these conditions. Intra-arterial administration of norepinephrine in the control group resulted in an increase of m. soleus contractions up to 1.210.17 g (p=0.048), and m. EDL up to 0.570.07 g (p=0.043). The administration of norepinephrine in spinalized animals caused an increase in the contraction of m. soleus up to 1.210.09 g (p=0.047), and m. EDL up to 0.660.05 g (p=0.043). The blocker of postsynaptic cholinergic receptors tubocurarine administration reduced the force of contraction of both muscle types in both control [m. soleus up to 0.390.03 g (p=0.039), m. EDL up to 0.110.02 g (p=0.042)] and spinalized [m. soleus up to 0.340.05 g (p=0.039), m. EDL up to 0.150.04 g (p=0.040)] animals. Conclusion. The data obtained demonstrate the presence of significant differences in the mechanisms of control of contractile activity in the fast and slow skeletal muscles of warm-blooded animals; the persistence of the similar effect of the basic modulators on the contraction of both muscles with such a striking reaction to spinalization highlights the contribution of neurotrophic control to the functioning of fast and slow motor units.

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