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  • 1
    Digitale Medien
    Digitale Medien
    Protein Kinase C Activation Enhances K+-Stimulated Endogenous Dopamine Release from Rat Striatal Synaptosomes in the Absence of an Increase in Cytosolic Ca2+ (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 52 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: The possibility that protein kinase C modulates neurotransmitter release in brain was investigated by examining the effects of 12-O-tetradecanoylphorbol 13-acetate (TPA) on Ca2+ transport and endogenous dopamine release from rat striatal synaptosomes. TPA (0.16 and 1.6 μM) significantly increased dopamine release by 24 and 33%, respectively, after a 20-min preincubation with TPA followed by 60 s of depolarization with 30 mM KCl. Depolarization-induced 45Ca2+ uptake, measured simultaneously with dopamine release, was not significantly increased by TPA. Neither 45Ca2+ uptake nor dopamine release was altered under resting conditions. When the time course of K+-stimulated 45Ca2+ uptake and dopamine release was examined, TPA (1.6 μM) enhanced dopamine release after 15, 30, and 60 s, but not 1, 3, or 5 s, of depolarization. A slight increase in 45Ca2+ uptake after 60 s of depolarization was also seen. The addition of 30 mM KCl to synaptosomes which had been preloaded with the Ca2+-sensitive fluorophore fura-2 increased the cytosolic free Ca2+ concentration ([Ca2+]i) from 445 nM to 506 nM after 10 s of depolarization and remained elevated after 60 s. TPA had no effect on [Ca2+]i under depolarizing or resting conditions. Replacing extracellular Ca2+ with 100 μM EGTA reduced K+-stimulated (60 s) endogenous dopamine release by 53% and decreased [Ca2+]i to 120 nM. In Ca2+-free medium, 30 mM KCl did not produce an increase in the [Ca2+]i. TPA (1.6 μM) did not alter the [Ca2+]i under resting or depolarizing conditions, but did increase K+-stimulated dopamine release in Ca2+-free medium. The inactive 4α-phorbol had no effect under any of the above experimental conditions. The demonstration that TPA induced an increase in dopamine release without an increase in the [Ca2+]i may suggest that protein kinase C increases the sensitivity of the exocytotic release process to Ca2+.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07275.x
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  • 2
    Digitale Medien
    Digitale Medien
    Correlation of Rates of Calcium Entry and Release of Endogenous Norepinephrine in Rat Brain Region Synaptosomes (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 46 (1986), S. 0 
    Details
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: Voltage-dependent 45Ca2+ uptake and endogenous norepinephrine (NE) release were measured simultaneously in synaptosomes isolated from rat hypothalamus, brainstem, and cerebellum at 1, 3, 5, 15, and 30 s. In synaptosomes depolarized by 125 mM KCl, 45Ca2+ uptake and NE release exhibited fast and slow components. Rates of NE release and 45Ca2+ uptake were fastest from 0 to 1 s. NE release and 45Ca2+ uptake rates from 1 to 5 s were 〈15% of 0–1 s rates. Both resting (5 mM KCl) and depolarization-induced (125 mM KCl) NE release paralleled 45Ca2+ uptake from 1 to 30 s. Voltage-dependent NE release was approximately 1% and 2% of total synaptosomal NE content at 1- and 30-s measurement intervals, respectively, and did not differ between the three brain regions studied. Calcium and potassium dependence studies showed that NE release was stimulated by increased potassium and that depolarization-induced NE release was dependent on the presence of external calcium. These results show that calcium-dependent NE release from synaptosomes is correlated with calcium entry. Both processes exhibit fast and slow temporal components.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1471-4159.1986.tb12954.x
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  • 3
    Digitale Medien
    Digitale Medien
    Mechanism of Inhibition of N-Methyl-d-Aspartate-Stimulated Increases in Free Intracellular Ca2+ Concentration by Ethanol (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 56 (1991), S. 0 
    Details
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: Dissociated brain cells were isolated from newborn rat pups and loaded with fura-2. These cells were sensitive to low N-methyl-d-aspartate (NMDA) concentrations with EC50 values for NMDA-induced intracellular Ca2+ concentration ([Ca2+]i) increases of approximately 7–16 μM measured in the absence of Mg2+. NMDA-stimulated [Ca2+]j increases could be observed in buffer with Mg2+ when the cells were predepolarized with 15 mMKQ prior to NMDA addition. Under these predepolarized conditions, 100 mMethanol inhibited 25 μM NMDA responses by approximately 50%, which was similar to the ethanol inhibition observed in buffer without added Mg2+. Ethanol did not alter [Ca2+]i prior to NMDA addition. In the absence of Mg2+, 50 and 100 mM ethanol did not significantly alter the EC50 value for NMDA, but did inhibit NMDA-induced increases in [Ca2+]i in a concentration-dependent manner at 4, 16, 64, and 256 μM NMDA. Whereas NMDA-induced increases in [Ca2+]i were dependent on extracellular Ca2+ and were inhibited by Mg2+, the ability of 100 mM ethanol to inhibit 25 μM NMDA responses was independent of the external Ca2+ or Mg2+ concentrations. Glycine (1, 10, and 100 μM) enhanced 25 μM NMDA-induced increases in [Ca2+]i by approximately 50%. Glycine (1-100 μM) prevented the 100 mM ethanol inhibition of NMDA-stimulated [Ca2+]i observed in the absence of exogenous glycine. MK-801 (25-400 μM) inhibited 25 μM NMDA-stimulated rises in [Ca2+]i in a concentration-dependent manner. Unlike the additive inhibition observed with Mg2+ plus ethanol, as the concentration of MK-801 increased above 50 μM, ethanol (at 100 mM) did not produce further inhibition of NMDA responses compared with MK-801 alone. These results suggest that ethanol may produce a noncompetitive inhibition of NMDA-stimulated Ca2+ influx in dissociated brain cells, with interactions at the glycine and possibly the phencyclidine site on the NMDA-receptor complex.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1471-4159.1991.tb02048.x
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  • 4
    Digitale Medien
    Digitale Medien
    45Ca2+ Uptake into Rat Whole Brain Synaptosomes Unaltered by Dihydropyridine Calcium Antagonists (1983)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 41 (1983), S. 0 
    Details
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: Voltage-dependent 45Ca2+ uptake into rat whole brain synaptosomes was measured after 3-s KClinduced depolarization to investigate possible inhibitory effects of calcium antagonists, nitrendipine, nimodipine, and nisoldipine. At a Ca2+ concentration of 1.2 mM, nitrendipine, in concentrations ranging from 0.1 nM to 10 μM, had no effect on 45Ca2+ uptake. When the Ca2+ concentration was lowered to 0.06 and 0.12 μM, nitrendipine, 10 μM, inhibited 45Ca2+ uptake in response to 109 mM KC1 depolarization. However, in a separate concentration response study, nitrendipine, nimodipine, and nisoldipine, 0.1 μM to 10 μM, failed to alter the uptake of 45Ca2+ (0.06 mM Ca2+) into 30 mM KCl-depolarized synaptosomes. The high concentrations of these agents required to depress 45Ca2+ uptake indicate that the dihydropyridine calcium antagonists are considerably less potent in brain tissue than in peripheral tissue.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1111/j.1471-4159.1983.tb00845.x
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  • 5
    Digitale Medien
    Digitale Medien
    Calcium uptake in skeletal muscle mitochondria (1978)
    Springer
    European journal of applied physiology 39 (1978), S. 111-116 
    Details
    ISSN: 1439-6327
    Schlagwort(e): Fatigue ; Mitochondria ; Chelating agents ; Calcium ; Magnesium
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Female Wistar rats were used to determine the effects of the chelating agents, EDTA and EGTA, on the in vitro 45Ca2+ accumulation by mitochondria isolated from the skeletal muscle of fatigued animals. The rats were divided into three groups: sedentary-rested (SR), trained-rested (TR), trained-exhausted (TE). The trained groups were exercised on a treadmill for 1 h daily, five times a week, for 22 weeks. At the conclusion of the training program, the TE group was rapidly exercised to exhaustion immediately following their daily 1-h run. In the TR group EDTA reduced 45Ca2+ binding while both EDTA and EGTA appeared to increase mitochondrial Ca2+ and Mg2+ content. In the TE group, EDTA reduced endogenous mitochondrial Ca2+ and Mg2+ content, while both EDTA and EGTA increased 45Ca2+ binding. Since chelating Ca2+ and Mg2+ from the membrane may affect the structure and function of the mitochondria, it is suggested that the use of chelating agents during the isolation of mitochondria from the skeletal muscle of trained rats be viewed with caution.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00421715
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  • 6
    Digitale Medien
    Digitale Medien
    Calcium uptake in skeletal muscle mitochondria (1978)
    Springer
    European journal of applied physiology 39 (1978), S. 117-122 
    Details
    ISSN: 1439-6327
    Schlagwort(e): Mitochondria ; Calcium ; Magnesium ; Training ; Fatigue
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary In order to ascertain the effects of long-term exercise training and long-term exhaustive exercise on mitochondrial 45Ca2+ uptake and related variables in rat skeletal muscle, female rats were randomly divided into three groups: sedentary-rested (SR), trained-rested (TR), and trained-exhausted (TE). The trained groups were exercised five times per week on a treadmill for 22 weeks. At the conclusion of the training period, the TE group was exercised to exhaustion following their daily 1 h run. The 45Ca2+ uptake and endogenous mitochondrial Ca2+ content of skeletal muscle followed stepwise increases of approximately 25% and 50%, respectively, across the groups, suggesting that long-term exercise induces the mitochondria to play an important role as a Ca2+ ion buffer. A 75–83% reduction in 45Ca2+ binding in the TE group suggests a selective loss and partial saturation of membrane phospholipids with exhaustive exercise. The TE group had a two-fold greater content of mitochondrial Mg2+ than did the rested groups. It is speculated that the mitochondria accumulate Mg2+ during acute exercise to maintain the functional integrity of the membrane, thus offsetting the deleterious effects of excessive Ca2+ uptake.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00421716
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