Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.21 (CPT)
 4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study has monitored junctional and nonjunctional resistance, [Ca2+]i and [H+]i, and the effects of various drugs in crayfish septate axons exposed to neutral anesthetics. The uncoupling efficiency of heptanol and halothane is significantly potentiated by caffeine and theophylline. The modest uncoupling effects of isoflurane, described here for the first time, are also enhanced by caffeine. Heptanol causes a decrease in [Ca2+]i and [H+]i both in the presence and absence of either caffeine or theophylline. A similar but transient effect on [Ca2+]i is observed with halothane. 4-Aminopyridine strongly inhibits the uncoupling effects of heptanol. The observed decrease in [Ca2+]i with heptanol and halothane and negative results obtained with different [Ca2+]o, (Ca2+)-channel blockers (nisoldipine and Cd2+) and ryanodine speak against a Ca2+ participation. Negative results obtained with 3-isobutyl-1-methylxanthine, forskolin, CPT-cAMP, 8Br-cGMP, adenosine, phorbol ester and H7, superfused in the presence and absence of caffeine and/or heptanol, indicate that neither the heptanol effects nor their potentiation by caffeine are mediated by cyclic nucleotides, adenosine receptors and kinase C. The data suggest a direct effect of anesthetics, possibly involving both polar and hydrophobic interactions with channel proteins. Xanthines and 4-aminopyridine may participate by influencing polar interactions. The potentiating effect of xanthines on cell-to-cell uncoupling by anesthetics may provide some clues on the nature of cardiac arrhythmias in patients treated with theophylline during halothane anesthesia.
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PMID:Effects of the anesthetics heptanol, halothane and isoflurane on gap junction conductance in crayfish septate axons: a calcium- and hydrogen-independent phenomenon potentiated by caffeine and theophylline, and inhibited by 4-aminopyridine. 205 74

Intracellular free Ca2+ concentration ([Ca2+]i) was measured by laser scanning confocal microscope, using Ca2+ indicator Fluo-3 in cultured hippocampal CA1 neurons isolated from newborn rat. The results showed that acute anoxia induced a rapid increase of [Ca2+]i in hippocampal CA1 neurons, and this increase could be attenuated by 100 mumol/L adenosine significantly. This effect of adenosine could be suppressed by adenosine A1 receptor antagonist CPT or potassium channel blockers, 4-AP and glipizide. These results suggest that adenosine activates 4-AP- or ATP-sensitive potassium channels through A1 receptors, and consequently inhibits the [Ca2+]i elevation in hippocampal neurons during anoxia.
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PMID:[Effect of adenosine on intracellular free calcium in cultured rat hippocampal CA1 neurons during anoxia]. 981 94

The role of adenosine in reversible inhibition of synaptic function during the early stage of anoxia and its mechanisms were investigated with extracellular recording technique in rat hippocampal slices. The results showed that acute anoxia led to the reversible inhibition of synaptic function, which is similar to the response to addition of high concentration of exogenous adenosine. The reversible inhibition could be suppressed by adenosine A1 receptor antagonist CPT and potassium channel blocker 4-AP, whereas TEA and ATP-sensitive potassium channel blocker glipzide had no effect. These results suggest that during the early stage of anoxia, the enhanced release of endogenous adenosine can inhibit the synaptic transmission by activating 4-AP-sensitive potassium channels via A1 receptors and thus play a role in protenction against anoxic injury. ATP-sensitive potassium channels may not be involved in the mechanisms of adenosine action.
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PMID:[The role of adenosine in the early stage of anoxia of hippocampal slices and its mechanisms]. 1007 22