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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 12 (1971), S. 132-149 
    ISSN: 1432-1106
    Keywords: Cerebral cortex ; Spreading Depression ; Glutamic acid ; Excitation ; Depression ; Cat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Variations in the excitability of individual cortical neurones during the invasion of spreading depression (SD) have been monitored by observing the alterations of spontaneous and L-glutamate-induced firing. Invasion of many neurones during SD is marked by a brief burst of firing which occurs concurrently with the onset of the negative slow extracellular potential. Other neurones do not fire, although the microelectrode records a negative slow wave. Depression of glutamate-induced and spontaneous firing follows and may last for several minutes. The initial loss of excitability of those neurones that discharge during SD invasion may be due to excessive depolarization. This phase is rapidly succeeded by a period of depressed excitability, during which the neurones can be invaded by an antidromic spike or excited by increased amounts of L-glutamate. These findings indicate that SD propagation initially involves the release of an excitant substance, possibly glutamic acid. The continuing effects of SD are due to the reduction in cell excitability. As many neurones are depressed without undergoing an initial excitation, it appears that a depressant substance is also involved. This may be gamma-aminobutyric acid.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 67 (1996), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Changes in cerebral cortical adenine nucleotide and adenosine levels during 10-, 20-, or 40-min periods of four-vessel occlusion producing cerebral ischemia in rats and reperfusions of 10, 45, or 90 min were determined to evaluate the effects of ischemia duration on mitochondrial function. Substantial recovery was evident following 10 or 20 min of cerebral ischemia but not, however, after a 40-min period of ischemia. A secondary decline in the cortical levels of ATP became evident following 40 min of cerebral ischemia and 90 min of reperfusion. Longer periods of ischemia may be associated with a loss of adenosine, limiting the resynthesis of ATP during reperfusion. A separate group of rats, resuscitated with 100% O2, demonstrated a more rapid recovery of mitochondrial function compared with animals that received room air during reperfusion following 20 min of cerebral ischemia. No detrimental effects of 100% O2 were observed during the 90-min period of reperfusion, indicating that 100% O2 does not promote early mitochondrial dysfunction.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 723 (1994), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 182 (1958), S. 323-323 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] In the present investigation, ?-amino-n-butyric acid has been passed electrophoretically, as a cation, from one barrel of a multi-barrelled electrode. The responses, both of single cells and of groups of cells within the spinal cord of the cat, have been recorded from another barrel of the ...
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 183 (1959), S. 611-612 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] When these substances were similarly applied to the surface of motoneurones from the extracellular barrel of a co-axial electrode, the intracellular electrode recorded a membrane depolarization which, when summed with the depolarization arising either from current passed through the intracellular ...
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 217 (1968), S. 1076-1077 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Spinal cords of the toad Bufo marinus were isolated, hemisected and perfused with oxygenated amphibian Ringer solution. Experiments were performed during the Australian summer. The methods have been described in detail elsewhere9'10. The eighth dorsal root was stimulated every 10 s and a.c. or d.c. ...
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 207 (1965), S. 1253-1255 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] THE relationship between the functional state of the brain and its acetylcholine (ACh) content has been the subject of a number of investigations. Variations in the ACh level have been correlated with physiological changes in nervous activity, such as those occurring in the transition from sleep to ...
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 36 (1981), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Adenosine, a putative inhibitory transmitter or modulator in the brain, is rapidly transported by rat cerebral cortical synaptosomes. The uptake may represent a facilitated diffusion process, which is saturable and temperature-dependent. In this study, the uptake process was very rapid, reaching completion within 60 s of incubation at 37°C, and had an apparent Km value of 0.9μM and a Vmax value of 5.26 pmol/mg protein/ 30 s. Over 70% of the adenosine taken up remained unchanged, whereas 14% was metabolized to inosine. Twelve percent of the adenosine was converted to nucleotides. Rapid uptake of adenosine into rat cerebral cortical synaptosomes was partially inhibited by replacing Na+ with choline chloride in the medium. Ca2+ ion is important for the uptake process, as inhibition of adenosine uptake occurs in the presence of either Co2- or EGTA. Rapid uptake of adenosine is apparently mediated by a nucleoside carrier, a conclusion based on its inhibition by a variety of purine and pyrimidine nucleosides. Uptake was inhibited by dipyridamole, hexobendine, papaverine, flurazepam, and morphine. Over 60% of the adenosine taken up by the rapid uptake system (30 s) was released by depolarizing agents. In contrast, only 30% of the adenosine taken up during a 15-min incubation period was released under the same conditions. [3H]Adenosine was the predominant purine released in the presence or absence of depolarizing agents. The basal and KCl-evoked release mechanisms were found to be at least partially Ca2+-dependent, however, the release of adenosine by veratridine was increased in the presence of EGTA. This finding is in agreement with the reported Ca2+-independent release of ATP from brain synaptosomes. The present findings suggest that there are at least two functional pools of adenosine in synaptosomes. Adenosine taken up by different uptake systems may be destined for different uses (metabolism or release) in the neuron.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 64 (1995), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The present study investigated the effect of the administration of oxypurinol (40 mg/kg), an inhibitor of xanthine oxidase, on adenosine and adenine nucleotide levels in the rat brain during ischemia and reperfusion. The brains of the animals were microwaved before, at the end of a 20-min period of cerebral ischemia, and after 5, 10, 45, and 90 min of reperfusion. Cerebral ischemia was elicited by four-vessel occlusion with arterial hypotension to 45–50 mm Hg. Adenosine and adenine nucleotide levels in the oxypurinol-pretreated (administered intravenously 20 min before ischemia) rats were compared with those in nontreated animals exposed to the same periods of ischemia and reperfusion. Oxypurinol administration resulted in significantly elevated ATP levels at the end of ischemia and 5 min after ischemia, but not at 10 min after ischemia. ADP levels were also elevated, in comparison with those in the control rats, at the end of the ischemic period. Conversely, AMP levels were significantly reduced at the end of ischemia and during the initial (5 min) period of reperfusion. Adenosine levels were lower in oxypurinol-treated rats, during ischemia, and in the initial reperfusion phase. Oxypurinol administration resulted in a significant increase in the energy charge both during ischemia and after 5 min of reperfusion. Physiological indices, namely, time to recovery of mean arterial blood pressure and time to onset of respiration, were also shortened in the oxypurinol-treated animals. These beneficial effects of oxypurinol may have been a result of its purine-sparing (salvage) effects and of its ability to inhibit free radical formation by the enzyme xanthine oxidase. Preservation of high-energy phosphates during ischemia likely contributes to the cerebroprotective potency of oxypurinol.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 39 (1982), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The uptake of Ca2+ by a K+-depolarized rat brain cerebral cortical crude synaptosomal preparation (P2 fraction) was investigated. The characteristics of the Ca2+ uptake system are similar to those observed by other investigators. The preparation is also a suitable model with which to study the effects of adenosine on Ca2+ uptake and neurotransmitter release, as it is generally accepted that K+-evoked Ca2+ uptake is intimately related to depolarization-induced release of neurotransmitters. We have demonstrated that an extracellular receptor is involved in mediating the adenosine-evoked inhibition of K+-evoked Ca2+ uptake. The pharmacological properties of the receptor suggest that it may be similar in some respects to the A2-receptor associated with adenylate cyclase. The adenosine uptake inhibitor, dipyridamole, potentiated the action of adenosine, suggesting that re-uptake is important in controlling the extracellular adenosine concentration and thus in the regulation of the adenosine receptor. The adenosine receptor antagonist theophylline inhibited the effects of adenosine. Calmodulin inhibited K+- evoked uptake of Ca2+ by the synaptosomal fraction.
    Type of Medium: Electronic Resource
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