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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Metabolic brain disease 1 (1986), S. 205-220 
    ISSN: 1573-7365
    Keywords: ischemia ; high-energy phosphates ; glucose ; cyclic nucleotides ; glutamate ; gerbil
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present experiments were designed to determine the short-term regional changes in the cyclic nucleotides, certain glucose metabolites, high-energy phosphates, γ-aminobutyric acid (GABA), glutamate, and glutamine in the gerbil brain following bilateral ligation of the common carotid arteries. The brains of the animals were microwaved at 20, 40, 60, 90, 120, and 300 sec of ischemia and the metabolites were measured in the cerebral cortex, hippocampus, and striatum. There were significant decreases in ATP, P-creatine, and glucose within the first 20 sec of ischemia in all three regions examined, whereas the increases in phosphate and lactate, as well as the loss of glycogen, were evident only after 40 sec of ischemia. The high-energy phosphates were essentially depleted (〈 15% of control values) in all three regions by 2 min of ischemia, indicating that the energy imbalance elicited by ischemia was comparable in the three regions. In contrast, the magnitude of the changes in the cyclic nucleotides was greater in the hippocampus than in the cerebral cortex or striatum. In addition, the decrease in cyclic GMP levels at 20 sec of ischemia preceded the increases in cyclic AMP observed at 40 sec in all three regions. The use of microwave irradiation to fix the gerbil brains not only provides a more accurate assessment of the time course of the metabolite changes but also permits studies on the deeper regions of the brain than is possible with freezing techniques.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-7365
    Keywords: γ-aminobutyric acid (GABA) ; hippocampus ; delayed neuronal death ; selective vulnerability ; ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A series of putative neuroprotective agents was tested to determine their efficacy in preventing the loss of the CA 1 neurons of the hippocampus at 4 days following 5 min of bilateral ischemia in the gerbil. Agents associated with the GABAergic system were determined to be the most effective, but only when given prior to the ischemic episode, suggesting that there was aγ-aminobutyric acid (GABA)-related event during ischemia which triggers the delayed neuronal death of these cells. In this report, the unidirectional release of GABA and glutamate from gerbil hippocampal slices was determined under conditions mimicking anoxia and/or ischemia. Pentobarbital, the most effective of the GABAergic agents, had little or no effect on the time-dependent release of glutamate. In contrast, pentobarbital reduced in release of GABA in both anoxia and ischemia, but only after 25 to 30 min of incubation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 14 (1989), S. 1-7 
    ISSN: 1573-6903
    Keywords: Cerebral ischemia ; energy metabolism ; monoamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationship of neurotransmitters and neuroeffectors to the energy state of the brain was examined in the gerbil model of ischemia after 5 and 15 min of bilateral common carotid artery occlusion only or with 1 hr of reperfusion. The gerbil brains were fixed by microwave irradiation and a total of 15 metabolites were measured from a single piece of tissue from either the hippocampus or the striatum. The rapid alterations in energy-related compounds and cyclic nucleotides appeared to be directly related both to the loss of oxygen and glucose during ischemia and the resupply of these nutrients during reflow. Significant reduction in the level of monoamines occurred prinicipally during reflow, at a time when the energy-related metabolites were restored. It is proposed that the changes in monoamines were triggered by other ischemic-induced events unrelated to energy depletion.
    Type of Medium: Electronic Resource
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