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  • 1
    Electronic Resource
    Electronic Resource
    Metabolic alterations in fiber layers of the CA 1 region of the gerbil hippocampus following short-term ischemia: High-energy phosphates, glucose-related metabolites, and amino acids (1988)
    Springer
    Metabolic brain disease 3 (1988), S. 133-149 
    Details
    ISSN: 1573-7365
    Keywords: ischemia ; energy metabolism ; ATP ; selective vulnerability ; GABA ; glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The CA 1 neurons of the gerbil hippocampus die at 4 days following 5 min of bilateral ischemia. The fiber and somal layers of the CA 1 region of the gerbil hippocampus were analyzed for high-energy phosphates, glucose-related metabolites, and amino acids from 0.75 hr to 4 days of postischemia. The results were compared to those from two layers of the CA 3 region and the cerebral cortex. The metabolite changes in the fiber layers of the CA 1 region were qualitatively similar to those in the somal layer. The energy status of the tissues taken from the CA 1 region was never compromised for up to 2 days of recirculation, after which the ATP and P-creatine in the somal layer decreased to 43 and 56% of the control, respectively, whereas the average decreases in the CA 1 fiber layers were only 71 and 88% of the control, respectively. Thus, the high-energy phosphate response of the neuronal elements in the fiber layers was temporally similar to that found in the somal layer of the CA 1 region. The biphasic increases in glycogen, glucose, glucose-6-phosphate, and high-energy phosphates to values greater than the control indicated that the metabolic restoration following transient ischemia is a dynamic process which persists for up to 2 days of recirculation, even in resistant tissues. A similar pattern of delayed changes was observed in glutamate, γ-aminobutyric acid (GABA), and glutamine, but the change in each amino acid appeared to be independent of the others despite their close metabolic relationship. The delayed decreases in GABA would favor a loss of inhibition to the CA 1 neurons and may be related to the phenomenon of delayed neuronal death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01001014
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  • 2
    Electronic Resource
    Electronic Resource
    Energy metabolism in delayed neuronal death of CA1 neurons of the hippocampus following transient ischemia in the gerbil (1986)
    Springer
    Metabolic brain disease 1 (1986), S. 263-278 
    Details
    ISSN: 1573-7365
    Keywords: selective vulnerability ; ATP ; glucose ; glycogen ; ischemia ; hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The delayed death of CA1 neurons in the gerbil has been reported to occur at 4 days of reflow following 5 min of bilateral ischemia. Samples of the CA1 and CA3 somal region of the hippocampus, as well as of the parietal cortex, were dissected from frozen dried sections of gerbil brains frozenin situ between 1.5 and 96hr of reflow following 5 min of bilateral ischemia and the concentrations of the adenylates, P-creatine, glucose, glycogen, and lactate were determined. The values for high-energy phosphates were restored by 1.5hr of recirculation in all three regions and remained at or above control in the CA3 region and cortex for up to 96hr. In contrast, the P-creatine and ATP decreased in the CA1 region at 48 and 96hr of reflow, respectively. The total adenylates also decreased in the CA1 region at 96h, but the normal energy charge in this area indicated that the surviving tissue was metabolically viable. A glucose overshoot was exhibited in the three regions at all time periods except 6 and 96 hr. At 6 hr of reflow, there was a transient return of glucose levels toward those of control. By 96 hr, the glucose in the CA3 region and cortex was not significantly different from control but was elevated in the CA1 region. The lactate levels were depressed from 1.5 to 12 hr of recirculation in all areas, but the decrease was significant only in the cerebral cortex. The concentration of glycogen was significantly elevated at 6 hr in all regions, then was restored by 24 to 48 hr, only to increase once again in the affected CA1 region. The results clearly indicate that metabolic perturbations persist for long periods of time after ischemic durations that are compatible with the survival of the animal but that the loss of the CA1 neurons cannot be attributed to a failure in energy metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00999356
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    Paper (German National Licenses)
    Fulltext
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