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Metabolic Brain Disease

, Volume 1, Issue 4, pp 263–278 | Cite as

Energy metabolism in delayed neuronal death of CA1 neurons of the hippocampus following transient ischemia in the gerbil

  • Hajime Arai
  • Janet V. Passonneau
  • W. David Lust
Original Contributions

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.

Key words

selective vulnerability ATP glucose glycogen ischemia hippocampus 

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Copyright information

© Plenum Publishing Corporation 1986

Authors and Affiliations

  • Hajime Arai
    • 1
  • Janet V. Passonneau
    • 1
  • W. David Lust
    • 1
  1. 1.Laboratory of NeurochemistryNational Institute of Neurological and Communicative Disorders and Stroke, National Institutes of HealthBethesda

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