Amino Acids

, Volume 23, Issue 1, pp 221-229

First online:

Role of creatine and phosphocreatine in neuronal protection from anoxic and ischemic damage

  • M. BalestrinoAffiliated with Department of Neurological and Vision Sciences, University of Genova, Italy
  • , M. LensmanAffiliated with Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia
  • , M. ParodiAffiliated with Department of Neurological and Vision Sciences, University of Genova, Italy
  • , L. PerassoAffiliated with Department of Neurological and Vision Sciences, University of Genova, Italy
  • , R. RebaudoAffiliated with Department of Neurological and Vision Sciences, University of Genova, Italy
  • , R. MelaniAffiliated with Department of Neurological and Vision Sciences, University of Genova, Italy
  • , S. PolenovAffiliated with Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia
  • , A. CupelloAffiliated with Center for Cerebral Neurophysiology, National Research Council, Genova, Italy

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Summary.

 Phosphocreatine can to some extent compensate for the lack of ATP synthesis that is caused in the brain by deprivation of oxygen or glucose. Treatment of in vitro rat hippocampal slices with creatine increases the neuronal store of phosphocreatine. In this way it increases the resistance of the tissue to anoxic or ischemic damage. In in vitro brain slices pretreatment with creatine delays anoxic depolarization (AD) and prevents the irreversible loss of evoked potentials that is caused by transient anoxia, although it seems so far not to be active against milder, not AD-mediated, damage. Although creatine crosses poorly the blood-brain barrier, its administration in vivo at high doses through the intracerebroventricular or the intraperitoneal way causes an increase of cerebral phosphocreatine that has been shown to be of therapeutic value in vitro. Accordingly, preliminary data show that creatine pretreatment decreases ischemic damage in vivo.

Keywords: Creatine Phosphocreatine Ischemia Anoxia Stroke Guanidinoacetate methyltransferase deficiency Hyperornithinemia Protection