Effects of Oxygen Depletion on Phosphoinositide Breakdown in Rat Brain Slices

  • Haruaki Ninomiya
  • Takashi Taniguchi
  • Motohatsu Fujiwara
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 287)


Electrophysiological studies indicate that hypoxia exerts dual effects on neuronal excitability. The first effect of hypoxia is supression of excitability during hypoxia period which would lead to the impared synaptic transmission during hypoxia (Gorman, 1966; Dolivo, 1974; Hansen et al., 1982), and the second effect is an enhancement of the excitability after hypoxic period (Shiff and Balestrino, 1985; Shiff and Somjen, 1984, 1985, 1987). Biochemical studies have clearly established that hypoxia disrupts the biosynthesis of various neurotransmitters, including acetylcholine (Gibson and Duffy, 1981; Gibson et al., 1981) or catecholamines (Davis and Carlsson, 1973; Miwa et al., 1986). The first effect of hypoxia, viz., supression of excitability, may be readily explained by decreased neurotransmitter synthesis in the presynaptic terminals, but the cellular and molecular mechanisms underlying the posthypoxic hyperexcitability remain unclear. PI breakdown is an ubiquitous intracellular signal transduction system in the brain, and our initial motivation to start this study was to examine whether any alterations in PI metabolism would play a role in changes in neuronal excitability caused by hypoxia.


Brain Slice Hippocampal Slice Oxygen Depletion Cortical Slice Krebs Buffer 
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Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • Haruaki Ninomiya
    • 1
  • Takashi Taniguchi
    • 2
  • Motohatsu Fujiwara
    • 1
  1. 1.Department of Pharmacology, Faculty of MedicineKyoto UniversityKyoto 606Japan
  2. 2.Department of NeurobiologyKyoto Pharmaceutical UniversityKyoto 607Japan

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