Abstract
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.
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References
Bosley T. M., Woodhams P. L., Gordon R. D., and Balazs R. (1983) Effects of anoxia on the stimulated release of amino acid neurotransmitters in the cerebellum in vitro. J. Neurochem., 40, 189–201.
Brown E. D., Kendall D. A., and Nahorski S. R. (1984) Inositol phospholipid hydrolysis in rat cerebral cortical slices: I. Receptor characterization. J. Neurochem., 42, 1379–1387.
Chen C.-K., Silverstein F. S., Fisher S. K., Statman D., and Johnston M. V. (1988) Perinatal hypoxic-ischemic brain injury enhances quisqualic acid-stimulated phosphoinositide turnover. J. Neurochem., 51, 353–359.
Davis J.N. and Carlsson A. (1973) The effect of hypoxia on monoamine synthesis, levels and metabolism in rat brain. J. Neurochem., 21, 783–790.
Dolivo M. (1974) Metabolism of mammalian sympathetic ganglia. Fed. Proc., 33, 1043–1048.
Gibson G. E. and Duffy T. E. (1981) Impaired synthesis of acetylcholine by mild hypoxic hypoxia or nitrous oxide. J. Neurochem., 36, 28–33.
Gibson G. E., Peterson, C. and Sansone J. (1981) Decreases in amino acid and acetylcholine metabolism during hypoxia. J. Neurochem., 37, 192–201.
Gorman A. L. F. (1966) Differential patterns of activation of the pyramidal system elicited by surface anodal and cathodal cortical stimulation. J. Neurophysiol., 29, 547–564.
Hansen A. J., Haunsgaard J. and Jahnsen H. (1982) Anoxia increases potassium conductance in hippocampal nerve cells, Acta Physiol. Scand., 115, 301–310.
Jolles J., Zwiers H., Dekker A., Wirtz K. W. A. and Gispen W. H. (1981) Corticotropin-(1–24)-tetracosapeptide affects protein phosphorylation and polyphosphoinositide metabolism in bat brain. Biochem. J., 194, 283–291.
Lowry O. H., Rosebrough N. J., Farr A. L., and Randall R.J. (1951) Protein measurement with the Folin phenol reagent. J. Biol. Chem., 193, 265–275.
Miwa S., Fujiwara M., Inoue M. and Fujiwara M. (1986) Effects of hypoxia on the activities of noradrenergic and dopaminergic neurons in the rat brain. J. Neurochem., 47, 63–69.
Ninomiya H., Taniguchi T., Fujiwara M. and Kameyama M. (1988) Increased binding of [3H]muscimol and [3H]flunitrazepam in the rat brain under hypoxia. J. Neurochem., 51, 1111–1117.
Ninomiya H., Taniguchi T., Fujiwara M. and Kameyama M. (1989) Effects phosphoinositide turnover in rat brain slices. J. Neurochem., 53, 183–190.
Shiff S. J. and Balestrino M. (1985) Possible mechanism of posthypoxic hyperexcitabi1ity in hippocampal slices. Soc. Neurosci. Abstr. 11, 374.
Schiff S.J. and Somjen G. G. (1984) Hypoxia and synaptic function. Clin. Neuropharmacol. 7 (suppl 1), 498–499.
Schiff S.J. and Somjen G. G. (1985) Hyperexcitability following moderate hypoxia in hippocampal tissue slices. Brain Res., 337, 337–340.
Schiff S.J. and Somjen G. G. (1987) The effect of graded hypoxia on the hippocampal slice: A in vitro model of the ischemic penumbra. Stroke, 18, 30–37.
Seren M.S., Aldinio C., Zanoni R., Leon A. and Nicoletti F. (1989) Stimulation of inositol phospholipid hydrolysis by excitatory amino acids is enhanced in brain slices from vulnerable regions after transient global ischemia. J. Neurochem., 53, 1700–1705.
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© 1991 Plenum Press, New York
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Ninomiya, H., Taniguchi, T., Fujiwara, M. (1991). Effects of Oxygen Depletion on Phosphoinositide Breakdown in Rat Brain Slices. In: Kito, S., Segawa, T., Olsen, R.W. (eds) Neuroreceptor Mechanisms in Brain. Advances in Experimental Medicine and Biology, vol 287. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5907-4_11
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DOI: https://doi.org/10.1007/978-1-4684-5907-4_11
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