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Bo K. Siesjö

evidence that Ca 2+ influx is normally stimulated by excitatory amino acids, and that it then predominantly occurs at postsynaptic sites, notably in apical dendrites of neocortical and limbic pyramidal cells. 74, 75 It is not known where Ca 2+ accumulates during ischemia; however, it seems likely that cells with high Ca 2+ conductances also have a large Ca 2+ influx. This assumption receives support from experiments showing that induced seizures lead to accumulation of Ca 2+ in the mitochondria of hippocampal pyramidal cells. 63 Fig. 11. Changes in

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Edward G. Jones

categorically that a number of excitatory amino acids, notably glutamate (Glu), are endogenous cortical transmitters even though they have a powerful action on cortical cells. Acetylcholine and the monoamines, dopamine, noradrenaline, and serotonin, by contrast with their powerful rapid effects on peripheral or brain-stem synapses, have rather weak, slow, and prolonged effects when iontophoresed onto cortical neurons. 158 This has generally delayed further analysis. Finally, many of the neuropeptides are not easy to work with, commonly requiring particularly large ejection

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Tony L. Yaksh

Locus Although the evidence outlined above emphasizes an action on primary afferents, equally convincing data also support a direct action on nonafferent neurons. Thus, as noted, even extensive rhizotomy produces only a subtotal loss of dorsal horn opioid binding, and binding in the ventral horn is little affected. Iontophoretic application of the excitatory amino acid glutamate onto dorsal horn interneurons and spinothalamic cells as well as onto motor horn cells will directly depolarize the neuron by an increase in Na + conductance. This depolarizing effect of

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Reduction of cellular energy requirements

Screening for agents that may protect against CNS ischemia

Eric L. Zager and Adelbert Ames III

findings, together with the rapidity with which electrophysiological function recovered after elevated CO 2 in our system, suggest that this agent warrants further investigation, even though its effects on the cerebral vasculature will have to be taken into account. 2-Amino-5-phosphonovaleric acid (APV) is a potent representative of a new class of agents that inhibit excitotoxic amino acid receptors. 18 There is some evidence that synaptic release of these excitatory amino acid neurotransmitters (glutamate and aspartate) may contribute to neuronal death due to

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Alexander Baethmann, Klaus Maier-Hauff, Ludwig Schürer, Manfred Lange, Christine Guggenbichler, Wolfgang Vogt, Karl Jacob and Oliver Kempski

-induced convulsions and striatal aspartate accumulation in rats with frontal cortical ablation. J Neurochem 49: 121–127, 1987 26. Choi DW : Dextrorphan and dextromethorphan attenuate glutamate neurotoxicity. Brain Res 403 : 333 – 336 , 1987 Choi DW: Dextrorphan and dextromethorphan attenuate glutamate neurotoxicity. Brain Res 403: 333–336, 1987 27. Croucher MJ , Collins JF , Meldrum BS : Anticonvulsant action of excitatory amino acid antagonists. Science 216 : 899 – 901 , 1982 Croucher MJ

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Burton M. Onofrio and Tony L. Yaksh

. Yaksh TL : Behavioral and autonomic correlates of the tactile evoked allodynia produced by spinal glycine inhibition: effects of modulatory receptor systems and excitatory amino acid antagonists. Pain 37 : 111 – 123 , 1989 Yaksh TL: Behavioral and autonomic correlates of the tactile evoked allodynia produced by spinal glycine inhibition: effects of modulatory receptor systems and excitatory amino acid antagonists. Pain 37: 111–123, 1989 49. Yaksh TL : In vivo studies on spinal opiate receptor systems mediating

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Ronald L. Hayes, Bruce G. Lyeth, Larry W. Jenkins, Richard Zimmerman, Tracy K. McIntosh, Guy L. Clifton and Harold F. Young

(in conjunction with observations by others) argues that certain endogenous opioids may reduce rather than exacerbate the pathophysiological consequences of TBI. Both TBI and seizures may share common excitotoxic mechanisms related to excessive release of acetylcholine and excitatory amino acids 27, 47, 49 (see reviews of this topic 29, 35, 48 ). Since there is substantial evidence that certain exogenous and endogenous opioids may act as anticonvulsants, 31, 72 it is possible that some opioids may attenuate excitotoxic processes contributing to long-term deficits

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Jeffrey J. Olson, Robert Friedman, Kathryn Orr, Thomas Delaney and Edward H. Oldfield

-part approach was designed to better elucidate the mechanism by which pentobarbital decreases radiation sensitivity. 1) An evaluation of the importance of the temporal relationship between irradiation and pentobarbital administration for reducing radiosensitivity was undertaken. 2) Pentobarbital as administered clinically is a racemic mixture of (+) and (−) isomers. 31 The (−) isomer enhances gamma-aminobutyric acid (GABA) binding and function whereas the (+) isomer inhibits the postsynaptic conductance induced by excitatory amino acids. 31 Therefore, the potential

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Edward H. Oldfield, Robert Friedman, Timothy Kinsella, Ross Moquin, Jeffrey J. Olson, Kathryn Orr and Anne Marie DeLuca

modification of the initial chemical reactions of the ionized molecular targets of x-rays may render tissues less radiosensitive, 15 we postulated that neural activity during radiation exposure may influence tissue damage, as it does in ischemic neural injury. 2, 18, 26, 27, 31, 38, 45–47, 53 In ischemic injury, synaptic activity mediates death of hypoxic neurons in vitro 38 and synaptic blockade with hypothermia, barbiturates, or lidocaine, or by antagonists of excitatory amino acids protects the brain and spinal cord against focal ischemic injury in vivo . 2, 18, 26

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Kai U. Frerichs, Perttu J. Lindsberg, John M. Hallenbeck and Giora Z. Feuerstein

. Clin Phys Physiol Meas 9 : 65 – 74 , 1988 Eyre JA, Essex TJ, Flecknell PA, et al: A comparison of measurements of cerebral blood flow in the rabbit using laser Doppler spectroscopy and radionuclide labelled microspheres. Clin Phys Physiol Meas 9: 65–74, 1988 23. Faden AI , Demediuk P , Panter SS , et al : The role of excitatory amino acids and NMDA receptors in traumatic brain injury. Science 244 : 798 – 800 , 1989 Faden AI, Demediuk P, Panter SS, et al: The role of excitatory amino acids and NMDA