K I Ito

University of North Carolina at Greensboro, Greensboro, NC, United States

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Publications (3)8.62 Total impact

  • T P Hicks, K I Ito
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    ABSTRACT: Many studies on long-term potentiation (LTP) in hippocampal region CA1 focus on receptor-mediated events that are often presumed to be linked to postsynaptic processes. Whereas it is now well-known that LTP consists of multiple components involving increases in postsynaptic responsiveness as well as enhanced presynaptic release of transmitter, little specific information has accrued on the nature of the presynaptic receptor-linked events. In the course of a series of experiments examining the actions of several antagonists of N-methyl-D-aspartate (NMDA) receptors on LTP, we made certain observations that suggested the role of a novel type of amino acid receptor which possibly was located presynaptically and that seemed to contribute to the induction of LTP. LTP evoked in region CA1 following high frequency stimulation (HFS) of the Schaffer collateral-commissural pathway measured 20-30 min after HFS always was attenuated incompletely when induced during administration of DalphaAA at doses ranging from 50 mu M to as high as 1000 mu M, whereas 2-amino-5-phosphonopropionate (AP5), at a concentration of 30 mu M, always abolished the process completely. 6,7-Dinitroquinoxaline-2,3-dione (DNQX) (10 mu M) administered alone also did not block LTP completely unless delivered in combination with DalphaAA. These non-AP5-like effects of DalphaAA could not be attributed to incomplete antagonism of postsynaptic NMDA receptors, since DalphaAA (200 mu M) completely and reversibly blocked the membrane depolarising effects of NMDA, as assessed through intracellular recording. Furthermore, the pharmacologically isolated NMDA-receptor-mediated component of the low-frequency, stimulus-evoked synaptic response was always abolished reversibly by DalphaAA (200 mu M). The most parsimonious explanation of these data is that a receptor which is only activated during HFS, is sensitive to the antagonising actions of AP5 and possibly also to DNQX but not to DalphaAA, and which could conceivably exist on terminals of the Schaffer collateral-commissural fibres, makes a significant contribution to LTP.
    Neuroscience Research 02/1996; 24(2):139-50. · 2.20 Impact Factor
  • K I Ito, T P Hicks
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    ABSTRACT: In slices from the visual cortex of kittens maintained in vitro, long-term potentiation of synaptic transmission following high frequency stimuli (10 Hz, 2 min) delivered at low to medium stimulus intensities (80 to 200 microA), is accompanied by changes of certain electrophysiological measures recorded intracellularly, such as long-lasting depolarization of membrane potential and decreased threshold to elicitation of an action potential. These parameters have never before been shown to be altered following high frequency stimulation in other systems widely used in studying synaptic plasticity, such as in hippocampal neurons. Another important difference between results from these two systems is that the amplitude of the excitatory post-synaptic potential is enhanced after high frequency stimulation in hippocampal neurons, whereas in striate cortex from young kittens, we observed a decrease. We demonstrate here that this decrease can be reversed to show enhancement from the original amplitude, upon clamp of membrane potential back to the voltage observed prior to stimulation. Thus, what appears to be "long-term depression" of synaptic transmission, as recorded extracellularly and represented by diminished flow of synaptic current, can be reversed by stepping membrane voltage back to the pre-high frequency stimulation level, to produce responses that then become consistent with long-term potentiation.
    Experimental Brain Research 02/1994; 100(1):175-80. · 2.22 Impact Factor
  • T P Hicks, K I Ito
    Progress in brain research 02/1993; 95:297-303. · 4.19 Impact Factor

Publication Stats

4 Citations
8.62 Total Impact Points

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  • 1993–1996
    • University of North Carolina at Greensboro
      • • Department of Psychology
      • • Department of Biology
      Greensboro, NC, United States