Chapter 12 Modulation of LTP induction by NMDA receptor activation and nitric oxide release

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Abstract

In the CA1 hippocampal region, the induction of long-term potentiation (LTP) requires activation of N-methyl-D-aspartate receptors (NMDARs). However, untimely NMDAR activation either immediately prior to or following tetanic stimulation inhibits LTP generation. This NMDAR-mediated LTP inhibition is overcome by inhibitors of nitric oxide synthase (NOS) and hemoglobin, suggesting the involvement of NO. Additionally, NO inhibitors can promote the ability of weak tetanic stimuli to produce LTP under basal conditions in hippocampal slices. Recent experiments indicate that untimely NMDAR activation contributes to the failure of LTP induction during periods of low glucose exposure and hypoxia. Following hypoxia there is also a delayed form of LTP inhibition that is reversed by NMDAR antagonists and NO inhibitors. These results suggest that there are physiological and pathological conditions during which NMDAR activation and NO release modulate the induction of synaptic plasticity.

References (57)

  • Y. Izumi et al.

    Low concentrations of N-methyl-D-aspartate inhibit the induction of long-term potentiation in rat hippocampal slices

    Neurosci. Lett.

    (1992)
  • Y. Izumi et al.

    Norepi-nephrine reverses N-methyl-D-aspartate-mediated inhibition of long-term potentiation in rat hippocampal slices

    Neurosci. Lett.

    (1992)
  • Y. Izumi et al.

    Developmental changes in the effects of metabotropic glutamate receptor antagonists on CA1 long-term potentiation in rat hippocampal slices

    Neurosci. Lett.

    (1994)
  • K. Kato et al.

    Long-term potentiation during whole-cell recording in rat hippocampal slices

    Neuroscience

    (1993)
  • S.Z. Lei et al.

    Effect of nitric oxide production on the redox modulatory site of the NMDA receptor-channel complex

    Neuron

    (1992)
  • R.C. Malenka

    Synaptic plasticity in the hippocampus: LTP and LTD

    Cell.

    (1994)
  • O. Manzoni et al.

    Nitric oxide-induced blockade of NMDA receptors

    Neuron

    (1992)
  • R.M. Mulkey et al.

    Mechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus

    Neuron

    (1992)
  • E. Palmer et al.

    Glutamate receptors and phosphoinositide metabolism: Stimulation via quisqualate receptors is inhibited by N-methyl-D-aspartate receptor activation

    Mol. Brain Res.

    (1988)
  • E. Palmer et al.

    Changes in excitatory amino acid modulation of phoshoinositide metabolism during development

    Dev. Brain Res.

    (1990)
  • D.K. Selig et al.

    Independent mechanisms for long-term depression of AMPA and NMDA responses

    Neuron

    (1995)
  • M.J. Thomas et al.

    Activity-dependent β-adrenergic modulation of low frequency stimulation induced LTP in the hippocampal CA1 region

    Neuron

    (1996)
  • C.F. Zorumski et al.

    Nitric oxide and hippocampal synaptic plasticity

    Biochem. Pharmacol.

    (1993)
  • O. Arancio et al.

    Activity-dependent long-term enhancement of transmitter release by presynaptic 3’,5’-cyclic GMP in cultured hippocampal neurons

    Nature

    (1995)
  • E.L. Bienenstock et al.

    Theory for the development of neuron selectivity: Orientation specificity and binocular interaction in visual cortex

    J. Neurosci.

    (1982)
  • T.V.P. Bliss et al.

    A synaptic model of memory: Long-term potentiation in the hippocampus

    Nature

    (1993)
  • T. Bonhoeffer et al.

    Synaptic plasticity in rat hippocampal slice cultures: Local “Hebbian” conjunction of pre- and postsynaptic stimulation leads to distributed synaptic enhancement

    Proc. Natl. Acad. Sci. USA

    (1989)
  • C. Chen et al.

    Molecular genetic analysis of synaptic plasticity, activity-dependent neural development, learning and memory in the mammalian brain

    Annu. Rev. Neurosci.

    (1997)
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