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 Previous Article
Journal of Neuroscience, Vol 16, 418-424, Copyright © 1996 by Society for Neuroscience
The selective neuronal NO synthase inhibitor 7-nitro-indazole blocks both long-term potentiation and depotentiation of field EPSPs in rat hippocampal CA1 in vivo
C Doyle, C Holscher, MJ Rowan and R Anwyl
Department of Physiology, Trinity College, Dublin 2, Ireland.
The membrane-permeant gas NO is a putative intercellular messenger that has
been proposed on the basis of previous in vitro studies to be involved in
synaptic plasticity, especially the induction of long-term potentiation
(LTP) of excitatory synaptic transmission in the hippocampus and cortex. In
the present study, the role of NO in synaptic plasticity has been
investigated in vivo. In particular, the action of the novel and selective
neuronal NO synthase (nNOS) inhibitor 7-nitro-indazole (7-NI) has been
investigated on the induction of LTP and depotentiation (DP) of field EPSPs
in CA1 of the hippocampus in vivo. Unlike previously studied nonselective
NOS inhibitors, 7-NI does not increase arterial blood pressure. In
vehicle-injected rats, high- frequency stimulation consisting of a series
of trains at 200 Hz induced LTP. However, LTP induction was strongly
inhibited in 7-NI (30 mg/kg, i.p.)-treated animals. The inhibitory effect
of 7-NI on the induction of LTP was prevented by pretreatment with
L-arginine, the substrate amino acid used by NOS. In control animals,
low-frequency stimulation consisting of 900 stimuli at 10 Hz induced DP of
previously established LTP, whereas in 7-HI-treated animals only a
short-term depression was induced. This effect of 7-NI also was prevented
by D- arginine. The LTP and DP induced in control animals in this study
were NMDA receptor-dependent, the NMDA receptor antagonist 3-(R,S)-2-
carboxypiperazin-4-yl-propyl-1- phosphonic acid inhibiting the induction of
both forms of synaptic plasticity. The present experiments are the first to
demonstrate that an NOS inhibitor blocks the induction of the synaptic
component of LTP and DP in vivo and, therefore, these results strengthen
evidence that the production of NO is necessary for the induction of LTP
and DP.
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