A Role for Nitric Oxide in Long‐term Potentiation

Bon, Christelle L. M.; Böhme, Georg Andrees; Doble, Adam; Stutzmann, Jean‐Marie; Blanchard, Jean‐Charles

doi:10.1111/j.1460-9568.1992.tb00891.x

Cited by 144 publications

(58 citation statements)

References 41 publications

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“…NO, in its turn, enhances vesicular release by stimulating cGMP synthesis at the presynaptic site and upregulates trafficking of AMPA receptors at the postsynaptic site [67]. Thereby, it may contribute to the induction of ATPinduced LTP like it has been demonstrated for tetanusinduced LTP [68][69][70][71][72]. The present study indicates that longterm synaptic plasticity induced by ATP is cannabinoiddependent: ATP-induced LTP is inhibited by the activation CB1 receptors.…”

Section: Discussionsupporting

confidence: 72%

Modulation of ATP-induced LTP by cannabinoid receptors in rat hippocampus

Ievglevskyi

Palygin

Kondratskaya

et al. 2012

Purinergic Signalling

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Cannabinoids exert powerful action on various forms of synaptic plasticity. These retrograde messengers modulate GABA and glutamate release from presynaptic terminals by acting on presynaptic CB1 receptors. In particular, they inhibit long-term potentiation (LTP) elicited by electrical stimulation of excitatory pathways in rat hippocampus. Recently, LTP of the field excitatory postsynaptic potential (fEPSP) induced by exogenous ATP has been thoroughly explored. The present study demonstrates that cannabinoids inhibit ATP-induced LTP in hippocampal slices of rat. Administration of 10 μM of ATP led to strong inhibition of fEPSPs in CA1/CA3 hippocampal synapses. Within 40 min after ATP removal from bath solution, robust LTP was observed (fEPSP amplitude comprised 130.1± 3.8% of control, n010). This LTP never appeared when ATP was applied in addition to cannabinoid receptor agonist WIN55,212-2 (100 nM). Selective CB1 receptor antagonist, AM251 (500 nM), completely abolished this effect of WIN55,212-2. Our data indicate that like canonical LTP elicited by electrical stimulation, ATP-induced LTP is under control of CB1 receptors.

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Section: Discussionsupporting

confidence: 72%

Modulation of ATP-induced LTP by cannabinoid receptors in rat hippocampus

Ievglevskyi

Palygin

Kondratskaya

et al. 2012

Purinergic Signalling

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“…In these cells NO has been implicated in synaptic plasticity phenomena like long-term potentiation (LTP) in the hippocampus [1,2] and long-term synaptic depression (LTD) in the cerebellum [21]. In these processes NO is suggested to act as a possible retrograde messenger, carrying information from postsynaptic elements (e.g., CAI pyramidal neurons and cerebellar Purkinje cells) to presynaptic terminals [see ref .…”

Section: Discussionmentioning

confidence: 99%

Aldehyde fixation differentially affects distribution of diaphorase activity but not of nitric oxide synthase immunoreactivity in rat brain

Buwalda

Nyakas

Gast

et al. 1995

Brain Research Bulletin

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Aldehyde fixation differentially affects distribution of diaphorase activity but not of nitric oxide synthase immunoreactivity in rat brain Buwalda, Bauke; Nyakas, C.; Gast, J.; Luiten, P.G.M. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. ABSTRACT: The effect of aldehyde fixation on NADPH-and NADH-dependent diaphorase (d) histochemistry and nitric oxide synthase (NOS) immunocytochemislry in the brain was investigated by comparing the distribution of these enzymes in in situ nitrocellulose blots of unfixed brain sections with that in aidehyde-fixed brain sections. Substitution of NADPH by NADH yielded no gross differences in cellular distbribution in the native blot, whereas in fixed sections NADH produced nonspecific staining of the entire section. In the in situ blot NADPHd histoohemislry therafore visualized general nitroblue tatrazolium reductass (NBTr) activity, which was particularly strong in hippocampal pyramidal neurons and cerabellar Purkinje cells. Aldehyde fixation abolished the anatomical pattern of general NBTr activity and changed the hiatochemical distribution in that of the NADPHd activity associated with the distribution of NOS-I immunoreacfivity (ir). Fixation intensified NADPHd histochemical staining in specific neurone, resulting in outstanding, Golgilike staining of these neurons in several brain regions, whereas the general NBTr activity in pyramidal and Purkinje cells disappeared, in contrast to the histochemical diaphorase dislribution, the distribution of NOS-I ir on blots and in aldehyde-fixed brain sections was similar. No NOS was observed in hippocampal pyramidal and carebellar Purkinje neurons. In regions like cerebral and cerebellsr cortex and striatum the applied anti NOS-I serum had a higher affinity for the native protein. It is concluded that aldehydes, rather than to progressively suppress NOS-unrelated enzymes, differentially elicit NADPHd activity in some groups of neurons while leaving NOS-ir unaffected.

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“…However, a few groups have had some www.annualreviews.org/aronline Annual Reviews success. Bohme and colleagues (Bohme et al 1991, Bon et al 1992 have shown that extracellular application of two different NO donors, hydroxylamine and sodium nitroprusside, can potentiate synaptic transmission in a manner that occludes normal synaptically-induced LTP. Direct application of NO has also been demonstrated to augment synaptic transmission: in cultured hippocampal neurons NO increases the frequency of spontaneous miniature synaptic events (O'Dell et al 1991).…”

Section: Long-term Potentiationmentioning

confidence: 99%