NMDA-induced release of nitric oxide potentiates aspartate overflow from cerebellar slices

Dickie, Brian G.M.; Lewis, Malcolm J.; Davies, John A.

doi:10.1016/0304-3940(92)90492-p

Cited by 83 publications

(19 citation statements)

References 25 publications

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“…Inhibitors of nitric oxide synthase prevent the development of LTP (1, 2, 4, 37) and decrease neurotransmitter release from synaptosomes and other preparations (38)(39)(40)(41). These results have been used to argue that NO ⅐ enhances LTP by potentiating presynaptic release of glutamate neurotransmitter.…”

Section: Discussionmentioning

confidence: 94%

Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures

Pan

Segal

Lipton

1996

Proc. Natl. Acad. Sci. U.S.A.

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Nitric oxide (NO ⅐ ) does not react significantly with thiol groups under physiological conditions, whereas a variety of endogenous NO donor molecules facilitate rapid transfer to thiol of nitrosonium ion (NO ؉ , with one less electron than NO ⅐ ). Here, nitrosonium donors are shown to decrease the efficacy of evoked neurotransmission while increasing the frequency of spontaneous miniature excitatory postsynaptic currents (mEPSCs). In contrast, pure NO ⅐ donors have little effect (displaying at most only a slight increase) on the amplitude of evoked EPSCs and frequency of spontaneous mEPSCs in our preparations. These findings may help explain heretofore paradoxical observations that the NO moiety can either increase, decrease, or have no net effect on synaptic activity in various preparations.A number of experiments, most of which have used inhibitors of endogenous nitric oxide synthase, have suggested that nitric oxide (NO ⅐ ) acts presynaptically to enhance the amplitude of evoked synaptic potentials during long-term potentiation (LTP) (1-5). Yet, a variety of exogenous NO donors produce a reversible depression (and only rarely an enhancement) of synaptic transmission (1, 6-10). Apparent discrepancies between effects of various endogenous and exogenous NO donors on neurotoxicity or neuroprotection were attributed at least in part to different redox-related species of the NO group and their disparate chemical reactivities (11,12). With this in mind, the present study was undertaken to determine if different redox-related forms of NO could contribute to differential effects on neurotransmission.Under physiological conditions, free nitric oxide (NO ⅐ ) reacts only very slowly with thiolate anions [the negatively charged form of thiol or -SH (sulfhydryl) groups]. Instead, the NO group in an alternative redox state from NO ⅐ reacts with protein thiol, producing transfer of NO ϩ equivalents to the thiolate anion (RS Ϫ ), resulting in RS-NO formation (11,(13)(14)(15)(16). Under physiological conditions NO ϩ does not exist in a free state in the nervous system, but extensive evidence exists in vivo that the NO group exists in a form that can be donated as NO ϩ . For example, S-nitroso-glutathione, S-nitrosohemoglobin, iron-nitrosyl complexes, nitroso-albumen, and N-nitrosamines are all present in biologic tissue, including the nervous system, and each of these chemical species can donate NO ϩ (15, 17, 18). We report here that donors with NO ϩ character, but not NO ⅐ , decrease evoked neurotransmission, apparently via reaction with thiol groups. Concomitantly, the frequency of spontaneous miniature excitatory postsynaptic currents (mEPSCs) is increased. MATERIALS AND METHODSNO Donors. Preparations of nitroglycerin (NTG), Snitrosocysteine (SNOC), diethylamine͞nitric oxide complex (DEA͞NO), N-ethylmaleimide (NEM), and their control solutions have been described (11,(19)(20)(21). These reagents were mixed in the extracellular solution, adjusted to pH 7.2, applied via bath superfusion for Ϸ2 min, and then washed ou...

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Section: Discussionmentioning

confidence: 94%

Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures

Pan

Segal

Lipton

1996

Proc. Natl. Acad. Sci. U.S.A.

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“…It has been suggested that NO acts as a retrograde messenger that modulates increased transmitter release after postsynaptic activation to enhance transmission in a use-dependent way (Dickie et al 1992;Bliss and Collingridge 1993;Guevara-Guzman et al 1994). The same role had been allocated to arachidonic acid in previous investigations (Lynch et al 1989;Zhang and Dorman 1993).…”

Section: -Ni Impairs Learning In the Ratmentioning

confidence: 90%

7-Nitro indazole, a selective neuronal nitric oxide synthase inhibitor in vivo, impairs spatial learning in the rat.

Hölscher

McGlinchey²,

Anwyl³

et al. 1996

Learn. Mem.

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Nitric oxide (NO) is an intercellular messenger that has been suggested to have a role in learning and memory formation. Previous studies with nonselective NO synthase inhibitors have produced contradictory results in learning experiments. However, these drugs also produced blood pressure changes, as NO is an endothelial-derived relaxing factor. A novel NO synthase inhibitor, 7-nitro indazole (7-NI), as a dose (30 mg/kg i.p.) shown previously to inhibit neuronal NO synthase by 85% without affecting blood pressure, produced amnesic effects both in a water maze and in an 8-arm radial maze. Latency as well as distance was greater in the 7-NI group in the water maze while swim speed was not affected. Latency, working memory (WM), and reference memory (RF) errors were also higher in the 7-NI group in the 8-arm maze. At the end of the second training day, these differences were no longer apparent. However, on the fourth training day, a transfer test in the water maze showed that 7-NI had produced a spatial memory deficit, reducing quadrant bias and the number of annulus crossings. Learning of a visual cue task was not affected. No difference between groups was visible in an open field test. We conclude that neuronal NO sythase activity plays a role in learning and memory formation in the rat. 3Corresponding author.

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“…It has been shown to regulate neurotransmitter release in the cerebellum (Dickie et al, 1992), basal forebrain (Prast and Philippu, 1992), and hippocampus . Although the mechanism by which NO produces such a wide array of biological responses is not known, a prevailing theory suggests that NO binds to the heme moiety of guanylate cyclase, which then results in an increase in cGMP (Katsuki et al, 1977).…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide induces calcium‐dependent release of [³H]dopamine release from striatal slices

Lónárt

Cassels

Johnson

1993

J of Neuroscience Research

131

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Hydroxylamine (0.01-30 mM), a nitric oxide (NO) generator, produced a concentration-dependent release of [3H]dopamine ([3H]DA) from rat striatal slices. Hemoglobin (10 microM), a NO scavenger, reduced basal [3H]DA release and blocked hydroxylamine (100 microM)-stimulated [3H]DA efflux. Tetrodotoxin (0.5 microM) had no significant effect. Sodium cyanide was used as a model compound to test the possibility that NO acted through blockade of mitochondrial electron transport. Calcium-free experimental buffer (1 mM EGTA) reduced basal release and the hydroxylamine response, while sodium cyanide-induced release did not change under these experimental conditions. Cadmium (200 microM), a non-selective inhibitor of voltage-dependent calcium channels, reduced the hydroxylamine response by 69%. Methylene blue (10 microM), an inhibitor of guanylate cyclase, produced a 3-fold increase in the basal release but had no significant effect on the hydroxylamine response. These data suggest that NO induces calcium-dependent [3H]DA release from the striatum via a mechanism which is independent of blockade of electron transport or activation of guanylate cyclase.

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NMDA-induced release of nitric oxide potentiates aspartate overflow from cerebellar slices

Cited by 83 publications

References 25 publications

Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures

Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures

7-Nitro indazole, a selective neuronal nitric oxide synthase inhibitor in vivo, impairs spatial learning in the rat.

Nitric oxide induces calcium‐dependent release of [³H]dopamine release from striatal slices

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NMDA-induced release of nitric oxide potentiates aspartate overflow from cerebellar slices

Cited by 83 publications

References 25 publications

Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures

Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures

7-Nitro indazole, a selective neuronal nitric oxide synthase inhibitor in vivo, impairs spatial learning in the rat.

Nitric oxide induces calcium‐dependent release of [3H]dopamine release from striatal slices

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Nitric oxide induces calcium‐dependent release of [³H]dopamine release from striatal slices