nitroarginine and 2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide

NO-producing neuron exhibited an excitatory response to the decrease in NO concentration, which was induced by NO synthase inhibitor N-nitro-L-arginine or specific NO acceptor 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. Addition of NO donors to the medium inhibits neuronal activity. The excitatory effects of N-nitro-L-arginine and 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide were preserved, while the inhibitory action of NO donors significantly decreased after isolation of the neuron. These findings indicate that NO regulates activity of these neurons by the negative feedback mechanism. This regulation includes the following complementary mechanisms: (1) endogenous mechanism of cell self-activation in response to the decrease in NO concentration; and (2) exogenous mechanism of cell-mediated inhibition in response to NO excess.

Topics: Animals; Cyclic N-Oxides; Electrophysiology; Imidazoles; Neurons; Nitric Oxide; Nitric Oxide Donors; Nitroarginine; Nitroprusside; Snails

When seedlings are grown in the dark, proplastids of the developing leaf differentiate into etioplasts. Greening of etiolated plastids is stimulated by light, which is sensed by various types of photoreceptors. Nitric oxide (NO) has been shown to be a bioactive molecule that could take part in this light-mediated process in plants. In this paper, we show that emission of NO in barley seedlings increased concomitantly with increasing activities of nitric oxide synthase (NOS) during the greening. Treatment with sodium nitroprusside (SNP), a NO donor, increased the accumulation of chlorophyll contents, enhanced the accumulation of thylakoid membrane proteins, such as light harvesting complex of photosystem II (LHCII) and PSIA/B, and then improved the effective quantum yield of photosystem II (PSII) (Phi(PSII)) in the light. Instead, treatment with either NO scavenger 2-phenyl-4,4,5,5-tetramentylimidazoline-1-oxyl-3-xide (PTIO) or NOS inhibitor N(omega)-nitro-l-arginine (l-NNA) retarded the greening of etiolated-seedlings. Moreover, sodium ferrocyanide, an analog of SNP, nitrite and nitrate, two NO-decomposition products did not have any effect on the greening process. These results indicated that NO, as an endogenous signaling molecule, participates in light-mediated greening of barley seedlings, and exogenous NO accelerates this process.

Topics: Blotting, Western; Chlorophyll; Cyclic N-Oxides; Electron Transport; Ferrocyanides; Hordeum; Imidazoles; Light; Light-Harvesting Protein Complexes; Membrane Proteins; Nitric Oxide; Nitric Oxide Synthase; Nitroarginine; Nitroprusside; Photosynthesis; Photosystem I Protein Complex; Plant Proteins; Plastids; Seedlings; Signal Transduction; Thylakoids

Methyl jasmonate (MeJA), a methyl ester of jasmonic acid (JA), is a well-established signal molecule in plant defense responses and an effective inducer of secondary metabolite accumulation in plant cell cultures such as the valuable anticancer diterpenoid taxol (paclitaxel) in Taxus spp. This work examines the involvement of nitric oxide (NO) in MeJA-induced plant defense responses and secondary metabolism in Taxus chinensis cell cultures. Exogenously supplied MeJA at 100 microM induced rapid production of NO in the Taxus cell cultures, reaching a maximum within 6 h of MeJA supply. Several other responses occurred concomitantly, including the production of hydrogen peroxide (H2O2), and the increases in intracellular malondialdehyde (MDA) content, lipoxygenase (LOX) and phenylalanine ammonium-lyase (PAL) activities. The MeJA-induced H2O2 production was suppressed by an NO donor, sodium nitroprusside (SNP), but enhanced by NO inhibitors, N (omega)-nitro-L-arginine (L-NNA) and 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (PTIO). In contrast, the MeJA-induced MDA, LOX and PAL were all enhanced by the NO donor but suppressed by the NO inhibitors. The NO inhibitors also suppressed MeJA-induced taxol accumulation. These results are suggestive of a role for NO as a signal element for activating the MeJA-induced defense responses and secondary metabolism activities of plant cells.

Topics: Acetates; Cyclic N-Oxides; Cyclopentanes; Free Radical Scavengers; Hydrogen Peroxide; Imidazoles; Lipid Peroxidation; Lipoxygenase; Models, Biological; Nitric Oxide; Nitric Oxide Donors; Nitroarginine; Nitroprusside; Oxylipins; Paclitaxel; Phenylalanine Ammonia-Lyase; Plant Growth Regulators; Signal Transduction; Taxus

Previous studies suggest that abscisic acid (ABA) stimulates the activities of antioxidant enzymes under normal and chilling temperature and enhanced chilling resistance in Stylosanthes guianensis. The objective of this study was to test whether nitric oxide (NO) is involved in the ABA-induced activities of the antioxidant enzymes in Stylosanthes guianensis due to its nature as a second messenger in stress responses. Plants were treated with NO donors, ABA, ABA in combination with NO scavengers or the nitric oxide synthase (NOS) inhibitor and their effects on the activity of antioxidant enzymes and NO production were compared. The results showed that ABA increased the activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX). The effect of ABA on antioxidant enzyme activities was suppressed by the NOS inhibitor, N(omega)-nitro-L-arginine (L-NNA), and the NO scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl3-oxide (PTIO). NO content increased after 5 h of ABA treatment. The NO-scavenger, PTIO, and the NOS-inhibitor, L-NNA, inhibited the accumulation of NO in ABA-treated Stylosanthes guianensis. NO donor treatment enhanced the activities of SOD, CAT, and APX. The results suggested that NO was involved in the ABA-induced activities of SOD, CAT, and APX in Stylosanthes guianensis. ABA triggered NO production that may lead to the stimulation of antioxidant enzyme activities.

Topics: Abscisic Acid; Antioxidants; Ascorbate Peroxidases; Catalase; Cyclic N-Oxides; Enzyme Inhibitors; Fabaceae; Free Radical Scavengers; Imidazoles; Nitric Oxide; Nitric Oxide Donors; Nitric Oxide Synthase; Nitroarginine; Peroxidases; Superoxide Dismutase

Long-term changes of synaptic transmission in slices of rat visual cortex were induced by intracellular tetanization: bursts of short depolarizing pulses applied through the intracellular electrode without concomitant presynaptic stimulation. Long-term synaptic changes after this purely postsynaptic induction were associated with alterations of release indices, thus providing a case for retrograde signalling at neocortical synapses. Both long-term potentiation and long-term depression were accompanied by presynaptic changes, indicating that retrograde signalling can achieve both up- and down-regulation of transmitter release. The direction and the magnitude of the amplitude changes induced by a prolonged intracellular tetanization depended on the initial properties of the input. The inputs with initially high paired-pulse facilitation (PPF) ratio, indicative of low release probability, were most often potentiated. The inputs with initially low PPF ratio, indicative of high release probability, were usually depressed or did not change. Thus, prolonged postsynaptic activity can lead to normalization of the weights of nonactivated synapses. The dependence of polarity of synaptic modifications on initial PPF disappeared when plastic changes were induced with a shorter intracellular tetanization, or when the NO signalling pathway was interrupted by inhibition of NO synthase activity or by application of NO scavengers. This indicates that the NO-dependent retrograde signalling system has a relatively high activation threshold. Long-term synaptic modifications, induced by a weak postsynaptic challenge or under blockade of NO signalling, were nevertheless associated with presynaptic changes. This suggests the existence of another retrograde signalling system, additional to the high threshold, NO-dependent system. Therefore, our data provide a clear case for retrograde signalling at neocortical synapses and indicate that multiple retrograde signalling systems, part of which are NO-dependent, are involved.

Topics: Animals; Cyclic N-Oxides; Electric Stimulation; Excitatory Postsynaptic Potentials; Free Radical Scavengers; Imidazoles; In Vitro Techniques; Long-Term Potentiation; Neocortex; Neuronal Plasticity; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitroarginine; Rats; Rats, Wistar; Reaction Time; Receptors, AMPA; Signal Transduction; Synapses; Synaptic Transmission; Visual Cortex

1. Electrical field stimulation (EFS) of muscle strips in vitro elicited a tetrodotoxin (TTX)-sensitive biphasic contractile response consisting of a phasic component followed by a tonic one. 2. The amplitude of both components of the response was impaired by N omega-nitro-L-arginine and potentiated by sodium nitroprusside. Cystamine caused a reduction in amplitude of both phasic and tonic components of the response to EFS. Neither N omega-nitro-L-arginine, sodium nitroprusside, nor cystamine induced changes in the resting muscle tone, or in the contractile response to exogenous agonists ATP and noradrenaline (NA). 3. The nitric oxide scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, induced a reduction in amplitude of both components of the response to EFS. 4. These results reveal a facilitatory prejunctional modulatory role for nitric oxide in sympathetic neurotransmission in rat vas deferens. Endogenous nitric oxide released in the extracellular space is presumed to potentiate neurotransmission by acting at prejunctional level via cGMP.

Topics: Animals; Cyclic N-Oxides; Cystamine; Electric Stimulation; Enzyme Inhibitors; Guanylate Cyclase; Imidazoles; Male; Muscle Contraction; Nitric Oxide; Nitric Oxide Synthase; Nitroarginine; Nitroprusside; Rats; Rats, Wistar; Sympathetic Nervous System; Vas Deferens