An electrochemical microprobe for detecting nitric oxide release in brain tissue

Shibuki, Katsuei

doi:10.1016/0168-0102(90)90048-j

Cited by 380 publications

(175 citation statements)

References 19 publications

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“…In this context, it should be noted that very different NO concentrations have been reported in vivo. In rat cerebellar slices, electrical stimulation elevated NO by ϳ6 -60 nM (Shibuki, 1990;Maffei et al, 2003). In contrast, Rivot et al (1997) estimated a basal extracellular NO concentration of ϳ0.5 M in rat dorsal horn, and concentrations exceeding 3 M were reported after electrical stimulation of sensory neurons (Schulte and Millar, 2003).…”

Section: Robustness Of Predicted Spread To Altering the Parameter Valuesmentioning

confidence: 99%

Modeling Cooperative Volume Signaling in a Plexus of Nitric Oxide Synthase-Expressing Neurons

Philippides¹,

Ott²,

Husbands³

et al. 2005

J. Neurosci.

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Invertebrateandinvertebratebrains,nitricoxide(NO)synthase(NOS)isfrequentlyexpressedinextensivemeshworks(plexuses)ofexceedingly fine fibers. In this paper, we investigate the functional implications of this morphology by modeling NO diffusion in fiber systems of varying fineness and dispersal. Because size severely limits the signaling ability of an NO-producing fiber, the predominance of fine fibers seems paradoxical. Our modeling reveals, however, that cooperation between many fibers of low individual efficacy can generate an extensive and strong volume signal. Importantly, the signal produced by such a system of cooperating dispersed fibers is significantly more homogeneous in both space and time than that produced by fewer larger sources. Signals generated by plexuses of fine fibers are also better centered on the active region and less dependent on their particular branching morphology. We conclude that an ultrafine plexus is configured to target a volume of the brain with a homogeneous volume signal. Moreover, by translating only persistent regional activity into an effective NO volume signal, dispersed sources integrate neural activity over both space and time. In the mammalian cerebral cortex, for example, the NOS plexus would preferentially translate persistent regional increases in neural activity into a signal that targets blood vessels residing in the same region of the cortex, resulting in an increased regional blood flow. We propose that the fineness-dependent properties of volume signals may in part account for the presence of similar NOS plexus morphologies in distantly related animals.

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Section: Robustness Of Predicted Spread To Altering the Parameter Valuesmentioning

confidence: 99%

Modeling Cooperative Volume Signaling in a Plexus of Nitric Oxide Synthase-Expressing Neurons

Philippides¹,

Ott²,

Husbands³

et al. 2005

J. Neurosci.

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“…Shibuki firstly introduced a miniature electrochemical probe consisting in a Pt electrode covered with a gas-permeable membrane to successfully monitor endogenous NO Å production (8-58 nM) in rat cerebellar slices (Shibuki, 1990). Later, Shibuki's probe enabled WPI (Sarasota, USA) to develop the first widely commercially available nitric oxide sensor, the ISO-NO.…”

Section: Measurement Of No å In Hippocampal Subregions Using Electrocmentioning

confidence: 99%

Nitric oxide in brain: diffusion, targets and concentration dynamics in hippocampal subregions

Ledo

Frade

Barbosa

et al. 2004

Molecular Aspects of Medicine

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Nitric oxide (NO Å ) is a diffusible regulatory molecule involved in a wide range of physiological and pathological events. At the tissue level, a local and temporary increase in NO Å concentration is translated into a cellular signal. From our current knowledge of biological synthesis and decay, the kinetics and mechanisms that determine NO Å concentration dynamics in tissues are poorly understood. Generally, NO Å mediates its effects by stimulating (e.g., guanylate cyclase) or inhibiting (e.g., cytochrome oxidase) transition metal-containing proteins and by post-translational modification of proteins (e.g., formation of nitrosothiol adducts). The borderline between the physiological and pathological activities of NO Å is a matter of controversy, but tissue redox environment, supramolecular organization and compartmentalisation of NO Å targets are important features in determining NO Å actions. In brain, NO Å synthesis in the dependency of glutamate NMDA receptor is a paradigmatic example; the NMDA-subtype glutamate receptor triggers intracellular signalling pathways that govern neuronal plasticity, development, senescence and disease, suggesting a role for NO Å in these processes. Measurements of NO Å in the different subregions of hippocampus, in a glutamate NMDA receptor-dependent fashion, by means of electrochemical selective microsensors illustrate the concentration dynamics of NO Å in the sub-regions of this brain area. The analysis of NO Å concentration-time profiles in the hippocampus requires consideration of at least two interrelated issues, also addressed in this review. NO Å diffusion in a biological medium and regulation of NO Å activity. Ó 2004 Elsevier Ltd. All rights reserved.Abbreviations: CAPON, Carboxy-terminal PDZ ligand of nNOS; DOPAC, dihydroxyphenylacetic acid; EPR, electron paramagnetic resonance; LTP, long-term potentiation; NMDA, N-methyl-D D -aspartate; NOS, nitric oxide synthase; PDZ, PSD-95 discs large/ZO-1 homology domain; PSD-95, post-synaptic density protein 95

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“…GST-TPH-CC was treated with varying concentrations of the NO generator sodium nitroprusside (SN P) (Feelisch and Noack, 1987;Shibuki, 1990;Southam and Garthwaite, 1991). Because the generation of NO from SN P depends on a reductant such as DTT, all experiments with SN P were performed Ϯ1 mM DTT.…”

Section: Methodsmentioning

confidence: 99%

Molecular Mechanism of the Inactivation of Tryptophan Hydroxylase by Nitric Oxide: Attack on Critical Sulfhydryls that Spare the Enzyme Iron Center

Kuhn

Arthur²

1997

J. Neurosci.

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Tryptophan hydroxylase (TPH), the initial and rate-limiting enzyme in the biosynthesis of the neurotransmitter serotonin (5-HT), is irreversibly inactivated by nitric oxide (NO). We have expressed brain TPH as a recombinant glutathione-Stransferase fusion protein and delineated the catalytic domain of the enzyme as the region spanning amino acids 99-444. Highly purified TPH catalytic core, like the native enzyme from brain, is inactivated by NO in a concentration-dependent manner. Removal of iron from TPH produces an apoenzyme with low activity that can be reconverted to its highly active holoform by the addition of ferrous iron. Apo-TPH exposed to NO cannot be reactivated by iron. Treatment of holo-TPH (ironloaded) with the disulfide 5,5Ј-dithio-bis (2-nitrobenzoic acid) (DTNB) causes an inactivation of TPH that is readily reversed by dithiothreitol (DTT). DTNB-treated TPH [sulfhydryl (SH)-protected] exposed to NO is returned to full activity by thiol reduction with DTT. The inactivation of native TPH by NO cannot be reversed by either iron or DTT. These data indicate that NO inactivates TPH by selective action on critical SH groups (i.e., cysteine residues) while sparing catalytic iron sites within the enzyme. The results are interpreted with reference to the substituted amphetamines, which are neurotoxic to 5-HT neurons, that inactivate TPH in vivo and are now known to produce NO and other reactive oxygen species in vivo. Key words: tryptophan hydroxylase; nitric oxide; sulfhydryls; catalytic iron site; serotonin; neurotoxic amphetaminesTryptophan hydroxylase [EC 1.14.16.4; L-tryptophan, tetrahydropteridine: oxygen oxidoreductase (5-hydroxylating)] (TPH) is the initial and rate-limiting enzyme in the biosynthesis of the neurotransmitter serotonin (5-HT) (Jequier et al., 1967). The synthesis of 5-HT can proceed only through this enzymecatalyzed step. The activity of TPH controls the amount of 5-HT produced and released from neurons (Gartside et al., 1992;Oluyomi et al., 1994), indicating that this enzyme regulates not just 5-HT synthesis but its f unction as well. As a neurotransmitter, 5-HT mediates pain, sleep, thermoregulation, and food intake. From a clinical perspective, altered 5-HT f unction has been implicated in depression, obsessive-compulsive disorder, autism, and impulsive self-destructive behaviors such as aggression, suicide, and drug taking (Schatzberg and Nemeroff, 1995).Selected amphetamines have profound effects on the 5-HT neuronal system. Methylenedioxymethamphetamine (ecstasy) (MDM A) and p-chloroamphetamine cause extensive destruction of 5-HT neurons. An early manifestation of their effects is a significant inactivation of TPH (for reviews, see Gibb et al., 1993;Steele et al., 1994;Seiden and Sabol, 1996). The mechanisms underlying these effects on TPH are not known, but emerging data implicate drug-induced production of reactive oxygen species (ROS) and nitric oxide (NO). The cellular effects of ROS or NO cannot be predicted a priori: NO can be toxic to some cells (Lipton et al., 1993;Da...

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An electrochemical microprobe for detecting nitric oxide release in brain tissue

Cited by 380 publications

References 19 publications

Modeling Cooperative Volume Signaling in a Plexus of Nitric Oxide Synthase-Expressing Neurons

Modeling Cooperative Volume Signaling in a Plexus of Nitric Oxide Synthase-Expressing Neurons

Nitric oxide in brain: diffusion, targets and concentration dynamics in hippocampal subregions

Molecular Mechanism of the Inactivation of Tryptophan Hydroxylase by Nitric Oxide: Attack on Critical Sulfhydryls that Spare the Enzyme Iron Center

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