Nitric oxide: A radical neurotransmitter in the central nervous system

Vincent, Steven R.

doi:10.1016/0301-0082(94)90023-x

Cited by 452 publications

(252 citation statements)

References 411 publications

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“…NO has been implicated in mediating long-term potentiation and long-term depression in the central nervous system; that is changes in efficiency of synapses due to usage which may be important in memory formation [4]. Levels of NO measured during induction of long-term depression in cerebellar slices were 20-75 nM [26].…”

Section: Brain and Synapsementioning

confidence: 99%

“…Nitric oxide (NO) has a number of physiological roles, including: (a) relaxation of smooth muscle; (b) neurotransmission and neuromodulation; (c) inhibition of platelet aggregation and adhesion; and (d) killing of pathogens (reviewed in [1][2][3][4][5]). NO can also be toxic to host cells, and has been implicated in variety of pathological processes.…”

Section: Introductionmentioning

confidence: 99%

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Nitric oxide regulates mitochondrial respiration and cell functions by inhibiting cytochrome oxidase

Brown¹

1995

FEBS Letters

514

283

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Nitric oxide (NO) reversibly inhibits mitochondrial respiration by competing with oxygen at cytochrome oxidase. Concentrations of NO measured in a range of biological systems are similar to those shown to inhibit cytochrome oxidase and mitochondrial respiration. Inhibition of NO synthesis results in a stimulation of respiration in a number of systems. It is proposed that NO exerts some of its main physiological and pathological effects on cell functions by inhibiting cytochrome oxidase. Further NO may be a physiological regulator of the affinity of mitochondrial respiration for oxygen, enabling mitochondria to act as sensors of oxygen over the physiological range.

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Section: Brain and Synapsementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Nitric oxide regulates mitochondrial respiration and cell functions by inhibiting cytochrome oxidase

Brown¹

1995

FEBS Letters

514

283

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“…Three isoforms of this enzyme have been purified, cloned, and sequenced: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS) (Nathan and Xie, 1994). In the striatum, NO is generated primarily via activation of nNOS which is localized to a subclass of medium aspiny interneurons known to synthesize neuropeptide Y, somatostatin, and GABA (Bredt et al, 1990Dawson et al, 1991;Kubota et al, 1993;Vincent, 1994). Considerable evidence has accumulated indicating that striatal NOS interneurons play a critical role in the integration of glutamatergic and dopaminergic neurotransmission within striatal neural networks (for a review, see Calabresi et al, 2000a;.…”

Section: Introductionmentioning

confidence: 99%

Phasic Dopaminergic Transmission Increases NO Efflux in the Rat Dorsal Striatum via a Neuronal NOS and a Dopamine D1/5 Receptor-Dependent Mechanism

Sammut

Dec

Mitchell

et al. 2005

Neuropsychopharmacol

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Dysfunctional neurotransmission within striatal networks is believed to underlie the pathophysiology of several neurological and psychiatric disorders. Nitric oxide (NO)-producing interneurons have been shown to play a critical role in modulating striatal synaptic transmission. These interneurons receive synaptic contacts from midbrain dopamine (DA) neurons and may be regulated by DA receptor activation. In the current study, striatal NO efflux was measured in anesthetized male rats using an NO-selective electrochemical microsensor and the role of DA in modulating NO synthase (NOS) activity was assessed during electrical or chemical (bicuculline) stimulation of the substantia nigra (SN). Electrical stimuli were patterned to approximate the natural single spike or burst firing activity of midbrain DA neurons. Electrical stimulation of the SN at low frequencies induced modest increases in striatal NO efflux. In contrast, train stimulation of the SN robustly increased NO efflux in a stimulus intensity-dependent manner. NO efflux evoked by SN stimulation was similar in chloral hydrate-and urethane-anesthetized rats. The facilitatory effect of train stimulation on striatal NO efflux was transient and attenuated by systemic administration of the neuronal NOS inhibitor 7-nitroindazole and the nonselective NOS inhibitor methylene blue. Moreover, the increase in NO efflux observed during chemical and train stimulation of the SN was attenuated following systemic administration of the DA D 1/5 receptor antagonist SCH 23390. SCH 23390 also blocked NO efflux induced by systemic administration of the D 1/5 agonist SKF 81297. These results indicate that neuronal NOS is activated in vivo by nigrostriatal DA cell burst firing via a DA D 1/5 -like receptor-dependent mechanism.

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“…NO is synthesized from L-arginine and molecular oxygen by the enzyme NO-synthase (NOS) (Bredt & Snyder, 1990), that, using as cofactor NADPH, displays NADPH diaphorase (NADPHd) activity (Garthwaite,1991;Vincent, 1994;Johansson & Carlberg, 1995); the formation of NO is a Ca 2+ / calmodulin-dependent process (Garthwaite et al, 1988).…”

confidence: 99%

Nitric oxide synthase-dependent NADPH-diaphorase activity in the optic lobes of male and female Ceratitis capitata mutants

et al. 2009

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Nitric oxide (NO) is acknowledged as a messenger molecule in the nervous system with a pivotal role in the modulation of the chemosensory information. It has been shown to be present in the optic lobes of several insect species. In the present study, we used males and females from four different strains of the medfly Ceratitis capitata (Diptera, Tephritidae): or; or,wp (both orange eyed); w,M360 and w,Heraklion (both white eyed), as models to further clarify the involvement of NO in the mutants' visual system and differences in its activity and localization in the sexes.Comparison of the localization pattern of NO synthase (NOS), through NADPH-diaphorase (NADPHd) staining, in the optic lobes of the four strains, revealed a stronger reaction intensity in the retina and in the neuropile region lamina than in medulla and lobula. Interestingly, the intensity of NADPHd staining differs, at least in some strains, in the optic lobes of the two sexes; all the areas are generally strongly labelled in the males of the or and w,M360 strains, whereas the w,Heraklion and or,wp mutants do not show evident sexdependent NADPHd staining. Taken as a whole, our data point to NO as a likely transmitter candidate in the visual information processes in insects, with a possible correlation among NOS distribution, eye pigmentation and visual function in C. capitata males. Moreover, NO could influence behavioural differences linked to vision in the two sexes.

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Nitric oxide: A radical neurotransmitter in the central nervous system

Cited by 452 publications

References 411 publications

Nitric oxide regulates mitochondrial respiration and cell functions by inhibiting cytochrome oxidase

Nitric oxide regulates mitochondrial respiration and cell functions by inhibiting cytochrome oxidase

Phasic Dopaminergic Transmission Increases NO Efflux in the Rat Dorsal Striatum via a Neuronal NOS and a Dopamine D1/5 Receptor-Dependent Mechanism

Nitric oxide synthase-dependent NADPH-diaphorase activity in the optic lobes of male and female Ceratitis capitata mutants

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