Dynamic changes in NADPH-diaphorase staining reflect activity of nitric oxide synthase: Evidence for a dopaminergic regulation of striatal nitric oxide release

Morris, Brian J.; Simpson, C.S.; Mundell, Stuart J.; MacEachern, K.E.; Johnston, Heather; Nolan, A. M.

doi:10.1016/s0028-3908(97)00159-7

Cited by 96 publications

(89 citation statements)

References 62 publications

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“…These findings are consistent with previous reports that D 1/5 receptor activation increases indirect measures of NOS activity (Altar et al, 1990;Morris et al, 1997) and firing activity of electrophysiologically identified NOS interneurons (Centonze et al, 2002). Thus, striatal NOS interneurons may be potently activated by DA cell burst firing in specific behavioural contexts.…”

Section: Discussionsupporting

confidence: 92%

“…This effect was observed in animals which also exhibited increases in NO efflux during train stimulation of the SN, indicating that NOS neurons are activated by endogenous DA and D 1/5 agonist in these rats. These results extend previous histochemical studies showing that NOS activity, assayed via NADPH-diaphorase staining, is reduced following the administration of the D 1/5 antagonist SCH 23390 (Morris et al, 1997). Consistent with our findings, D 1/5 agonist administration has been shown to robustly stimulate the firing activity of electrophysiologically identified NOS interneurons in a manner sensitive to SCH 23390 administration (Centonze et al, 2002).…”

Section: Sn Stimulation Increases No Efflux Via a D 1/5 Receptor-depesupporting

confidence: 92%

“…Given the proximity of glutamatergic and dopaminergic inputs on the NOS interneuron dendrites (Fujiyama and Masuko, 1996;Hidaka and Totterdell, 2001), it is likely that these afferents interact via presynaptic and/ or postsynaptic mechanisms to regulate striatal NOS activity. This is supported by histochemical evidence that both NMDA and D 1/5 receptor antagonists decrease NOS activity measured ex vivo (Morris et al, 1997). Interestingly, D 1/5 receptor activation increases striatal tissue levels of the NO second messenger cGMP via an unknown mechanism (Altar et al, 1990).…”

Section: Introductionmentioning

confidence: 91%

“…Effective doses of SCH 23390 (100, 500 mg/kg, i.p.) and SKF 81297 (50 mg/ml/kg, i.v) were derived from the range previously reported in the literature (Gonon, 1997;Morris et al, 1997;Reynolds et al, 2001;Brady and O'Donnell, 2004). In studies using SKF 81297, drug was administered intravenously (via a lateral tail vein) after obtaining 150 s of basal activity.…”

Section: Drug Preparation and Administrationmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 92%

Section: Sn Stimulation Increases No Efflux Via a D 1/5 Receptor-depesupporting

confidence: 92%

Section: Introductionmentioning

confidence: 91%

Section: Drug Preparation and Administrationmentioning

confidence: 99%

See 2 more Smart Citations

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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“…Mice of each group were sacrificed by decapitation under deep anesthesia and diaphragm muscle was resected to evaluate a NOS activity by NADPH diaphorase staining [9,10]. The diaphragm was quickly excised, and the tissue pieces were frozen in O.C.T.…”

Section: Nadph Diaphorase Stainingmentioning

confidence: 99%

Diaphragm Muscle Contraction Decrease in a Mouse Model of Ovalbumin-Induced Allergic Airway Inflammation

Yamaguchi¹,

Shindoh²,

Miura³

2017

J Allergy Ther

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Objective: We investigated diaphragm contractile and inflammatory properties of mice with OVA sensitization and challenge.Methods: BALB/c mice were sensitized to OVA by intraperitoneal (i.p.) injection at 0 and 7 days, and challenged with aerosolized OVA on 21, 22, and 23 days (O/O group). Budesonide/Formoterol combination was inhaled on days 21, 22, and 23 before OVA challenge on those same days (O/OC group). Control mice were sensitized and challenged with an aerosolized saline (O-group). The diaphragm contractile and inflammatory properties were measured on day 24. NOS activity in the diaphragm muscle was evaluated by NADPH diaphorase staining. IL-4 and IL-13 levels of BALF, as well as lung tissue and diaphragm muscle homogenates were measured by ELISA. Conclusions:OVA sensitization and challenge decreased diaphragm muscle contraction, increased NOS activity, IL-4 levels of diaphragm in a mouse model. Budesonide/Formoterol combination could protect diaphragm muscle weakness and inflammation. According to the traditional concept of the contemporary Immunology, neither autoimmune diseases nor allergic diseases can be cured completely. Nevertheless, a fortunate coincidence led me to discovery of a novel concept that eliminations of the causes of these diseases are possible. In other words, combinations of pathogenic antibodies with responsible cells, namely, cytolytic T lymphocytes in cases of autoimmune diseases and mast cells in cases of allergic diseases, can be decomposed by replacing the pathogenic antibodies with non-specific antibodies. In more detail, intradermal injections with a non-specific antigen preparation induce production of non-specific antibodies in the body of the patient. Repetitions of the injections bring about an accumulation of them. Accumulated non-specific antibodies will occupy most of the receptors on the surface of responsible cells. When the accumulation reaches the sufficient level, virtually no pathogenic antibodies would remain on the receptors. That is, no causes of the diseases remain. Naturally, where there is no cause, there is no disease. Details are demonstrated elsewhere.

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NADPH diaphorase activity in the rabbit retina is modulated by glutamatergic pathways

Zemel

Perlman

2001

J. Comp. Neurol.

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NADPH diaphorase activity in the rabbit retina is modulated by the state of visual adaptation. In this study, we tested possible glutamatergic control of this phenomenon. Rabbits were injected intravitreally with agonists and antagonists of glutamate. After adaptation (3 hours) to either room light or darkness, the rabbits were killed and the retinae were prepared for NADPH diaphorase histochemistry. Kainic acid significantly reduced the number of NADPH diaphorase amacrine cells but augmented NADPH diaphorase activity in horizontal cells in both light- and dark-adapted animals. 6,7-Dinitroquinoxaline-2,3(1H,4H)-dione exerted no effect on amacrine cells but eliminated NADPH diaphorase activity in horizontal cells. 2-Amino-4-phosphono butyric acid did not affect NADPH diaphorase activity in horizontal cells but reduced the degree of staining in the neuronal processes of amacrine cells. MK-801 and N-methyl-D-aspartic acid (NMDA) had no effect on NADPH diaphorase activity in horizontal cells. However, MK-801 reduced staining in the neuronal processes of amacrine cells but not in their cell bodies. NMDA effects were expressed in a significant reduction in the number and size of amacrine cells that were NADPH diaphorase positive. These results indicate that activation of NADPH diaphorase in horizontal cells by darkness is mediated by the activation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainic acid (KA)-type glutamate receptors. The ON pathway in the retina is probably involved in modulation of NADPH diaphorase in the neuronal processes of amacrine cells. Amacrine cells that are NADPH diaphorase positive contain NMDA-type and AMPA/KA-type receptors and are highly susceptible to NMDA and kainic acid toxicity.

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Dynamic changes in NADPH-diaphorase staining reflect activity of nitric oxide synthase: Evidence for a dopaminergic regulation of striatal nitric oxide release

Cited by 96 publications

References 62 publications

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

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

Diaphragm Muscle Contraction Decrease in a Mouse Model of Ovalbumin-Induced Allergic Airway Inflammation

NADPH diaphorase activity in the rabbit retina is modulated by glutamatergic pathways

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