Nitric oxide as modulator of neuronal function

Prast, H.; Philippu, A.

doi:10.1016/s0301-0082(00)00044-7

Cited by 856 publications

(542 citation statements)

References 184 publications

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“…Nitric oxide (NO) is a gaseous messenger molecule that can serve both as an extracellular and intracellular transmitter in the brain, most likely through modulation of classical neurotransmitter release (Kano et al, 1998;Segovia and Mora, 1998;Whitton, 2000, 2001;Wegener et al, 2000;Prast and Philippu, 2001). The main effector of NO signaling is cGMP formed by soluble guanylyl cyclase (sGC) (Karatinos et al, 1995) even if NO, to a lesser extent, may act through cAMP formation by adenylyl cyclase and protein nitrosylation.…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide Signaling in the Medial Prefrontal Cortex is Involved in the Biochemical and Behavioral Effects of Phencyclidine

Fejgin

Pålsson

Wass

et al. 2007

Neuropsychopharmacol

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The prefrontal cortex (PFC) is believed to play an important role in the cognitive impairments observed in schizophrenia and has also been shown to be involved in the modulation of prepulse inhibition (PPI), a measure of preattentive information processing that is impaired in schizophrenic individuals. Phencyclidine (PCP), a noncompetitive inhibitor of the NMDA receptor, exerts psychotomimetic effects in humans, disrupts PPI, and causes hypofrontality in rodents and monkeys. We have previously demonstrated that interfering with the production of nitric oxide (NO) can prevent a wide range of PCP-induced behavioral deficits, including PPI disruption. In the present study, the role of NO signaling for the behavioral and biochemical effects of PCP was further investigated. Dialysate from the medial PFC of mice receiving systemic treatment with PCP and/or the NO synthase inhibitor, N G -nitro-L-arginine methyl ester (L-NAME, 40 mg/kg), was analyzed for cGMP content. Furthermore, a specific inhibitor of NO-sensitive soluble guanylyl cyclase (sGC), 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (ODQ, 0.01-1 mM), was administered into the medial PFC of mice in combination with systemic injections of PCP, followed by PPI and locomotor activity testing. PCP (5 mg/kg) caused an increase in prefrontal cGMP that could be attenuated by pretreatment with the NO synthase inhibitor, L-NAME. Moreover, bilateral microinjection of the sGC inhibitor, ODQ, into the medial PFC of mice attenuated the disruption of PPI, but not the hyperlocomotion, caused by PCP. The present study shows that NO/sGC/cGMP signaling pathway in the medial PFC is involved in specific behavioral effects of PCP that may have relevance for the disabling cognitive dysfunction found in patients with schizophrenia.

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Section: Introductionmentioning

confidence: 99%

Nitric Oxide Signaling in the Medial Prefrontal Cortex is Involved in the Biochemical and Behavioral Effects of Phencyclidine

Fejgin

Pålsson

Wass

et al. 2007

Neuropsychopharmacol

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“…It may be immediately seen from this that the neural sensitization theory overlaps with the nitric oxide/peroxynitrite theory. Furthermore, nitric oxide has an important role in LTP, acting as a retrograde messenger (Bliss and Collingridge 1993;Prast and Phillipu 2001;Snyder 1992), increasing the release of neurotransmitters including glutamate, which in turn stimulate the NMDA receptors. Thus, we have a potential vicious cycle in the nervous system, with excessive NMDA activity producing excessive nitric oxide leading to excessive NMDA activity ( Figure 1).…”

Section: Fusion Of the Nitric Oxide/peroxynitrite Theory With The Neumentioning

confidence: 99%

Elevated nitric oxide/peroxynitrite theory of multiple chemical sensitivity: central role of N-methyl-D-aspartate receptors in the sensitivity mechanism.

Pall

2003

Environ Health Perspect

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The elevated nitric oxide/peroxynitrite and the neural sensitization theories of multiple chemical sensitivity (MCS) are extended here to propose a central mechanism for the exquisite sensitivity to organic solvents apparently induced by previous chemical exposure in MCS. This mechanism is centered on the activation of N-methyl-D-aspartate (NMDA) receptors by organic solvents producing elevated nitric oxide and peroxynitrite, leading in turn to increased stimulating of and hypersensitivity of NMDA receptors. In this way, organic solvent exposure may produce progressive sensitivity to organic solvents. Pesticides such as organophosphates and carbamates may act via muscarinic stimulation to produce a similar biochemical and sensitivity response. Accessory mechanisms of sensitivity may involve both increased blood-brain barrier permeability, induced by peroxynitrite, and cytochrome P450 inhibition by nitric oxide. The NMDA hyperactivity/ hypersensitivity and excessive nitric oxide/peroxynitrite view of MCS provides answers to many of the most puzzling aspects of MCS while building on previous studies and views of this condition.

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“…There are molecules like NO which are particularly complex from a functional point of view (Prast and Philippu, 2001). In fact, NO is a biological signaling molecule that is important in the physiology and pathophysiology of many different tissues (Schulz et al, 1995).…”

Section: Nos Induction After Axotomymentioning

confidence: 99%

Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection

et al. 2002

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When vestibular damage occurs, nitric oxide synthase (NOS) expression in rat cerebellar flocculus is affected. Since compensation for postural symptoms occurs and Purkinje cells play an important role in movement coordination and motor learning, we analyzed in situ the induction of NOS in the Purkinje cell population of the cerebellum (corpus cerebelli) of frog after unilateral transection of the eighth statoacoustic nerve to gain insight into the role of NO in neural plasticity after injury. Three days after neurectomy, the early effects induced NADPH diaphorase reactivity in most of the Purkinje cells on the ipsilateral side, while on the contralateral side the highest labeling was observed at 15 days. This finding can give information on the dynamics of vestibular compensation, in which NOS involvement was investigated. At 30 days, NADPH diaphorase reactivity was present in a large number of Purkinje cells of the whole cerebellum, while at 60 days a down-regulation for NADPH diaphorase reactivity was evident. A similar trend was observed for NOS-immunoreactivity, which was still present at 60 days in a high percentage of Purkinje cells, mainly on the ipsilateral side. On the basis of cell density evaluations, it was proposed that the early induction of NOS after neurectomy was linked to the degeneration of a part of the Purkinje neurons, while the permanence of NOS labeling might be due to a neuroprotective role of NO in the restoration phase of the vestibular compensation process. Anat Rec 268: 73-83, 2002.

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Nitric oxide as modulator of neuronal function

Cited by 856 publications

References 184 publications

Nitric Oxide Signaling in the Medial Prefrontal Cortex is Involved in the Biochemical and Behavioral Effects of Phencyclidine

Nitric Oxide Signaling in the Medial Prefrontal Cortex is Involved in the Biochemical and Behavioral Effects of Phencyclidine

Elevated nitric oxide/peroxynitrite theory of multiple chemical sensitivity: central role of N-methyl-D-aspartate receptors in the sensitivity mechanism.

Nitric oxide synthase in the frog cerebellum: Response of Purkinje neurons to unilateral eighth nerve transection

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