Effects of selective neuronal nitric oxide synthase inhibition on sleep and wakefulness in the rat

Cavas, M.; Navarro, José Francisco

doi:10.1016/j.pnpbp.2005.06.013

Cited by 24 publications

(13 citation statements)

References 74 publications

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“…Inhibition of NO synthase (NOS) by L-NAME has been described to reduce both NREMS and REMS in rats [32]; however, also the exact opposite effect has been reported [33]. The specific neuronal NOS (nNOS) inhibitor, 7-nitro-indazole, has been demonstrated to decrease REMS exclusively [33], to reduce both REMS and NREMS as well as EEG amplitude [34], or to have most of all an effect on NREMS [35], respectively. Inhibition of soluble guanylyl cyclase, which generates cGMP upon activation by NO, promoted NREMS and suppressed REMS [36].…”

Section: Discussionmentioning

confidence: 99%

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cGMP-Dependent Protein Kinase Type I Is Implicated in the Regulation of the Timing and Quality of Sleep and Wakefulness

et al. 2009

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Many effects of nitric oxide (NO) are mediated by the activation of guanylyl cyclases and subsequent production of the second messenger cyclic guanosine-3′,5′-monophosphate (cGMP). cGMP activates cGMP-dependent protein kinases (PRKGs), which can therefore be considered downstream effectors of NO signaling. Since NO is thought to be involved in the regulation of both sleep and circadian rhythms, we analyzed these two processes in mice deficient for cGMP-dependent protein kinase type I (PRKG1) in the brain. Prkg1 mutant mice showed a strikingly altered distribution of sleep and wakefulness over the 24 hours of a day as well as reductions in rapid-eye-movement sleep (REMS) duration and in non-REM sleep (NREMS) consolidation, and their ability to sustain waking episodes was compromised. Furthermore, they displayed a drastic decrease in electroencephalogram (EEG) power in the delta frequency range (1–4 Hz) under baseline conditions, which could be normalized after sleep deprivation. In line with the re-distribution of sleep and wakefulness, the analysis of wheel-running and drinking activity revealed more rest bouts during the activity phase and a higher percentage of daytime activity in mutant animals. No changes were observed in internal period length and phase-shifting properties of the circadian clock while chi-squared periodogram amplitude was significantly reduced, hinting at a less robust oscillator. These results indicate that PRKG1 might be involved in the stabilization and output strength of the circadian oscillator in mice. Moreover, PRKG1 deficiency results in an aberrant pattern, and consequently a reduced quality, of sleep and wakefulness, possibly due to a decreased wake-promoting output of the circadian system impinging upon sleep.

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Section: Discussionmentioning

confidence: 99%

“…Divergent findings might be due to variances in times of treatment [37] and/or drug dose [30], [35]. In addition, it is important to note that not all effects of NO must be mediated via cGMP and PRKGs.…”

Section: Discussionmentioning

confidence: 99%

cGMP-Dependent Protein Kinase Type I Is Implicated in the Regulation of the Timing and Quality of Sleep and Wakefulness

et al. 2009

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“…Nitric oxide (NO) performs multiple roles in CNS function like 539 maintaining cognitive function, neurotransmitter secretion, sleep 540 wake cycle, appetite control body temperature homeostasis and 541 neuroprotection [107]. It has been well documented that NO seems 542 to protect the neurons from excitotoxicity through its effect on 543 NMDA receptors as well as caspase inhibition [108].…”

Section: Modulators Of Nos 538mentioning

confidence: 99%

A review on Alzheimer's disease pathophysiology and its management: an update

Kumar

Singh

Ekavali

2015

Pharmacological Reports

1,314

850

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Alzheimer's disease acknowledged as progressive multifarious neurodegenerative disorder, is the leading cause of dementia in late adult life. Pathologically it is characterized by intracellular neurofibrillary tangles and extracellular amyloidal protein deposits contributing to senile plaques. Over the last two decades, advances in the field of pathogenesis have inspired the researchers for the investigation of novel pharmacological therapeutics centered more towards the pathophysiological events of the disease. Currently available treatments i.e. acetylcholinesterase inhibitors (rivastigmine, galantamine, donepezil) and N-methyl d-aspartate receptor antagonist (memantine) contribute minimal impact on the disease and target late aspects of the disease. These drugs decelerate the progression of the disease, provide symptomatic relief but fail to achieve a definite cure. While the neuropathological features of Alzheimer's disease are recognized but the intricacies of the mechanism have not been clearly defined. This lack of understanding regarding the pathogenic process may be the likely reason for the non-availability of effective treatment which can prevent onset and progression of the disease. Owing to the important progress in the field of pathophysiology in the last couple of years, new therapeutic targets are available that should render the underlying disease process to be tackled directly. In this review, authors will discusses the different aspects of pathophysiological mechanisms behind Alzheimer's disease and its management through conventional drug therapy, including modern investigational therapeutic strategies, recently completed and ongoing.

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“…In fact, NO meets some of the criteria for sleep regulatory substances (Gautier-Sauvigne et al, 2005). Systemic administration of the nNOS inhibitors 3-bromo-7-nitroindazole (Cavas and Navarro, 2006) and N G -nitro-L-arginine (L-NAME; Kapas et al, 1994b) during the light phase of the LD cycle reduced the amount of time spent in SWS, as did intracerebroventricular injection (Kapas et al, 1994a). However, when the same compound was administered at dark onset, only suppression of SWA occurred and time spent in SWS increased (Ribeiro and Kapas, 2005).…”

Section: Neuronal No As a Sleep-inducing Factor: Local Regulation Of mentioning

confidence: 99%

Sleep-Active Neuronal Nitric Oxide Synthase-Positive Cells of the Cerebral Cortex: A Local Regulator of Sleep?

Wisor

Gerashchenko²,

Kilduff³

2011

CTMC

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Our recent report demonstrated that a small subset of GABAergic interneurons in the cerebral cortex of rodents expresses Fos protein, a marker for neuronal activity, during slow wave sleep (Gerashchenko et al., 2008). The population of sleep-active neurons consists of strongly immunohistochemically-stained cells for the enzyme neuronal nitric oxide synthase. By virtue of their widespread localization within the cerebral cortex and their widespread projections to other cortical cell types, cortical neuronal nitric oxide synthase-positive neurons are positioned to play a central role in the local regulation of sleep waveforms within the cerebral cortex. Here, we review the possible functions of neuronal nitric oxide synthase and its diffusible gas product, nitric oxide, in regulating neuronal activity, synaptic plasticity and cerebral blood flow within the context of local sleep regulation in the cerebral cortex. We also summarize what is known, in addition to their expression of neuronal nitric oxide synthase, about the biochemical phenotype, synaptic connectivity and electrophysiological properties of this novel sleep-active population of cells. Finally, we raise some critical unanswered questions about the role of this population in local sleep regulation within the cerebral cortex and describe some experimental approaches that might be used to address those questions.

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Effects of selective neuronal nitric oxide synthase inhibition on sleep and wakefulness in the rat

Cited by 24 publications

References 74 publications

cGMP-Dependent Protein Kinase Type I Is Implicated in the Regulation of the Timing and Quality of Sleep and Wakefulness

cGMP-Dependent Protein Kinase Type I Is Implicated in the Regulation of the Timing and Quality of Sleep and Wakefulness

A review on Alzheimer's disease pathophysiology and its management: an update

Sleep-Active Neuronal Nitric Oxide Synthase-Positive Cells of the Cerebral Cortex: A Local Regulator of Sleep?

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