Nitric oxide and neurological disorders

Duncan, Andrew; Heales, Simon

doi:10.1016/j.mam.2004.09.004

Cited by 169 publications

(125 citation statements)

References 165 publications

(173 reference statements)

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“…Astrocytes support damaged neural tissues through release of neurotrophic factors, antioxidants, and degradation of extracellular deposits (WyssCoray and Mucke, 2002). In contrast, release of reactive oxygen species, cytokines, nitric oxide, and proteases by reactive astrocytes contribute to neurodegenerative disorders (Tacconi, 1998;Mrak and Griffin, 2001;Duncan and Heales, 2005). In the present study, the microarray data provide a view of the reactive astrocyte transcriptome in response to activated EGFR that suggests new experimental approaches to dissect the role of reactive astrocytes in CNS disorders.…”

Section: Discussionmentioning

confidence: 69%

Epidermal Growth Factor Receptor Activation: An Upstream Signal for Transition of Quiescent Astrocytes into Reactive Astrocytes after Neural Injury

et al. 2006

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Modulating the behaviors of reactive astrocytes is a potential therapeutic strategy for neurodegenerative diseases. We found that upregulation and activation of the epidermal growth factor receptor (EGFR) occur in astrocytes after different injuries in optic nerves in vivo. Activation of EGFR regulates genes and cellular processes representing most major markers of reactive astrocytes and genes related with glaucomatous optic neuropathy and other neural disorders. These results suggest that activation of EGFR is a common, regulatory pathway that triggers quiescent astrocytes into reactive astrocytes in response to neural injuries in the optic nerve, and perhaps other parts of the CNS. Targeting EGFR activation using an EGFR tyrosine kinase inhibitor prevents the loss of retinal ganglion cells in a model of glaucomatous optic neuropathy. Because these inhibitors are currently used clinically, our results present an approach to reactive astrocytes as a potential new target for the treatment of neurodegenerations.

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Section: Discussionmentioning

confidence: 69%

Epidermal Growth Factor Receptor Activation: An Upstream Signal for Transition of Quiescent Astrocytes into Reactive Astrocytes after Neural Injury

et al. 2006

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“…Because of their abilities to rapidly spread from the site of production to adjacent cells, and to activate a signal transduction pathway involving cyclic GMP and kinases, nitric oxide and carbon monoxide may have important roles in many different physiological processes, including relaxation of blood vessels, regulation of reproductive functions, learning and memory, and immune responses to pathogens. However, excessive production of nitric oxide is implicated in the pathogenesis of major diseases, including cardiovascular disease, diabetes, cancer, stroke and neurodegenerative disorders (Hofseth et al, 2003;Duncan et al, 2005;Pacher et al, 2005).…”

Section: Endogenous Neurotoxins and The Pathological Second Phase Of mentioning

confidence: 99%

Awareness of Hormesis Will Enhance Future Research in Basic and Applied Neuroscience

Mattson

2008

Critical Reviews in Toxicology

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Hormesis is defined operationally as responses of cells or organisms to an exogenous or intrinsic factor (chemical, temperature, psychological challenge, etc.) in which the factor induces stimulatory or beneficial effects at low doses and inhibitory or adverse effects at high doses. The compendium of articles by Calabrese entitled "Neuroscience and Hormesis" provides a broad range of examples of neurobiological processes and responses to environmental factors that exhibit biphasic dose responses, the signature of hormesis. Nerve cell networks are the "first responders" to environmental challenges-they perceive the challenge and orchestrate coordinated adaptive responses that typically involve autonomic, neuroendocrine, and behavioral changes. In addition to direct adaptive responses of neurons to environmental stressors, cells subjected to a stressor produce and release molecules such as growth factors, cytokines, and hormones that alert adjacent and even distant cells to impending danger. The discoveries that some molecules (e.g., carbon monoxide and nitric oxide) and elements (e.g., selenium and iron) that are toxic at high doses play fundamental roles in cellular signaling or metabolism suggest that during evolution, organisms (and their nervous systems) coopted environmental toxins and used them to their advantage. Neurons also respond adaptively to everyday stressors, including physical exercise, cognitive challenges, and dietary energy restriction, each of which activates pathways linked to the production of neurotrophic factors and cellular stress resistance proteins. The development of interventions that activate hormetic signaling pathways in neurons is a promising new approach for the preventation and treatment of a range of neurological disorders. COMMENTARY ON NEUROSCIENCE AND HORMESISThe biphasic nature of responses to neurotransmitters, neurotrophic factors, cytokines, drugs of abuse, and treatments for a range of neurological disorders is underappreciated and often ignored in basic and applied neuroscience research. Calabrese demonstrates a broad understanding of basic principles of neuroscience, to which he applies his expertise in toxicology and hormesis to catalog hundreds of examples of "toxins," pharmacological agents, intrinsic signaling molecules, and behavioral factors that exhibit biphasic dose responses. The focus throughout the series of articles in "Neuroscience and Hormesis" is on the results of cell culture and in vivo experiments in which the effects of increasing doses of exogenous agents (toxins, neurotransmitters, peptide, hormones, drugs of abuse, etc.) on neuronal survival or plasticity or on animal behavior has been investigated. Calabrese aptly explores the existence of hormesis in most of the major areas of the field of neuroscience, ranging from developmental mechanisms (cell survival and neurite outgrowth) to synaptic plasticity to behavior to

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“…neuroprotective vs. neurotoxic) it plays in neurodegenerative disorders is still ambiguous. Substantial evidence demonstrates a causative role for NO in the degeneration of DAergic neurons of the nigrostriatal pathway in PD Di Matteo et al 2006;Duncan and Heales 2005;Zhang et al 2006;Eve et al 1998;Nisbet et al 1994;Hunot et al 1996). Consistently, NOS polymorphisms increased expression of astroglial iNOS, and nNOS have been reported in PD patients and in different toxin-induced experimental models of PD.…”

Section: Involvement Of No In Neurodegeneration Of Dopaminergic Nigromentioning

confidence: 66%

Nitric Oxide Modulation of the Dopaminergic Nigrostriatal System: Focus on Nicotine Action

Matteo

Pierucci

Benigno

et al. 2009

Advances in Behavioral Biology

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Nitric oxide (NO) signalling plays an important role in the integration of information processed by the basal ganglia nuclei. Accordingly, considerable evidence has emerged indicating a role for NO in pathophysiological conditions such as Parkinson's disease (PD), schizophrenia and drug addiction. To further investigate the NO modulation of dopaminergic function in the basal ganglia circuitry, in this study we used in vivo electrophysiology and microdialysis in freely-moving rats. Pharmacological manipulation of the NO system did not cause any significant changes either in the basal firing rate and bursting activity of the dopamine (DA) neurons in the substantia nigra pars compacta (SNc) or in DA release in the striatum. In contrast, the disruption of endogenous NO tone was able to counteract the phasic dopaminergic activation induced by nicotine treatment in both experimental approaches. These results further support the possibility that nicotine acts via a NO mechanism and suggest a possible state-dependent facilitatory control of NO on the nigrostriatal DA pathway. Thus, NO selectively modulates the DA exocytosis associated with increased DA function.

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Nitric oxide and neurological disorders

Cited by 169 publications

References 165 publications

Epidermal Growth Factor Receptor Activation: An Upstream Signal for Transition of Quiescent Astrocytes into Reactive Astrocytes after Neural Injury

Epidermal Growth Factor Receptor Activation: An Upstream Signal for Transition of Quiescent Astrocytes into Reactive Astrocytes after Neural Injury

Awareness of Hormesis Will Enhance Future Research in Basic and Applied Neuroscience

Nitric Oxide Modulation of the Dopaminergic Nigrostriatal System: Focus on Nicotine Action

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