Nitric oxide and <i>S</i>‐nitrosylation: excitotoxic and cell signaling mechanism

Nelson, Eric J.; Connolly, Jon H.; McArthur, Peter

doi:10.1016/s0248-4900(03)00004-2

Cited by 58 publications

(39 citation statements)

References 30 publications

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“…The NMDA receptor is closely linked to the neuronal enzyme nitric oxide synthase (NOS) via PSD-95 interactions. Calcium entering through NMDA receptors stimulates NO production by NOS, which is neurotoxic at high levels [44,45]. This observation may explain why calcium entering through NMDA receptors is more neurotoxic than calcium entering through voltage-dependent calcium channels or non-NMDA ionotropic glutamate receptors [46].…”

Section: Events Underlying Excitotoxicitymentioning

confidence: 99%

Protein phosphatases and their potential implications in neuroprotective processes

Gee

Mansuy

2005

CMLS, Cell. Mol. Life Sci.

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Several neurological disorders such as stroke, amyotrophic lateral sclerosis and epilepsy result from excitotoxic events and are accompanied by neuronal cell death. These processes engage multiple signalling pathways and recruit numerous molecular components, in particular several families of protein kinases and protein phosphatases. While many investigations have examined the importance of protein kinases in excitotoxicity, protein phosphatases have not been well studied in this context. However, recent advances in understanding the functions of protein phosphatases have suggested that they may play a neuroprotective role. In this review, we summarize some of the recent findings that illustrate the pleiotropic and complex functions of tyrosine and serine/threonine protein phosphatases in the cascade of events leading to neuronal cell death, and highlight their potential intervention in limiting the extent of neuronal death.

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Section: Events Underlying Excitotoxicitymentioning

confidence: 99%

Protein phosphatases and their potential implications in neuroprotective processes

Gee

Mansuy

2005

CMLS, Cell. Mol. Life Sci.

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“…The physiological functions of NO are mediated by activation of sGC, which generates cGMP (Gibb et al, 2003a). Under pathological conditions such as cerebral ischemia, sGC-independent mechanism appears to be involved in the neurotoxic action of NO (Nelson et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Glial‐mediated neuroprotection: Evidence for the protective role of the NO‐cGMP pathway via neuron–glial communication in the peripheral nervous system

Thippeswamy

McKay

Morris

et al. 2004

Glia

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The NO-cGMP pathway has emerged as a neuroprotective signaling system involved in communication between neurons and glia. We have previously shown that axotomy or nerve growth factor (NGF)-deprivation of dorsal root ganglion (DRG) neurons leads to increased production of NO and at the same time an increase in cGMP production in their satellite glia cells. Blockade of NO or its receptor, the cGMP synthesizing enzyme soluble guanylate cyclase (sGC), results in apoptosis of neurons and glia. We now show that co-culture of neonatal DRG neurons with either Schwann cells pre-treated with an NO donor or a membrane-permeant cGMP analogue; or neurons maintained in the medium from Schwann cell cultures treated in the same way, prevents neuronal apoptosis. Both NO donor and cGMP treatment of Schwann cells results in synthesis of NGF and NT3. Furthermore, if the Schwann cells are previously infected with adenoviral vectors expressing a dominant negative sGC mutant transgene, treatment of these Schwann cells with an NO donor now fails to prevent neuronal apoptosis. Schwann cells treated in this way also fail to express neither cGMP nor neurotrophins. These findings suggest NO-sGC-cGMP-mediated NGF and NT3 synthesis by Schwann cells protect neurons.

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“…Both peroxynitrite and cGMP have been shown to influence ion channel physiology and the subsequent release of neurotransmitters [88,114]. In addition, NO mediates the down-regulation of excitatory amino acid receptors (AMPA and NMDA) via NO cGMP-dependent and -independent (S-nitrosylation) pathways [86,112,[115][116][117][118][119]. The results presented suggest that NO has a dual role in the retina.…”

Section: Involvement Of No/cgmpmentioning

confidence: 99%

“…In addition, NO mediates the down-regulation of excitatory amino acid receptors (AMPA and NMDA) via NO cGMP-dependent and -independent (S-nitrosylation) pathways [86,112,[115][116][117][118][119].…”

Section: No/cgmp Mediates Srif's Neuroprotective Effectsmentioning

confidence: 99%

Somatostatin and Neuroprotection in Retina

Thermos

2011

Hormones in Neurodegeneration, Neuroprotection, and Neurogenesis

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Nitric oxide and S‐nitrosylation: excitotoxic and cell signaling mechanism

Cited by 58 publications

References 30 publications

Protein phosphatases and their potential implications in neuroprotective processes

Protein phosphatases and their potential implications in neuroprotective processes

Glial‐mediated neuroprotection: Evidence for the protective role of the NO‐cGMP pathway via neuron–glial communication in the peripheral nervous system

Somatostatin and Neuroprotection in Retina

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