Inducible nitric oxide synthase appears and is co-expressed with the neuronal isoform in interneurons of the rat hippocampus after transient ischemia induced by middle cerebral artery occlusion

Corsani, Letizia; Bizzoco, Elisa; Pedata, Felicita; Gianfriddo, Marco; Faussone–Pellegrini, Maria Simonetta; Vannucchi, Maria Giuliana

doi:10.1016/j.expneurol.2008.02.008

Cited by 20 publications

(18 citation statements)

References 28 publications

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“…NOS1 (nNOS or neuronal NOS) is one of three major isoforms of NO synthase, the others being NOS2 (iNOS or inducible NOS) and NOS3 (eNOS or endothelial NOS). Many cell types in the body can express NOS2, including immune response cells (Hickey, 2001), glial cells (Nomura and Kitamura, 1993) and neurons (Corsani et al, 2008). Unlike NOS1 and NOS3 that are expressed constitutively, NOS2 is induced by inflammatory cytokines (Saha and Pahan, 2006).…”

Section: Molecular Pathways For the Action Of Nomentioning

confidence: 99%

The role of nitric oxide in pre-synaptic plasticity and homeostasis

Hardingham

Dachtler

Fox

2013

Front. Cell. Neurosci.

234

166

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Since the observation that nitric oxide (NO) can act as an intercellular messenger in the brain, the past 25 years have witnessed the steady accumulation of evidence that it acts pre-synaptically at both glutamatergic and GABAergic synapses to alter release-probability in synaptic plasticity. NO does so by acting on the synaptic machinery involved in transmitter release and, in a coordinated fashion, on vesicular recycling mechanisms. In this review, we examine the body of evidence for NO acting as a retrograde factor at synapses, and the evidence from in vivo and in vitro studies that specifically establish NOS1 (neuronal nitric oxide synthase) as the important isoform of NO synthase in this process. The NOS1 isoform is found at two very different locations and at two different spatial scales both in the cortex and hippocampus. On the one hand it is located diffusely in the cytoplasm of a small population of GABAergic neurons and on the other hand the alpha isoform is located discretely at the post-synaptic density (PSD) in spines of pyramidal cells. The present evidence is that the number of NOS1 molecules that exist at the PSD are so low that a spine can only give rise to modest concentrations of NO and therefore only exert a very local action. The NO receptor guanylate cyclase is located both pre- and post-synaptically and this suggests a role for NO in the coordination of local pre- and post-synaptic function during plasticity at individual synapses. Recent evidence shows that NOS1 is also located post-synaptic to GABAergic synapses and plays a pre-synaptic role in GABAergic plasticity as well as glutamatergic plasticity. Studies on the function of NO in plasticity at the cellular level are corroborated by evidence that NO is also involved in experience-dependent plasticity in the cerebral cortex.

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Section: Molecular Pathways For the Action Of Nomentioning

confidence: 99%

The role of nitric oxide in pre-synaptic plasticity and homeostasis

Hardingham

Dachtler

Fox

2013

Front. Cell. Neurosci.

234

166

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“…Several studies have provided increasing evidence that most of the effects of relaxin depend on its ability to modulate the activity and/or gene expression of the various NOS isoforms (6,7,8,27,36). In this regard, numerous reports have demonstrated that the same cell type can express multiple NOS isoforms (45,39,4,13) and, by immunohistochemical and biochemical studies, it has been shown that each isoform has proper subcellular location and a potentially distinct role (24,44,20,25,43,39). However, all NOS share a common effector, e.g., NO, a diffusible gas easily crossing the cell membranes and acting at relatively long distance as an inhibitor of neurotransmission and/or muscle contraction.…”

Section: Discussionmentioning

confidence: 99%

“…The eNOS variants are one full-length and two shorter variants (26). Finally, it has been also demonstrated that the two constitutive NOS can also be induced and the iNOS can be constitutively expressed (4,11,13,39,40).…”

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confidence: 97%

Relaxin exerts two opposite effects on mechanical activity and nitric oxide synthase expression in the mouse colon

Baccari

Traini

Garella

et al. 2012

American Journal of Physiology-Endocrinology and Metabolism

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Baccari MC, Traini C, Garella R, Cipriani G, Vannucchi MG. Relaxin exerts two opposite effects on mechanical activity and nitric oxide synthase expression in the mouse colon. Am J Physiol Endocrinol Metab 303: E1142-E1150, 2012. First published August 28, 2012 doi:10.1152/ajpendo.00260.2012.-The hormone relaxin exerts a variety of functions on the smooth muscle of reproductive and nonreproductive organs, most of which occur through a nitric oxide (NO)-mediated mechanism. In the stomach and ileum, relaxin causes muscle relaxation by modulating the activity and expression of different nitric oxide synthase (NOS) isoforms region-dependently. Nothing is known on the effects of relaxin in the colon, the gut region expressing the highest number of neuronal (n) NOS␤-immunoreactive neurons and mainly involved in motor symptoms of pregnancy and menstrual cycle. Therefore, we studied the effects of relaxin exposure in the mouse proximal colon in vitro evaluating muscle mechanical activity and NOS isoform expression. The functional experiments showed that relaxin decreases muscle tone and increases amplitude of spontaneous contractions; the immunohistochemical results showed that relaxin increases nNOS␤ and endothelial (e) NOS expression in the neurons and decreases nNOS␣ and eNOS expression in the smooth muscle cells (SMC). We hypothesized that, in the colon, relaxin primarily increases the activity and expression of nNOS␤ and eNOS in the neurons, causing a reduction of the muscle tone. The downregulation of nNOS␣ and eNOS expression in the SMC associated with increased muscle contractility could be the consequence of continuous exposue of these cells to the NO of neuronal origin. These findings may help to better understand the physiology of NO in the gastrointestinal tract and the role that the "relaxin-NO" system plays in motor disorders such as functional bowel disease. nitric oxide synthase isoforms; nitric oxide synthase splice variants; immunohistochemistry; mechanical responses RELAXIN, a 6,000 Da hormone peptide mainly produced by the corpus luteum, has been shown to exert a variety of physiological effects on the smooth muscle of reproductive and nonreproductive organs, most of which occur through a nitric oxide (NO)-mediated mechanism (1,12,17,33). The latter effects can be direct on the smooth muscle cells (SMC) or mediated by the endothelial cells (2,12,17,30,36). In the gastrointestinal tract, relaxin has been shown to cause depression of muscle contractility by modulating the activity and expression of the different nitric oxide synthase (NOS) isoforms (8,3,4,40). Interestingly, the depression of muscle contractility reported in the mouse stomach and ileum was mediated by different NOS isoforms. While in the stomach relaxin induced an increase in both the constitutive NOS isoforms, i.e., neuronal (n) NOS and endothelial (e) NOS (3, 40), in the ileum it increased the expression of eNOS and of inducible (i) NOS isoforms (8, 4). In summary, relaxin is able to act on different NOS isoforms depending on the gut...

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“…microglial cells) [33]. There is also evidence that cells other than inflammatory cells can produce iNOS following exposure to ischemia [34]. In addition, minocycline was reported to inhibit the transcription of the p38 mitogen activated protein kinase cascade (MAPK).…”

Section: Anti-inflammatory Effectsmentioning

confidence: 99%

The Role of Minocycline in Ischemia-Reperfusion Injury: A Comprehensive Review of an Old Drug with New Implications

Ulgen¹,

Field²,

Qureshi³

et al. 2011

PRC

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Minocycline is a semi-synthetic tetracycline that inhibits bacterial protein synthesis and hence is used for the treatment of many infectious diseases. Over the years, many other interesting properties of minocycline have been identified and been used to make patents which include anti-inflammatory, anti-apoptotic, matrix metalloproteinase inhibitor and free oxygen radical scavenger activity. Ischemia-reperfusion injury is a concern for almost every clinical specialty and minocycline seems to be an attractive cytoprotective agent that can ameliorate the damage due to these properties. Ischemia-reperfusion injury is a complex process and involves various pathways that lead to cell death. This review focuses on the body of evidence describing various proposed mechanisms of action of minocycline and its current experimental use in various animal models of ischemia-reperfusion injury.

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Inducible nitric oxide synthase appears and is co-expressed with the neuronal isoform in interneurons of the rat hippocampus after transient ischemia induced by middle cerebral artery occlusion

Cited by 20 publications

References 28 publications

The role of nitric oxide in pre-synaptic plasticity and homeostasis

The role of nitric oxide in pre-synaptic plasticity and homeostasis

Relaxin exerts two opposite effects on mechanical activity and nitric oxide synthase expression in the mouse colon

The Role of Minocycline in Ischemia-Reperfusion Injury: A Comprehensive Review of an Old Drug with New Implications

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