Development of neuron-specific enolase immunoreactivity in avian nervous tissue in vivo and in vitro

Maxwell, Gerald D.; Whitehead, Mark C.; Connolly, Susan M.; Marangos, Paul J.

doi:10.1016/0165-3806(82)90007-4

Cited by 42 publications

(11 citation statements)

References 34 publications

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“…NSE has been used as a neuronal marker for structural damage and as a marker for neuronal metabolic properties (43). It has also been reported that the expression of NSE coincides with the onset of synaptic connections (44). Therefore, enolase is not only involved in metabolism but also in cell differentiation and normal growth in the brains.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Analysis of Protein Expression and Oxidative Modification in R6/2 Transgenic Mice

Perluigi

Poon

Maragos

et al. 2005

Molecular & Cellular Proteomics

165

145

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Huntington disease (HD) is a hereditary neurodegenerative disorder characterized by motor, psychiatric, and cognitive symptoms. The genetic defect responsible for the onset of the disease, expansion of CAG repeats in exon 1 of the gene that codes for huntingtin on chromosome 4, has been unambiguously identified. On the other hand, the mechanisms by which the mutation causes the disease are not completely understood yet. However, defects in energy metabolism of affected cells may cause oxidative damage, which has been proposed as one of the underlying molecular mechanisms that participate in the etiology of the disease. In our effort to investigate the extent of oxidative damage occurring at the protein level, we used a parallel proteomic approach to identify proteins potentially involved in processes upstream or downstream of the disease-causing huntingtin in a well established HD mouse model (R6/2 transgenic mice). We have demonstrated that the expression levels of dihydrolipoamide S-succinyltransferase and aspartate aminotransferase increase consistently over the course of disease (10-week-old mice). In contrast, pyruvate dehydrogenase expression levels were found to be decreased in 10-week-old HD transgenic mice compared with young (4-week-old) mice. Our experimental approach also led to the identification of oxidatively modified proteins. Six proteins were found to be significantly oxidized in old R6/2 transgenic mice compared with either young transgenic mice or non-transgenic mice. These proteins are ␣-enolase, ␥-enolase (neuron-specific enolase), aconitase, the voltage-dependent anion channel 1, heat shock protein 90, and creatine kinase. Because oxidative damage has proved to play an important role in the pathogenesis and the progression of Huntington disease, our results for the first time identify specific oxidatively modified proteins that potentially contribute to the pathogenesis of Huntington disease.

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Section: Discussionmentioning

confidence: 99%

Proteomic Analysis of Protein Expression and Oxidative Modification in R6/2 Transgenic Mice

Perluigi

Poon

Maragos

et al. 2005

Molecular & Cellular Proteomics

165

145

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“…The ethidium homodimer was added to the medium of both sets of cultures for 1 hr to label cells in each that were dead or dying. Both sets of cultures were then fixed and immunostained with antibodies to NSE to identify postmitotic neurons (Schmechel et al, 1980;Maxwell et al, 1982;Baetge et al, 1990b). For each culture, the total number of cells, the number of neurons, and the number of dying or dead cells were determined (Fig.…”

Section: A Subset Of Neurons That Develop In Response To Nt-3 Becomesmentioning

confidence: 99%

Neurotrophin-3 Is Required for the Survival–Differentiation of Subsets of Developing Enteric Neurons

et al. 2001

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Neurotrophin-3 (NT-3) promotes enteric neuronal development in vitro; nevertheless, an enteric nervous system (ENS) is present in mice lacking NT-3 or TrkC. We thus analyzed the physiological significance of NT-3 in ENS development. Subsets of neurons developing in vitro in response to NT-3 became NT-3 dependent; NT-3 withdrawal led to apoptosis, selectively in TrkC-expressing neurons. Antibodies to NT-3, which blocked the developmental response of enteric crest-derived cells to exogenous NT-3, did not inhibit neuronal development in cultures of isolated crest-derived cells but did so in mixed cultures of crest-and non-neural crest-derived cells; therefore, the endogenous NT-3 that supports enteric neuronal development is probably obtained from noncrest-derived mesenchymal cells. In mature animals, retrograde transport of 125 I-NT-3, injected into the mucosa, labeled neurons in ganglia of the submucosal but not myenteric plexus; injections of 125 I-NT-3 into myenteric ganglia, the tertiary plexus, and muscle, labeled neurons in underlying submucosal and distant myenteric ganglia. The labeling pattern suggests that NT-3-dependent submucosal neurons may be intrinsic primary afferent and/or secretomotor, whereas NT-3-dependent myenteric neurons innervate other myenteric ganglia and/or the longitudinal muscle. Myenteric neurons were increased in number and size in transgenic mice that overexpress NT-3 directed to myenteric ganglia by the promoter for dopamine ␤-hydroxylase. The numbers of neurons were regionally reduced in both plexuses in mice lacking NT-3 or TrkC. A neuropoietic cytokine (CNTF) interacted with NT-3 in vitro, and if applied sequentially, compensated for NT-3 withdrawal. These observations indicate that NT-3 is required for the normal development of the ENS.

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“…It was reported that y-enolase immunoreactivity occurs after at least some dorsal root ganglion cells have both peripheral and central connections (12). Schmechel et al (16) showed that the faintly stained dorsal root ganglion cells in culture do not have spontaneous activity.…”

Section: Peripheral Neuronsmentioning

confidence: 99%

“…This finding is consistent with the rostral-to-caudal gradient in the production of spinal motor neurons studied using thymidine autoradiography and rat embryos (4) . Maxwell et al (12) reported that, in the anterior horn cells at the level of the hind limb of the developing chick embryo, y-enolase immunoreactivity appeared only after functional connections with muscle targets had been made. They hypothesized that the appearance of y-enolase immunostaining cells suggests a certain level of functional maturation of neurons.…”

Section: Motor Neurons In the Basal Plate Of The Neural Tubementioning

confidence: 99%

Development of .GAMMA.-enolase immunoreactive cells in the nervous system of human embryos.

Shinohara

Tanaka

1986

Acta Histochem. Cytochem

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Development of neuron-specific enolase immunoreactivity in avian nervous tissue in vivo and in vitro

Cited by 42 publications

References 34 publications

Proteomic Analysis of Protein Expression and Oxidative Modification in R6/2 Transgenic Mice

Proteomic Analysis of Protein Expression and Oxidative Modification in R6/2 Transgenic Mice

Neurotrophin-3 Is Required for the Survival–Differentiation of Subsets of Developing Enteric Neurons

Development of .GAMMA.-enolase immunoreactive cells in the nervous system of human embryos.

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