[20] Techniques in the tissue culture of rat sympathetic neurons

Johnson, Mary I.; Argiro, Vincent

doi:10.1016/s0076-6879(83)03022-0

Cited by 86 publications

(55 citation statements)

References 18 publications

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“…Cultures of sympathetic neurons from the superior cervical ganglia (SCG) were prepared based on the protocol described in Johnson and Argiro (1983). Briefly, SCG were dissected from postnatal day (P)-1 Sprague-Dawley rats (Harlan, Indianapolis, IN) into L15 medium.…”

Section: Methodsmentioning

confidence: 99%

Mixed-Lineage Kinase Inhibitors Require the Activation of Trk Receptors to Maintain Long-Term Neuronal Trophism and Survival

Wang

Paden

Johnson

2004

J Pharmacol Exp Ther

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Section: Methodsmentioning

confidence: 99%

Mixed-Lineage Kinase Inhibitors Require the Activation of Trk Receptors to Maintain Long-Term Neuronal Trophism and Survival

Wang

Paden

Johnson

2004

J Pharmacol Exp Ther

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“…[71][72][73] Briefly, SCGs were dissected from newborn animals and incubated for 30 min each with 1 mg/ml collagenase and 2.5 mg/ml trypsin at 371C. The ganglia were dissociated by triturating through a 200-ml micropipet tip; cells were plated on collagen-coated plastic tissue culture plates at the appropriate densities.…”

Section: Neuronal Culturementioning

confidence: 99%

Cytosine arabinoside rapidly activates Bax-dependent apoptosis and a delayed Bax-independent death pathway in sympathetic neurons

Besirli

Deckwerth²,

Crowder

et al. 2003

Cell Death Differ

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Cytosine arabinoside (ara-C) is a nucleoside analog used in the treatment of hematologic malignancies. One of the major side effects of ara-C chemotherapy is neurotoxicity. In this study, we have further characterized the cell death induced by ara-C in sympathetic neurons. Similar to neurons undergoing trophic factor deprivation-induced apoptosis, ara-C-exposed neurons became hypometabolic before death and upregulated c-myb, c-fos, and Bim. Bax deletion delayed, but did not prevent, ara-C toxicity. Neurons died by apoptosis, indicated by the release of mitochondrial cytochrome-c and caspase-3 activation. p53-deficient neurons demonstrated decreased sensitivity to ara-C, but neither p53 nor multiple p53-regulated genes were induced. Mature neurons showed increased ara-C resistance. These results demonstrate that molecular mechanisms underlying ara-C-induced death are similar to those responsible for trophic factor deprivation-induced apoptosis. However, substantial differences in neuronal death after these two distinct stress stimuli exist since ara-C toxicity, unlike the developmental death, can proceed in the absence of Bax.

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“…65 Briefly, the dissected ganglia were treated with collagenase (1 mg/ml), then trypsin (2.5 mg/ ml) for 30 min each at 378C. The ganglia were triturated and the dissociated cells were plated on collagen-coated dishes in NGFcontaining medium (AM50); NGF was purchased from Harlan (Indianapolis, IN, USA).…”

Section: Sympathetic Neuronal Cultures and Mediamentioning

confidence: 99%

Staurosporine-induced neuronal death: multiple mechanisms and methodological implications

Deshmukh

Johnson

2000

Cell Death Differ

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To examine whether multiple pathways of cell death exist in sympathetic neurons, we studied the cell death pathway induced by staurosporine (STS) in sympathetic neurons and compared it with the well-characterized NGF deprivationinduceddeathpathway.IncreasingconcentrationsofSTSwere found to induce sympathetic neuronal death with different biochemical and morphological characteristics. One hundred nM STS induced metabolic changes, loss of cytochrome c, and caspase-dependent morphological degeneration which closely resembled the apoptotic death induced by NGF deprivation. In contrast, sympathetic neurons treated with 1 mM STS showed no loss of cytochrome c but exhibited extensive, caspase-independent, chromatin changes that were not TUNEL positive. One mM STS-treated sympathetic neurons had greatly reduced metabolic activities and became committed to die rapidly, yet maintained soma structure and appeared viable by other criteria even up to 48 h after STS treatment, illustrating the need to assess cell death by multiple criteria. Lastly, in contrast to the cell death-inducing activities of 100 nM STS or 1 mM STS, very low concentrations of STS (1 nM STS) inhibited sympathetic neuronal death by acting either at or prior to c-jun phosphorylation in the NGF deprivation-induced PCD pathway. Cell Death and Differentiation (2000) 7, 250 ± 261.

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[20] Techniques in the tissue culture of rat sympathetic neurons

Cited by 86 publications

References 18 publications

Mixed-Lineage Kinase Inhibitors Require the Activation of Trk Receptors to Maintain Long-Term Neuronal Trophism and Survival

Mixed-Lineage Kinase Inhibitors Require the Activation of Trk Receptors to Maintain Long-Term Neuronal Trophism and Survival

Cytosine arabinoside rapidly activates Bax-dependent apoptosis and a delayed Bax-independent death pathway in sympathetic neurons

Staurosporine-induced neuronal death: multiple mechanisms and methodological implications

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