The effects of ruthenium red, dantrolene and nimodipine, alone or in combination, in NMDA induced neurotoxicity of cerebellar granular cell culture of rats

Düzenli, Selma; Bakuridze, K; Gepdíremen, Akçahan

doi:10.1016/j.tiv.2005.03.007

Cited by 24 publications

(11 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These observations may explain why nimodipine action is only observed at higher concentrations in this ( fig. 8 E) and related studies [Koh and Cotman, 1992;Moulder et al, 2002;Duzenli et al, 2005]. Nevertheless, the dramatic loss in neuronal viability at these higher concentrations suggests that a threshold has to be achieved below which toxicity is not apparent.…”

Section: Direct Exposure Of Neurons To Calcium-reducing Agents Promotmentioning

confidence: 85%

Widespread Neonatal Brain Damage following Calcium Channel Blockade

et al. 2006

View full text Add to dashboard Cite

An abundance of evidence exists that shows calcium channel blockade promotes injury in cultured neurons. However, few studies have addressed the in vivo toxicity of such agents. We now show that the L-type calcium channel antagonist nimodipine promotes widespread and robust injury throughout the neonatal rat brain, in an age-dependent manner. Using both isolated neuronal as well as brain slice approaches, we address mechanisms behind such injury. These expanded studies show a consistent pattern of injury using a variety of agents that lower intracellular calcium. Collectively, these observations indicate that postnatal brain development represents a transitional period for still developing neurons, from being highly sensitive to reductions in intracellular calcium to being less vulnerable to such changes. These observations directly relate to current therapeutic strategies targeting neonatal brain injury.

show abstract

Section: Direct Exposure Of Neurons To Calcium-reducing Agents Promotmentioning

confidence: 85%

Widespread Neonatal Brain Damage following Calcium Channel Blockade

et al. 2006

View full text Add to dashboard Cite

show abstract

“…To date, much effort has been put on the understanding of the neuroprotective effect of nimodipine on oxygen-glucose deprivation (OGD)-induced [16,24], bilirubin-induced [25] or NMDA-induced [26] cell death. The neuroprotective capability of nimodipine was also analyzed previously regarding inflammation-mediated degeneration of neurons and showed significantly better results for nimodipine-treated compared with non-treated cell cultures [27].…”

Section: Discussionmentioning

confidence: 99%

Investigation of the Neuroprotective Impact of Nimodipine on Neuro2a Cells by Means of a Surgery-Like Stress Model

Herzfeld

Strauß

Simmermacher

et al. 2014

IJMS

View full text Add to dashboard Cite

Nimodipine is well characterized for the management of SAH (subarachnoid hemorrhage) and has been shown to promote a better outcome and less DIND (delayed ischemic neurological deficits). In rat experiments, enhanced axonal sprouting and higher survival of motoneurons was demonstrated after cutting or crushing the facial nerve by nimodipine. These results were confirmed in clinical trials following vestibular Schwannoma surgery. The mechanism of the protective competence of nimodipine is unknown. Therefore, in this study, we established an in vitro model to examine the survival of Neuro2a cells after different stress stimuli occurring during surgery with or without nimodipine. Nimodipine significantly decreased ethanol-induced cell death of cells up to approximately 9% in all tested concentrations. Heat-induced cell death was diminished by approximately 2.5% by nimodipine. Cell death induced by mechanical treatment was reduced up to 15% by nimodipine. Our findings indicate that nimodipine rescues Neuro2a cells faintly, but significantly, from ethanol-, heat- and mechanically-induced cell death to different extents in a dosage-dependent manner. This model seems suitable for further investigation of the molecular mechanisms involved in the neuroprotective signal pathways influenced by nimodipine.

show abstract

“…influx, mitochondrial dysfunction, overproduction of NO and oxidative stress in cultured glial cells [169] Lacidipine Reduced infarction size before or after ischemic injury [170] Neurol Sci (2012) 33:223-237 231 usefulness. The need for very early administration and the dose-dependent neurobehavioral toxicity in humans limit their usefulness [173].…”

Section: Drugs Inhibiting Glutamate-induced Cell Injurymentioning

confidence: 99%

The role of glutamate in neuronal ischemic injury: the role of spark in fire

2011

View full text Add to dashboard Cite

Although being a physiologically important excitatory neurotransmitter, glutamate plays a pivotal role in various neurological disorders including ischemic neurological diseases. Its level is increased during cerebral ischemia with excessive neurological stimulation causing the glutamate-induced neuronal toxicity, excitotoxicity, and this is considered the triggering spark in the ischemic neuronal damage. The glutamatergic stimulation will lead to rise in the intracellular sodium and calcium, and the elevated intracellular calcium will lead to mitochondrial dysfunction, activation of proteases, accumulation of reactive oxygen species and release of nitric oxide. Interruption of the cascades of glutamate-induced cell death during ischemia may provide a way to prevent, or at least reduce, the ischemic damage. Various therapeutic options are suggested interrupting the glutamatergic pathways, e.g., inhibiting the glutamate synthesis or release, increasing its clearance, blocking of its receptors or preventing the rise in intracellular calcium. Development of these strategies may provide future treatment options in the management of ischemic stroke.

show abstract

The effects of ruthenium red, dantrolene and nimodipine, alone or in combination, in NMDA induced neurotoxicity of cerebellar granular cell culture of rats

Cited by 24 publications

References 30 publications

Widespread Neonatal Brain Damage following Calcium Channel Blockade

Widespread Neonatal Brain Damage following Calcium Channel Blockade

Investigation of the Neuroprotective Impact of Nimodipine on Neuro2a Cells by Means of a Surgery-Like Stress Model

The role of glutamate in neuronal ischemic injury: the role of spark in fire

Contact Info

Product

Resources

About