Journals / Turkish Journal of Medical Sciences / 2000 / Cilt: 30 - Sayı: 3

Nimodipine Aggravates Systemic Kainic Acid Toxicity in Retinal Ganglion Cells of Intact Mice

Pages
213–217
Publication Date
2022-11-05
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Blocking of calcium channels may lead to the rebound activation of sodium channels or stimulate the release of intracellular calcium by activating ryanodine sensitive calcium channels.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:The aim of the present study was to investigate the role of the L-type voltage dependent Ca2+ channel blocker, nimodipine, in kainate induced toxicity in retinal ganglion cells of mice.
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Key Findings & Data:Kainate in 10mg/kg was administered intraperitoneally following the vehicle or nimodipine.
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Conclusion & Impact:Blocking of calcium channels may lead to the rebound activation of sodium channels or stimulate the release of intracellular calcium by activating ryanodine sensitive calcium channels.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Kainate · retina · nimodipine

Abstract

The aim of the present study was to investigate the role of the L-type voltage dependent Ca2+ channel blocker, nimodipine, in kainate induced toxicity in retinal ganglion cells of mice. Kainate in 10mg/kg was administered intraperitoneally following the vehicle or nimodipine. Nimodipine, 45 minutes prior to kainate in 10, 15, 25, 50, 100 and 250 mg/kg doses was administered intraperitoneally. Surprisingly, nimodipine potentiated the ganglional cell death induced by kainate, with respect to the control and kainate+vehicle treated group. In accordance with our results, blockage of L-type calcium channels by nimodipine may worsen the prognosis and survival of retinal neurons in kainate receptor stimulated toxicity. Blocking of calcium channels may lead to the rebound activation of sodium channels or stimulate the release of intracellular calcium by activating ryanodine sensitive calcium channels.

Özet

The aim of the present study was to investigate the role of the L-type voltage dependent Ca2+ channel blocker, nimodipine, in kainate induced toxicity in retinal ganglion cells of mice. Kainate in 10mg/kg was administered intraperitoneally following the vehicle or nimodipine. Nimodipine, 45 minutes prior to kainate in 10, 15, 25, 50, 100 and 250 mg/kg doses was administered intraperitoneally. Surprisingly, nimodipine potentiated the ganglional cell death induced by kainate, with respect to the control and kainate+vehicle treated group. In accordance with our results, blockage of L-type calcium channels by nimodipine may worsen the prognosis and survival of retinal neurons in kainate receptor stimulated toxicity. Blocking of calcium channels may lead to the rebound activation of sodium channels or stimulate the release of intracellular calcium by activating ryanodine sensitive calcium channels.

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Cite This Article

GEPDİREMEN, A., GÜNDOĞDU, C., KOÇER, İ., KAYA, M. (2022). Nimodipine Aggravates Systemic Kainic Acid Toxicity in Retinal Ganglion Cells of Intact Mice. Turkish Journal of Medical Sciences, Cilt: 30 - Sayı: 3, 213–217. https://ajindex.com/articles/612403

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