Role of Cav2.1 Channel Signaling in Glutamate-Related Brain Injury

Kim, Tae Yeon; Niimi, Kimie; Takahashi, Eiki

doi:10.4172/2168-975x.1000226

Cited by 1 publication

(2 citation statements)

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“…Numerous studies highlight the important role of VGCC blockers to treat glutamate excitotoxicity (Godoy et al, 2021;Higley & Sabatini, 2012;Kim et al, 2016;Zyśk et al, 2018). In the light of the results summarized in the literature, N-type blockers are known to have protective effects toxicity of NMDAR-mediated Ca 2+ entry (Kimura et al, 1999;Vallazza-Deschamps et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Ca 2+ homeostasis is essential for the survival of neurons, on the other hand increased intracellular Ca 2+ concentration disrupts calcium homeostasis, and free oxygen radicals formation which could degenerate neurons and synaptic loss (Godoy et al, 2021) (5). For this reason, blocking excitotoxicity through inhibition of VGCC activity in neurons are an especially appealing point for neuroprotection (Godoy et al, 2021;Higley & Sabatini, 2012;Kim et al, 2016). By contrast to neuroprotective effects of P/Q-type and N-type calcium channel blockers, there is a gap for L-type calcium channels blockers in relation to glutamate excitotoxicity (Vallazza-Deschamps et al, 2005;Wheeler et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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The Difference Between The Response To Glutamate Excitotoxicity and The Role Of Ca2+ Channel Blockers in Cortical Neuron and SH-SY5Y Cells Cultures

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et al. 2022

Journal of Anatolian Environmental and Animal Sciences

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Cortical neuron and SH-SY5Y cells are widely used in glutamate excitotoxicity studies, but it is unclear which one better reflects this model. Generally, glutamate induces toxicity conditions by leading to L and L/N-Ca 2+ channels activation and cell death via lethal Ca 2+ influx. To evaluate this hypothesis, the effects of L and L/N-Ca 2+ channel blockers, lacidipine, and amlodipine under excitotoxic conditions were evaluated. At the same time, in this study, we aimed to determine that these two cell lines better reflect this model. To induce excitotoxicity, cortical neuron and SH-SY5Y cells were incubated with glutamate 10 -5 mM. After 30 min incubation with glutamate, agents of different concentrations (1, 2, and 4 µg lacidipine and 20, 50, and 100 µM amlodipine) were applied to these cells. Possible neuroprotective roles of lacidipine and amlodipine were investigated through cell viability, oxidative stress, and apoptotic alterations. Our results showed that SH-SY5Y cells are the more ideal cell line for oxidative stress-mediated glutamate toxicity. Although 4 µg lacidipine and 100 µM amlodipine have important neuroprotective roles in these cells, the most protective effect was also detected in SH-SY5Y cells at 100 µM amlodipine concentration. The highest viability rate on cell lines was found at 88.8 % in SH-SY5Y cells treated with 100 μM amlodipine. Results from the TAC, TOS, LDH assays, and flow cytometry analysis were correlated to our MTT results. Taken together, our results indicate that SH-SY5Y cells are more effective at reflecting glutamate-induced excitotoxicity and 100μM amlodipine has a more protective effect in treating this toxicity.

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