ArticleNeurochemical research2006
Increased response to high KCl-induced elevation in the intracellular-Ca(2+) concentration in differentiated NG108-15 cell and the inhibitory effect of the L-type Ca(2+) channel blocker, calciseptine.
Article in Neurochemical research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
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- Zinc regulates a key transcriptional pathway for epileptogenesis via metal-regulatory transcription factor 1.Nature communications · 2015Article
- TRPC1-mediated Ca²⁺ entry is essential for the regulation of hypoxia and nutrient depletion-dependent autophagy.Cell death & disease · 2015Article
- Regulator of G-protein signaling 14 protein modulates Ca²+ influx through Cav1 channels.Neuroreport · 2010Article
- Characteristics for enhanced response of serotonin-evoked ion dynamics in differentiated NG108-15 cells.Neurochemical research · 2009Article
- Enhancement of sodium current in NG108-15 cells during neural differentiation is mainly due to an increase in NaV1.7 expression.Neurochemical research · 2007Article
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6 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Characteristics of the increasing effect for the concentration of intracellular calcium ions ([Ca(2+)](i)) by high-KCl application were investigated in the neuroblastomaxglioma hybrid NG108-15 cell line (NG108-15 cells). The present study confirmed that the increasing effect of [Ca(2+)](i) by high-KCl application in single NG108-15 cells, differentiated with dibutyryl cAMP (Bt(2)cAMP), was significantly enhanced, compared to undifferentiated cells. The following observations were made at first: (1) The response to high-KCl application, in both undifferentiated and differentiated cells, was significantly inhibited by calciseptine (CaS), an L-type Ca(2+) channel blocker, but not by N-, P- and R-type Ca(2+) channel blockers. The IC(50) values for CaS in both undifferentiated and differentiated cell was almost identical. (2) The inhibitory effect of CaS was irreversible. (3) The increasing effect for [Ca(2+)](i) by high-KCl application was completely dependent on the presence of extracellular calcium ions. (4) The increased [Ca(2+)](i) by high-KCl application under a plateau concentration was quickly decreased to basal levels when the high-KCl solution was exchanged for a high-KCl solution containing EGTA (without CaCl(2)). Together, these results suggest that the enhancement of the response effect of [Ca(2+)](i) by high-KCl application in differentiated single NG108-15 cells was mainly due to the quantitative increase of L-type voltage-sensitive calcium channels (VSCCs), which were irreversibly inhibited by CaS.
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