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Calcium influx through multiple types of VDCCs was involved in the electrical stimulation-induced inhibition.
Current influx through all channel subtypes exhibited an activity-dependent depression.
Our findings demonstrate that simulated weightlessness induces Ca2+ influx through stretch-activated channels, then results in microfilament disruption.
Calcium influx through voltage-dependent Ca2+ channels is critical for many neuronal processes required for learning and memory.
Ca2+ mobilization by Ca2+ influx through voltage-dependent Ca2+ channels is involved in this heterologous desensitization of β-adrenoceptors.
Further, there is likely an appropriate range of calcium influx through VDCC which ensures effective axonal membrane resealing.
We measure calcium influx through specific isoforms and measure cell capacitance as an index of granule fusion.
Therefore, neuronal death induced during glycolysis inhibition involves calcium influx through NMDA receptors and calcium release from intracellular ER stores [17, 24].
These drugs inhibit calcium influx through voltage-sensitive L-type calcium channels in vascular smooth muscle cells inducing arteriolar vasodilation and reducing SVR.
Together with above results, our data suggest that ethanol increases basal [Ca2+]i, but it also inhibits the extracellular Ca2+ influx through VDCC and ionophore channel.
However, the differential role of calcium influx through the injury site and through voltage dependent calcium channels (VDCC) has not been examined in detail.
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