Sentence examples for membrane depolarization increases from inspiring English sources

Individual types of SPM were exposed to human, immortalized bronchial-tracheal epithelial cells (i.e. BEAS-2B) and endpoints of biological activation (i.e. membrane depolarization, increases in intracellular calcium (i.e. [Ca2+]i) levels, IL-6 release) were measured.

According to our model, membrane depolarization increases the probability of CaV1.2 sparklet occurrence.

Membrane depolarization increases ciliary [Ca2+], but only marginally alters cilia beating and cilia-driven fluid velocity within short (~1 min) time frames.

Excitation of the ependymal cell by membrane depolarization increases ciliary [Ca2+] with only minor changes in motility and fluid movement, suggesting that beating of ependymal motile cilia is not significantly regulated by the activity of ciliary or cytoplasmic CaV channels.

Mitochondria are crucial to intracellular Ca2+ homeostasis and accumulation of Ca2+ induced by excitotoxic insults leads to mitochondrial membrane depolarization, increased production of oxygen free radicals and caspase-dependent or -independent oligodendrocyte death.

Using Drosophila and mouse models, we show here that an early effect of PINK1 deficiency is the disruption of Complex I function, which results in mitochondrial membrane depolarization, increased sensitivity to apoptotic stress and synaptic transmission deficits in Drosophila neurons.

We observed an increase (15 ± 5%; P ≤ 0.05) in mitochondrial membrane depolarization (increased ratio of green to red fluorescence) in the AR-65Q cells compared to AR-24Q cells (Fig.  3A) and a 38 ± 3% (P ≤ 0.05) increase in the PC12 cells expressing mutant AR (Fig.  3B).

Under normal conditions, Ca2+ influx elicited by brief membrane depolarizations increases [Ca2+]i to high levels within discrete microdomains and triggers the exocytosis of closely associated insulin granules.

We show that membrane depolarizations increased BK channel activity in LNCaP cells expressing Cav3.2 T-type Ca2+ channels.

Moreover we found that membrane depolarization, which increases the driving force for Cl− in the inward direction, has a strongly depressive effect on EPSP amplitude (Figure 1A, C; the mean reversal potential of mixed PSPs was −62.03±1.37 mV, n = 22).

Although BK channels in IHCs appear to gate independently of intracellular [Ca2+] [25], it is possible that BK channels expressed in OHCs may be more similar to the BK channels found in other cells, which are synergistically activated by membrane depolarization and increases in intracellular [Ca2+] [30].