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CACNA1A activates sodium atom. 36 / 36
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36
sparser
"Distinctively different with the case observed in Na v 1.2α, BmK AS could move the voltage dependent activation of Na v 1.2 (α + β1) towards depolarization in a linear dose-dependent way ( xref , right, Pre AS): Prominent for 100 nM ( Δ V 1/2 = 6.43 mV, P < 0.001) and 10 nM ( Δ V 1/2 = 6.03 mV, P < 0.005), but less significant for 1 nM ( Δ V 1/2 = 2.05 mV, P < 0.05) ( xref and xref )."
sparser
"While the voltage-dependent activation of Na v 1.5 or Na v 1.7 was not affected by mexiletine and lidocaine, the steady-state fast and slow inactivation of Na v 1.5 and Na v 1.7 were significantly shifted to hyperpolarized direction by either mexiletine or lidocaine in dose-dependent manner."
sparser
"However, patch clamp recordings and Na + imaging studies of the AIS suggest that the density of functional Na + channels, while higher in the AIS than in the soma, may not be as high as suggested from immunohistochemistry, and that the lower threshold for AP initiation results from a hyperpolarized shift in I Na voltage-dependent activation and the presence of I NaP ( xref ; xref ; xref )."
sparser
"We found that: (1) some chemical mediators (e.g., adenosine 5'-triphosphate) produce a reduction or loss of superexcitability together with increased axonal excitability, indicating membrane depolarization; (2) blockade of axonal hyperpolarization-activated (Ih) currents produces an enhancement of superexcitability together with a decreased excitability, indicating membrane hyperpolarization; and (3) application of calcium produces an increase in membrane threshold without an alteration in superexcitability, indicating a non-specific increase in surface charge and a change in the voltage-dependent activation of sodium channels."
sparser
"When electrotonic propagation from the neighboring cells depolarizes the cell membrane to reach the threshold for Na + channel voltage-dependent activation, a large number of channels open giving rise to a huge depolarizing current (∼20–30 nA/pF at peak), which determines the upstroke phase of the AP."
sparser
"xref describes the effects of the β1 subunit on the voltage-dependent activation of Na v 1.6 sodium channels expressed in HEK293 cells. xref shows families of sodium currents, recorded using the indicated pulse protocol, from an individual representative cell expressing rat Na v 1.6 sodium channels and current – voltage plot of the peak transient sodium currents in these traces. xref shows sodium current traces and current – voltage relationships from an individual representative cell expressing Na v 1.6β1 sodium channels. xref shows conductance – voltage plots of data obtained from multiple cells expressing rat Na v 1.6 sodium channels either in the absence or presence of the β1 subunit, and xref summarizes the statistical analysis of these data."
sparser
"Despite the complete removal of inactivation by NBA, the voltage-dependent activation of sodium channels remains unaltered as determined by (a) sodium current turn-on kinetics, (b) sodium tail current kinetics, (c) voltage dependence of steady-state activation, and (d) sensitivity of sodium channels to external calcium concentration."
sparser
"The ionic conductances that are modulated by cholinergic receptor activation were assessed in voltage clamp experiments in the presence of TTX (0.5 µM) and ZD7288 (50 µM) to block voltage-dependent activation of sodium channels and the hyperpolarization-activated current I h , respectively."
sparser
"Together with the electrophysiological findings showing that the intrinsic properties, such as voltage-dependent activation and inactivation of Nav1.8 sodium channels, remained unchanged after the inoculation of tumor cells, the increased expression of Nav1.8 on the cell membrane provides a possible explanation for the enhanced density of Nav1.8- mediated sodium current in the DRG neurons of MRMT-1-treated rats, which actually represents the functional upregulation of Nav1.8 sodium channels in the DRG neurons of bone cancer rats."