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1  in long shut times and a robust increase in mean open time.
2 nel probability, while exerting no effect on mean open time.
3 ity of channel opening and increased channel mean open time.
4 y a single exponential, showed a decrease in mean open time.
5 L receptors had impaired gating with shorter mean open time.
6 nce markedly increases the small conductance mean open time.
7  longest closed time constant, so increasing mean open time.
8 e-channel conductance, reversal potential or mean open time.
9 hange in conductance, reversal potential, or mean open time.
10 , and a smaller increase in opening rate and mean open time.
11 ift could be accounted for by the changes in mean open time.
12 ly lower open probability (NP(o)) and longer mean open time.
13 el conductance but instead increased channel mean open time.
14 icant effect on unitary current amplitude or mean open time.
15 s (<6 mM) increased the open probability and mean open time.
16 osed time without significant changes in the mean open time.
17 bility of the receptor with no change in the mean open time.
18  in this range for dSlo had little effect on mean open time.
19 or 3000 microM then typically increased dSlo mean open time.
20 annel activity by increasing the duration of mean open times.
21 rease in mean closed times and a decrease in mean open times.
22                The F1304Q mutation increased mean open time (1.7 fold at -20 mV) and reduced the prob
23 % decrease in open probability by decreasing mean open time 2.5-fold and by increasing mean closed ti
24                                              Mean open time and burst duration were decreased in the
25                                              Mean open time and conductance of single channels in GIR
26                                         Both mean open time and desensitization were dependent primar
27  conductance was caused by decreased channel mean open time and increased channel mean closed time.
28 mine inhibited the channel by decreasing the mean open time and introducing transitions to a long clo
29  300 microM PB had similar main conductance, mean open time and mean burst duration as those activate
30 P increased reversibly the open probability, mean open time and mean burst duration of 4-AP-sensitive
31 II or protein kinase C activity, reduced the mean open time and mean open probability of 115 +/- 6 pS
32 x-2 treatment was found to increase both the mean open time and open probability of NMDA receptors.
33                            DCS increased the mean open time and open probability of NR1/NR2C receptor
34 ir influence, at least in part, by enhancing mean open time and single-channel conductance.
35       Block manifested as a reduction in the mean open time and the emergence of a closed state, with
36 eased P(open) at a given voltage, increasing mean open time and the number of openings per burst.
37 lpha6(R46W)beta2delta single-channel current mean open times and burst durations were reduced.
38  were characterized by drastically elongated mean open times and distinctly slower time constants of
39 ro M Ca(2+) by decreasing channel events and mean open times and increasing mean close times.
40 ed maximal open probability, and a shortened mean open-time and prolonged mean closed-time durations.
41 markedly increased apparent desensitization, mean open time, and peak current density.
42 reducing open probability (P(o)), shortening mean open time, and prolonging mean closed time.
43 rance of the residual state, increase in the mean open time, and slowing of the transition times betw
44                                  The overall mean open time at +60 mV was approximately 4 ms, compare
45 state probability of hemichannel opening and mean open times at negative potentials, was observed in
46 e in Popen (39 +/- 9 %; n = 5) by decreasing mean open time, burst length and total open time per bur
47 ctly phosphorylated PC2, which increased the mean open time but not the single channel conductance of
48 es the activation threshold and shortens the mean open time but unexpectedly leads to a complete loss
49                                CaM decreased mean open times but increased channel events, without si
50 dependent closings of channels after a given mean open time, but we found no correlation of terminati
51 e channel open probability by 9-fold and the mean open time by 12-fold.
52 rom dwell time histograms, but increased the mean open time by affecting the channel open probability
53 es that SP acts through reduction of channel mean open-time (cmot): GABA(A) cmot being reduced by app
54 gating kinetics of RyR1 channels, increasing mean open time, decreasing mean closed time, and thereby
55                                          The mean open times determined in selected mutants could be
56                                          The mean open time directly measured from 43 GABA-induced ch
57 robability of opening increased 4-fold while mean open time doubled.
58 of alpha1beta2 receptor channels by reducing mean open time due to a reduction in the proportion of l
59 lar to steroids, BI-2 acts by prolonging the mean open time duration through an effect on the duratio
60  and that binding of Gbetagamma prolongs its mean open time duration.
61            In global terms, PB increased the mean open time for events in clusters, without changing
62 -attached patch recordings revealed that the mean open time for single Cl- channels in response to 2
63                                          The mean open time for the 38 pS state (0.74 +/- 0.07 ms) wa
64  channels, 100 microM disopyramide decreased mean open time from 1.64 +/- 0.08 to 0.34 +/- 0.04 msec.
65                  Epo (2 U/mL) increased both mean open time (from 4.27 +/- 0.75 to 11.15 +/- 1.80 ms)
66 ts exhibited two conductances, each with two mean open times (gamma1 = 17 pS, tau1 = 3.7 msec, and ta
67                                          The mean open time in the presence of 100 microM picrotoxin
68 aracterized by extremely slow kinetics, with mean open times in the range of seconds.
69 the InsP3R/Ca2+ channel open probability and mean open time increased significantly.
70 obability increased by approximately 20% and mean open times increased by approximately 4 ms, compare
71 2+) in the range of 5 to 30 microM increases mean open time, increasing Cai2+ in this range for dSlo
72  shortened mean closed time without changing mean open time, indicating closed-channel destabilizatio
73 sed with transmembrane potential, making the mean open time moderately voltage dependent (tau(open) c
74 have two open-time populations with the same mean open times (MOTs).
75 t 50 mus in physiological conditions, with a mean open time of 0.5 ms.
76 h a mean chord conductance of 32 +/- 6 pS, a mean open time of 1.0 +/- 0.3 ms and a mean burst length
77 spectral density distribution gave a channel mean open time of 12.7+/-1.5 ms, range 6.37-23.42 ms.
78  mV with a reversal potential around 0 mV, a mean open time of 2.6 +/- 0.2 ms and a mean burst length
79 2+) reduces the frequency of opening and the mean open time of alpha7 nAChR channels, these data sugg
80             PNU-120596 increased the channel mean open time of alpha7 nAChRs but had no effect on ion
81 s resistance of the recording (R(A)) and the mean open time of AMPA channels.
82 10 microM PhTX-343 significantly reduced the mean open time of channel openings evoked by 1 microM AC
83 t caused only a small decrease (7.5%) in the mean open time of channel openings induced by 1 microM A
84                    Moreover, RXP-E increased mean open time of Cx43 channels.
85 7.4), but not pH 7.9, ifenprodil reduces the mean open time of GluN1/GluN2B receptors, which may be r
86 aesthetics either increased or decreased the mean open time of K+-selective ion channels without alte
87                                          The mean open time of KirNB channels (1.1 ms) was almost the
88                                 The apparent mean open time of NR1/NR2C receptors was brief (0.52 +/-
89  a weak correlation between ethanol IC50 and mean open time of NR2A(Met823) mutants that was dependen
90                  All three drugs reduced the mean open time of single channels and increased the prob
91 a voltage-independent manner and reduced the mean open time of single channels without affecting thei
92 el recordings revealed that NEFA reduces the mean open time of single NMDA-activated channels in a co
93 -trans-14,15-EETA (1-3 x 10(-6) m) increased mean open time of small conductance K(+) channels (13-14
94                 No significant change in the mean open time of subconductance states was observed wit
95      Picrotoxinin and picrotin decreased the mean open time of the channel in a concentration-depende
96 e channel kinetic analyses revealed that the mean open time of the channel increased monotonically wi
97                                          The mean open time of the channel was quite long, with a ran
98 t significantly affecting the conductance or mean open time of the channel.
99 showed a clear positive correlation with the mean open time of the channel.
100                                              Mean open time of the dominant kinetic component decreas
101  or decrease the rate of desensitization and mean open time of the ion channel.
102 cy of LCC reopening, and a slower decline in mean open time of the LCC.
103  unitary conductance, reversal potential and mean open time of the single-channel currents were simil
104 rtant regulatory mechanism that shortens the mean open time of these otherwise long-lasting high-volt
105 nce of the two channels was similar, but the mean open time of unitary events was shorter for express
106 le-exponential open-time distributions, with mean open times of 279 +/- 58 ms (n = 4) for IRK1 and 23
107  of open-time duration and the dependence of mean open time on [Ca2+] are explained by populations of
108 dent increase in both open probabilities and mean open times on KcsA in artificial bilayers.
109 g channel opening frequency without altering mean open time or EC(50) values for glutamate or glycine
110 n kinetics of mu 1-F1304Q but did not modify mean open time or fast-inactivation kinetics.
111 ers of single channel activity (conductance, mean open time or frequency of opening).
112 e-out patches without significantly changing mean open time or single-channel conductance, suggesting
113 he Na+ single channel current amplitude, the mean open time or the mean closed time, but increased th
114 th no change in unitary conductance, channel mean open times or burst durations.
115 lved from the open period distributions with mean open times reduced 5-fold by the weakest partial ag
116 F1651A and N1662A mutants also had increased mean open times relative to WT, indicating a slowed rate
117 as calmodulin binding reduced single channel mean open time, resulting in an overall reduction in P(o
118 s, pore size, single channel conductance and mean open time suggest that the rho1 homomeric receptor
119 2 mean closed time without changing the RyR2 mean open time, suggesting that ent-verticilide function
120                                              Mean open time (tau(o)) and mean closed time (tau(c)), o
121 tamoxifen shortens both mean closed time and mean open time; the latter is probably due to an interme
122  demonstrated that PS primarily affected the mean open time to produce its effects: positive modulati
123 pressed with CFTR exhibited decreased Po and mean open time under conditions optimal for PKA-mediated
124  channel open probability, with no change in mean open time, unitary conductance, or reversal potenti
125 ised from Xenopus oocytes, with no change in mean open time, unitary conductance, or reversal potenti
126                                          The mean open times varied from cell to cell, possibly owing
127                                          The mean open time was >11-fold longer for a channel mutagen
128 -40 mV and 68 picosiemens at +40 mV, and the mean open time was 0.9 ms at -40 mV.
129                                          The mean open time was 2.70 +/- 0.95 ms (range, 1.24-4.78 ms
130                                              Mean open time was 3.2 ms and closed times were 1.0 and
131                         Single Na(+) channel mean open time was longer in ankyrin(B)(-/-) versus WT a
132 re particularly brief in WT-Y145V, where the mean open time was reduced from 102 ms at -120 mV in wil
133               In single-channel experiments, mean open time was unaltered and unitary current was onl
134                 From the abbreviation of the mean open times, we estimated association rates of appro
135     At positive potentials Po and the longer mean open time were greatly increased.
136 d wild-type CFTR ion channels have identical mean open times when activated by different nucleotide l
137 ase with increased open probability (Po) and mean open time, whereas ENaC co-expressed with CFTR exhi
138  -30 mV and lengthened the longer of the two mean open times without significant effects on other kin

 
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