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1  generated upon repolarization after a large depolarizing pulse.
2 d cells remained unattenuated throughout the depolarizing pulse.
3 e same time course as the current during the depolarizing pulse.
4 does not inactivate appreciably during short depolarizing pulses.
5 50 ms pulses, with significant resistance to depolarizing pulses.
6 comparable with that triggered by a train of depolarizing pulses.
7  PGN fired on average only 1.4 spikes during depolarizing pulses.
8 e sustained Na+ currents at the end of 30-ms depolarizing pulses.
9 ivation that channels rapidly undergo during depolarizing pulses.
10 onship identical to that obtained for single depolarizing pulses.
11 ted patch mode and stimulated with trains of depolarizing pulses.
12  cells of Ca(2+) alternans produced by small depolarizing pulses.
13  monitor exocytosis in response to trains of depolarizing pulses.
14  in the releasable pool) was not affected by depolarizing pulses.
15 ancy between the currents during the initial depolarizing pulse and the tail current.
16 stsynaptic currents, pattern of discharge to depolarizing pulses and current-voltage relationships.
17 lar free Ca2+ in turtle hair cells evoked by depolarizing pulses and has delineated factors affecting
18 col, uses currents during a moderately large depolarizing pulse, and the other uses tail currents aft
19                              For short 20 ms depolarizing pulses, and interpulse intervals between 15
20 change in fluorescence can faithfully report depolarizing pulses as short as 2 ms.
21 cilitation was observed even during a single depolarizing pulse, as confirmed by two-pulse experiment
22                            Using long (20 s) depolarizing pulses both gating modes were activated, an
23  single channels open only once or twice per depolarizing pulse, but in the slow mode the channels de
24 ed in smaller exocytotic responses to single depolarizing pulses, but the normal relationship between
25 ail currents depended on the duration of the depolarizing pulse, consistent with a rise in intracellu
26 - 0.004 nA); (iv) firing of APs throughout a depolarizing pulse (duration <= 1 s) and one to four APs
27          In the presence of 4-aminopyridine, depolarizing pulses evoked transient outward currents an
28     Single step depolarizations or trains of depolarizing pulses evoked voltage-dependent, inward Ca2
29 mediating DAPs (IDAP), evoked by three brief depolarizing pulses, had a peak of 17 +/- 1 pA (mean +/-
30   Exocytotic events occur principally during depolarizing pulses, i.e., events are "stimulus-coupled"
31  activation time constant (tau(act))] during depolarizing pulses; (iii) slower deactivation [larger d
32 current was induced progressively after each depolarizing pulse in a train of stimuli, and this Na+ c
33  mode was maintained for the duration of the depolarizing pulse in the presence of the beta2a subunit
34  the subthreshold dynamics using optogenetic depolarizing pulses in hippocampal neuronal assemblies i
35 ed with single depolarizations and trains of depolarizing pulses in whole cell perforated patch clamp
36 id decay became shorter as the length of the depolarizing pulse increased but was unaffected by chang
37 f deactivation slowed as the duration of the depolarizing pulse increased.
38 eopenings for all three mutants during 40-ms depolarizing pulses, indicating a substantial impairment
39                                            A depolarizing pulse induced a release permeability with a
40 , and the decline in [Ca2+]i at the end of a depolarizing pulse is three to four times faster in toni
41                                 Responses to depolarizing pulses of various durations show that the s
42                   Finally, during a train of depolarizing pulses, paired pulse plasticity was signifi
43           Previous work has shown that small depolarizing pulses produce a beat to beat alternation i
44 lar myocytes, stimulating with small (20 mV) depolarizing pulses produced alternans of the amplitude
45                                              Depolarizing pulses produced rapid increases in capacita
46               However, after a brief (50 ms) depolarizing pulse, recovery from lidocaine block is sim
47                            As frequencies of depolarizing pulses rose from 2 to 20 Hz, the times to p
48 e-pulse of a few seconds or a burst of brief depolarizing pulses selectively augmented the subsequent
49  results imply excitation by hyperpolarizing-depolarizing pulse sequences at two separate sites.
50   The indo-1 transient elicited by an 800 ms depolarizing pulse showed a rapid initial rise which was
51                      Steady-state IKr during depolarizing pulses showed characteristic inward rectifi
52 otic Cm rise (delta Cm,s) that outlasted the depolarizing pulse stimulus.
53                                              Depolarizing pulses subthreshold to activating a Ca2+ sp
54              The sADPs generated by repeated depolarizing pulses summed to promote a plateau potentia
55 very is also dependent on the voltage of the depolarizing pulse that induces the inactivation, consis
56 es its current amplitudes elicited by strong depolarizing pulses that maximally activate the channels
57 rge elevation in [Ca2+]i at the start of the depolarizing pulse, there was an increase in I beta, the
58                                              Depolarizing pulses to 0 mV elicited large Ca2+ transien
59 Unitary current sweeps were evoked by 300-ms depolarizing pulses to 0 mV, from a holding potential of
60                                       During depolarizing pulses to the Cx45-expressing cell, Cx43 co
61                                              Depolarizing pulse trains also elicited a rapid increase
62 unt of total Ca2+ entry during a single long depolarizing pulse usually evoked a much larger secretor
63 verage 12.3 +/- 1.4 spikes during a 500 msec depolarizing pulse) versus phasic firing (1.2 +/- 0.2 sp
64                  'Decay' of release during a depolarizing pulse was defined as the difference between
65                         As the duration of a depolarizing pulse was increased (range 0.32-10 ms), the
66                      As the amplitude of the depolarizing pulse was increased from 10 to 30 mV the ma
67  the decaying phase of Na+ currents during a depolarizing pulse was significantly accelerated by all
68             The amount of Ca2+ releasable by depolarizing pulses was always equal to the amount of Ca
69             Ca2+ channel inactivation during depolarizing pulses was primarily voltage-dependent.
70  was no longer seen when the duration of the depolarizing pulses was reduced to 100 ms, but was clear
71 TX-resistant action potentials during 600 ms depolarizing pulses was significantly increased time dep
72                                     When the depolarizing pulses were applied at 3 Hz to mimic normal
73 on were observed when one to three preceding depolarizing pulses were applied, although there was a t
74                                When pairs of depolarizing pulses were applied, the increase in [Ca2+]
75 To investigate further the state dependence, depolarizing pulses were used to inactivate the channels
76 e receptor agonist (4-chloro-meta-cresol) or depolarizing pulses were used.
77 ivation, hyperpolarization and diminution of depolarizing pulses, were simulated from the experimenta
78 ndritic Ca2+ spikes evoked by suprathreshold depolarizing pulses, which could be terminated by superi
79          Thalamic neurons respond to a brief depolarizing pulse with a burst of action potentials; ho
80 red from the inactivation induced by a 60 ms depolarizing pulse with time constants of 1.6 ms (91 %)
81 -VSD deactivation kinetics were modulated by depolarizing pulses with durations in the intermediate t