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1 adening and also eliminated the depolarizing afterpotential.
2  prevented the induction of the depolarizing afterpotential.
3 on and suppression of prolonged depolarizing afterpotential.
4 ation or hyperpolarization referred to as an afterpotential.
5  resulted from modulation by mGluRs of three afterpotentials.
6 resident chaperone, neither inactivation nor afterpotential A (NinaA), lead to mild ER stress, protec
7 (+) influx would cause a larger depolarizing afterpotential, a condition favoring the repetitive disc
8                    Surprisingly, presynaptic afterpotentials after AP stimuli did not alter calcium c
9 is, presynaptic calcium entry is affected by afterpotentials after standard instant voltage jumps.
10 nse is affected significantly by presynaptic afterpotentials after voltage jumps.
11                              Hyperpolarizing afterpotential (AH)/type 2 neurons respond to 5-HT with
12 ptation and increases prolonged depolarizing afterpotential amplitude, whereas a reduced PP2A activit
13  brings about reduced prolonged depolarizing afterpotential amplitude.
14 euron models incorporating a hyperpolarising afterpotential and either a slow afterhyperpolarisation
15 re potassium channels limit the depolarizing afterpotential and the effects of depolarizing currents.
16 gle enzyme known as Neither Inactivation Nor Afterpotential B (NinaB).
17 low afterhyperpolarisation or a depolarising afterpotential, but many others could not.
18 toreceptors lacking neither inactivation nor afterpotential C (NINAC) myosin III, a motor protein/kin
19 n A (RDGA) and with Neither Inactivation Nor Afterpotential C (NINAC) proteins.
20 nd to interact with Neither Inactivation Nor Afterpotential C through Inactivation No Afterpotential
21 ase C (PKC), NINAC (neither inactivation nor afterpotential C) p174, which consists of fused protein
22 counteracting eye-PKC [INAC (inactivation no afterpotential C] in vivo, we performed ERG recordings.
23 ies with reduced Arr1 prolonged depolarizing afterpotential can be triggered with fewer light pulses,
24                                        These afterpotentials consisted either of a hyperpolarization,
25               We found that amplifying spike afterpotentials converted bistable persistent firing int
26 ikely via phosphorylation of inactivation no afterpotential D (INAD) and TRP (transient receptor pote
27 Nor Afterpotential C through Inactivation No Afterpotential D (INAD) in a light-dependent manner and
28                              Inactivation-no-afterpotential D (INAD) is an adaptor protein containing
29  player in the signalplex is inactivation no afterpotential D (INAD), a protein consisting of a tande
30 e complex is orchestrated by inactivation no afterpotential D (INAD), which colocalizes the transient
31 dent manner and that the CRY-Inactivation No Afterpotential D interaction is mediated by specific dom
32 s-1) scaffold protein, INAD (inactivation no afterpotential D).
33 n kinase C (aPKC) and INADL (inactivation-no-afterpotential D-like, also known as protein associated
34 ving an activity-dependent slow depolarising afterpotential (DAP) generated by a calcium-inactivated
35   We have demonstrated that the depolarizing afterpotential (DAP), which modulates bursting activity,
36  decreased the amplitude of the depolarizing afterpotential (DAP); this effect was not time-of-day de
37 eristics.SIGNIFICANCE STATEMENT Depolarizing afterpotentials (DAPs) are frequently observed in princi
38 a depolarization reminiscent of depolarizing afterpotentials (DAPs) recorded in vitro in MEC principa
39 membrane time constant, and the depolarizing afterpotential did not differ among groups.
40                    Surprisingly, presynaptic afterpotentials did not alter calcium current or neurotr
41 jection of CASPR2 mAbs showed characteristic afterpotentials following electrical stimulation.
42 hat the AP repolarization time course causes afterpotential-induced changes in calcium driving force
43     We show that the AP falling phase causes afterpotential-induced changes in electrical driving for
44 RIO domain protein, prolonged depolarization afterpotential is not apparent (PINTA), which binds to a
45             In some neurons the depolarizing afterpotential is sufficient to trigger spontaneous firi
46 ociated with the induction of a depolarizing afterpotential lasting minutes.
47                For uninjured RS neurons, the afterpotentials of action potentials had three component
48 ential for the induction of the depolarizing afterpotential probably by regulating calcium influx and
49             We hypothesized that presynaptic afterpotentials should alter neurotransmitter release by
50 ng from a relatively slow, late depolarizing afterpotential that approaches or exceeds spike threshol
51 ith a relatively early and fast depolarizing afterpotential that modulates the probability that rando
52 tosolic Ca2+ transient increases may lead to afterpotentials that ultimately trigger VF in these anim
53 zed RS neurons displayed firing patterns and afterpotentials that were similar to those of uninjured
54  therefore tested the effects of presynaptic afterpotentials using simultaneous presynaptic and posts
55 tion is required to trigger the depolarizing afterpotential, we eliminated frequency-dependent broade
56                         We hypothesized that afterpotentials, which often follow APs, affect calcium
57                      Next, we correlated the afterpotentials with the cells' propensity to fire burst