ライフサイエンスコーパス: afterpotential

1 on and suppression of prolonged depolarizing afterpotential.

2 ation or hyperpolarization referred to as an afterpotential.

3 adening and also eliminated the depolarizing afterpotential.

4 prevented the induction of the depolarizing 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 re potassium channels limit the depolarizing afterpotential and the effects of depolarizing currents.

15 toreceptors lacking neither inactivation nor afterpotential C (NINAC) myosin III, a motor protein/kin

16 n A (RDGA) and with Neither Inactivation Nor Afterpotential C (NINAC) proteins.

17 nd to interact with Neither Inactivation Nor Afterpotential C through Inactivation No Afterpotential

18 ase C (PKC), NINAC (neither inactivation nor afterpotential C) p174, which consists of fused protein

19 counteracting eye-PKC [INAC (inactivation no afterpotential C] in vivo, we performed ERG recordings.

20 ies with reduced Arr1 prolonged depolarizing afterpotential can be triggered with fewer light pulses,

21 ikely via phosphorylation of inactivation no afterpotential D (INAD) and TRP (transient receptor pote

22 Nor Afterpotential C through Inactivation No Afterpotential D (INAD) in a light-dependent manner and

23 Inactivation-no-afterpotential D (INAD) is an adaptor protein containing

24 player in the signalplex is inactivation no afterpotential D (INAD), a protein consisting of a tande

25 e complex is orchestrated by inactivation no afterpotential D (INAD), which colocalizes the transient

26 dent manner and that the CRY-Inactivation No Afterpotential D interaction is mediated by specific dom

27 s-1) scaffold protein, INAD (inactivation no afterpotential D).

28 n kinase C (aPKC) and INADL (inactivation-no-afterpotential D-like, also known as protein associated

29 ving an activity-dependent slow depolarising afterpotential (DAP) generated by a calcium-inactivated

30 We have demonstrated that the depolarizing afterpotential (DAP), which modulates bursting activity,

31 decreased the amplitude of the depolarizing afterpotential (DAP); this effect was not time-of-day de

32 membrane time constant, and the depolarizing afterpotential did not differ among groups.

33 Surprisingly, presynaptic afterpotentials did not alter calcium current or neurotr

34 hat the AP repolarization time course causes afterpotential-induced changes in calcium driving force

35 We show that the AP falling phase causes afterpotential-induced changes in electrical driving for

36 RIO domain protein, prolonged depolarization afterpotential is not apparent (PINTA), which binds to a

37 In some neurons the depolarizing afterpotential is sufficient to trigger spontaneous firi

38 ociated with the induction of a depolarizing afterpotential lasting minutes.

39 For uninjured RS neurons, the afterpotentials of action potentials had three component

40 ential for the induction of the depolarizing afterpotential probably by regulating calcium influx and

41 We hypothesized that presynaptic afterpotentials should alter neurotransmitter release by

42 ng from a relatively slow, late depolarizing afterpotential that approaches or exceeds spike threshol

43 ith a relatively early and fast depolarizing afterpotential that modulates the probability that rando

44 tosolic Ca2+ transient increases may lead to afterpotentials that ultimately trigger VF in these anim

45 zed RS neurons displayed firing patterns and afterpotentials that were similar to those of uninjured

46 therefore tested the effects of presynaptic afterpotentials using simultaneous presynaptic and posts

47 tion is required to trigger the depolarizing afterpotential, we eliminated frequency-dependent broade

48 We hypothesized that afterpotentials, which often follow APs, affect calcium