ライフサイエンスコーパス: quantal release

1 for regulating vesicle docking and, in turn, quantal release.

2 although synapsin did not affect the rate of quantal release.

3 tter into the lumen of synaptic vesicles for quantal release.

4 mpal synapses are not generally saturated by quantal release.

5 ic recordings to characterize the effects on quantal release.

6 -expressing mast cells as a model system for quantal release.

7 se by setting a single probability level for quantal release.

8 2-fold greater quantal size and frequency of quantal release.

9 ecreased the frequency of stimulation-evoked quantal release.

10 at it does not account for the properties of quantal release.

11 ic and postsynaptic sites by increasing both quantal release and expression of AChR subunits and othe

12 eveals largely normal synaptic transmission, quantal release and trans-synaptic homeostatic compensat

13 We investigated quantal release and ultrastructure in the neuromuscular

14 rably greater than typically measured during quantal release at cultured neurons.

15 taneous, as well as action potential-evoked, quantal release at nerve terminals and increases hormone

16 Osmotic pressure enhanced quantal release at the lowest f tested (1 Hz) but suppre

17 s increased the action potential-independent quantal release by 12-fold without affecting neuronal su

18 We evoked quantal release by brief electric stimulation at single

19 We enhanced the rate of quantal release by elevating the K+ concentration.

20 We adapted amperometric methods to observe quantal release directly from axonal varicosities of mid

21 ggest why each active zone averages only one quantal release event during every other action potentia

22 that a change in the efficacy of spontaneous quantal release events is sufficient to trigger the indu

23 The observation of quantal release from central catecholamine neurons has p

24 ral and spatial resolution required to study quantal release from single cells.

25 e and with a brief latency characteristic of quantal release from synaptic vesicles.

26 nsitive stores to undergo multiple partial ("quantal") releases has been assessed.

27 e calcimycin stimulate FM1-43 destaining and quantal release in csp mutants at 32 degrees C when depo

28 We propose that the decline in K+-stimulated quantal release in preparations treated with CCCP, oligo

29 e physiological Ca(2+) concentration (2 mM), quantal release in Syn II KO synapses was unaffected.

30 nals reduced vesicular docking and inhibited quantal release, indicating a direct and selective synap

31 neurons, the Ca-dependence of toxin-enhanced quantal release is based on Ca entry through toxin-induc

32 transfer of LEMS appears to occur only after quantal release is significantly impaired for an extende

33 he actual EPSC evoked by cones, supporting a quantal release model at the photoreceptor synapse.

34 uivalent synapses;p, the mean probability of quantal release; mu, mean; and sigma(2), variance of the

35 Therefore, quantal release must be regular, giving narrower distrib

36 Neither the spontaneous quantal release of acetylcholine (ACh) nor basal evoked

37 ting that they are caused by the spontaneous quantal release of acetylcholine (ACh).

38 otor endplate, i.e. they bring about massive quantal release of acetylcholine and eventually block ne

39 However, reductions in quantal release of ACh occur even after very short perio

40 Submaximal concentrations of ATP caused quantal release of Ca2+ from the ER, resulting in a dose

41 We conclude that quantal release of Ca2+ in response to caffeine in these

42 ATP is accompanied by a drastic fall in the quantal release of catecholamines.

43 ine (DA) and observed spontaneous and evoked quantal release of DA by amperometry.

44 ocytic neurotransmitter release, we measured quantal release of dopamine from pheochromocytoma PC12 c

45 cells, in which VMAT2 expression induced the quantal release of dopamine.

46 We have found that quantal release of GABA from interneurons elicits GABA(A

47 The quantal release of glutamate depends on its transport in

48 Kinetic analysis of miniature EPSCs revealed quantal release of mixed events associating AMPARs and N

49 olutions cause markedly enhanced spontaneous quantal release of neurotransmitter from many nerve term

50 lpha-Latrotoxin (alpha-LT) potently enhances quantal release of neurotransmitter from nerve terminals

51 that neurotransmission is determined by the quantal release of neurotransmitter.

52 bending or direct application of JA caused a quantal release of oxidizable material from gland cells

53 red as increases in membrane capacitance and quantal release of preloaded serotonin.

54 The quantal release of serotonin was quantitatively characte

55 Quantal release of the principal excitatory neurotransmi

56 vestigate the mechanism responsible for this quantal release phenomenon, [Ca2+] changes inside intrac

57 We investigated how elevated quantal release produced by motor nerve stimulation affe

58 aptic units are required to sustain the high quantal release rate needed to signal a single photon.

59 Unsurprisingly, higher quantal release rates (Q(rates)) yield higher efficienci

60 h components reflect variations in hair-cell quantal release rates and are eliminated by pharmacologi

61 h higher affinity for glutamate than AMPARs, quantal release resulted in similar occupancy levels in

62 kinase inhibitor H7 (100 microM) suppressed quantal release significantly stronger in Syn II KO syna

63 ty of the resting membrane potential, evoked quantal release, synaptic potentials, acetylcholine rece

64 Since HS also stimulated asynchronous quantal release, the observed effect of HS on facilitati

65 ipophylic dye FM1-43 and focal recordings of quantal release to investigate how synapsin affects vesi

66 sculpting extracellular DA transients after quantal release, using a model based on data from the li

67 Since quantal release was first described, it has been clear t

68 Whereas quantal release was highly synchronized at low frequenci

69 Quantal release was monitored by focal extracellular rec

70 If quantal release were Poisson, the distributions of quant

71 of presynaptic syt-IV increased spontaneous quantal release, whereas a loss of postsynaptic syt-IV i

72 gnificant increase in evoked and spontaneous quantal release, while at the physiological Ca(2+) conce

73 nt reduction in the frequency of spontaneous quantal release with no change in quantal size.