ライフサイエンスコーパス: afterdischarge

1 it ovulation by releasing hormones during an afterdischarge.

2 reproduction by secreting hormone during an afterdischarge.

3 t broadening of action potentials during the afterdischarge.

4 oductive behaviors by generating a prolonged afterdischarge.

5 )O(2) regulates cation channels to drive the afterdischarge.

6 as Type II neurons typically had a sustained afterdischarge.

7 the cation channel and, thereby, trigger the afterdischarge.

8 aneous action potentials referred to as the "afterdischarge.

9 rane to ensure adequate secretion during the afterdischarge.

10 tical effects occur when cognitive tasks end afterdischarges.

11 ly stimulated or to other electrodes showing afterdischarges.

12 restored the ability of stimulation to evoke afterdischarges.

13 unstimulated clusters inhibited the onset of afterdischarges.

14 slices, accompanied by the appearance of CA3 afterdischarges.

15 or the commissural system was used to elicit afterdischarges.

16 ala stimulation (baseline), (2) during focal afterdischarge (AD) and (3) during generalized AD.

17 as to test the hypothesis that an electrical afterdischarge (AD) causes prolonged elevation in cytoso

18 etized rat during the initiation of a single afterdischarge (AD) evoked by perforant path stimulation

19 GalKO showed increased duration of afterdischarge (AD) evoked from the dentate gyrus by per

20 Kindling trials and afterdischarge (AD) were controlled to ascertain their r

21 ain-wide circuit dynamics resulting from non-afterdischarge (AD)-generating stimulations and individu

22 ated kindling rate, defined as the number of afterdischarges (ADs) required to achieve the first stag

23 on the rapid kindling induced by a series of afterdischarges (ADs) triggered in hippocampus over a 3-

24 outs of synchronized network activity called afterdischarges (ADs).

25 Irrespective of the evoking conditions, afterdischarges always terminated first in the CA1 regio

26 tion, play important roles in generating the afterdischarge and triggering egg-laying behaviors.

27 ministration was also associated with longer afterdischarges and abnormal wind-up to transcutaneous e

28 tion velocity, (2) increase in IED secondary afterdischarges and their reverberation between CA3a and

29 y period, intact clusters were stimulated to afterdischarge, and neurons were isolated after the clus

30 ed spike failure, single spike transmission, afterdischarge, and spontaneous spiking.

31 In juvenile animals, such afterdischarges are inhibited by a high density of Ca2+

32 H(2)O(2), which is generated in response to afterdischarge-associated second messengers, may prompt

33 The likelihood of an afterdischarge at an individual site after stimulation w

34 Afterdischarge can be triggered in vitro by a variety of

35 When cognitive tasks ended afterdischarges, coherence varied similarly across the c

36 Adult bag cell neurons exhibit an afterdischarge, consisting of prolonged depolarization a

37 A neuron prone to afterdischarge could function normally unless it was swi

38 Normal, long-lasting afterdischarges could be triggered by stimulation of an

39 which focuses on the neuronal mechanisms of afterdischarges, demonstrates that a single pair of inte

40 Afterdischarge duration (ADD) was assessed via electroen

41 Two indices of seizure severity, afterdischarge duration (Mean +/- S.E.M., sec.) (stimula

42 red-pulse inhibition, decreased epileptiform afterdischarge durations during 8 hours of subsequent st

43 me and then to increase toward baseline when afterdischarges ended.

44 After a complete lesion was made, afterdischarges evoked on one half of a slice were not d

45 inch) stimulation and increased incidence of afterdischarge firing 2-3 days after injection.

46 We did this by studying cortical afterdischarges following electrical stimulation of the

47 nstrate that: (1) the threshold to elicit an afterdischarge from the BL was lower than that of either

48 Finally, H(2)O(2) evoked an afterdischarge from whole bag cell neuron clusters recor

49 A interneuron (Cr-Aint)] is responsible for afterdischarge generation in the network.

50 nature of the depolarization generating the afterdischarge, however, has remained unclear.

51 gs revealed increased spontaneous discharge, afterdischarge, hyperresponsiveness to innocuous and nox

52 as given below the threshold that elicits an afterdischarge (i.e., a neuronal discharge that occurs a

53 An increase in this current also follows an afterdischarge in mature animals, contributing to a subs

54 to adults, juvenile neurons did not exhibit afterdischarge in response to pleural-abdominal connecti

55 the anlage of the mechanism responsible for afterdischarge in the adult.

56 e to Conus textile venom (CtVm), triggers an afterdischarge in the bag cell neurones of Aplysia.

57 gh-frequency stimulation of the VTA provoked afterdischarge in the central amygdala and enhanced kind

58 clude that a subiculum--CA1 circuit supports afterdischarges in both regions and synchronizes their a

59 region between subiculum and CA1 eliminated afterdischarges in subicular and CA1 events, but did not

60 ulse excitation or inhibition or duration of afterdischarges in the intact hippocampal preparation.

61 In vivo stimulation of a paroxysmal afterdischarge increased both pan-BDNF and NGF mRNA leve

62 A single afterdischarge increased exon I-IV-containing mRNA level

63 nisomycin modestly attenuated the paroxysmal afterdischarge-induced increase of both transcripts.

64 rons, which initiate reproduction through an afterdischarge involving multiple Ca(2+)-dependent proce

65 The afterdischarge is followed by a prolonged (approximately

66 Moreover, the refractory period of the afterdischarge itself may also be initiated by Ca2+ entr

67 and the cluster, H(2)O(2) evokes prolonged, afterdischarge-like bursting by gating a nonselective vo

68 A vigorous, long-lasting sound-evoked afterdischarge (LSA) is seen in a subpopulation of both

69 Afterdischarge occurred at g(Na)/g(L) just below the thr

70 astic" slices were characterized by multiple afterdischarges, occurring at a significantly higher rep

71 various cation channels, causing an ~30 min afterdischarge of action potentials and the secretion of

72 The afterdischarge of Aplysia bag cell neurons has served as

73 stimulation of the CeM elicited seizures and afterdischarges of shorter duration than those evoked by

74 was to investigate the effects of electrical afterdischarge on protein kinase C (PKC) activity from b

75 lectrical stimulation (ES), subthreshold for afterdischarge, on delayed item RM in epilepsy patients

76 h electrical stimulation and CtVm to trigger afterdischarges or elevate [Ca2+]i is severely attenuate

77 During the afterdischarge, protein kinase C is also activated, whic

78 P levels or direct electrical stimulation of afterdischarge rapidly enhanced formation of these clust

79 Afterdischarges represent a prominent characteristic of

80 ges during cognitive tasks used to terminate afterdischarges studying multiple time segments and mult

81 The mechanism of afterdischarge termination in the various hippocampal re

82 itic layers associated with a low amplitude "afterdischarge termination oscillation" (ATO) at 40 to 8

83 tion of action potentials during a prolonged afterdischarge that triggers a series of reproductive be

84 evelopment allows mature neurons to generate afterdischarges that are required for reproduction.

85 ecordings revealed increased tetanus-induced afterdischarges that could be kindled in the absence of

86 During the first few seconds of this afterdischarge, the action potentials of the bag cell ne

87 were divided: one cluster was stimulated to afterdischarge, the other was a control.

88 After an approximately 30 min afterdischarge, these neurons enter an approximately 18

89 he left piriform cortex every 5 min for 6 h (afterdischarge threshold, 60 Hz, 1 ms, 1 s).

90 The rats were kindled once daily using afterdischarge-threshold electrical stimulation until th

91 Rats were kindled to stage 5 by afterdischarge-threshold electrostimulation of the left

92 d chronic antiepileptic action by increasing afterdischarge thresholds in perforant path (but not olf

93 antly higher spontaneous activity and longer afterdischarges to noxious mechanical stimuli than wide

94 lock, probably by preventing newly generated afterdischarges to travel backwards to the original focu

95 Afterdischarge triggered a rapid and persistent increase

96 the intensely discharging neurons during the afterdischarge triggers propagating waves of depolarizat

97 Vocalization afterdischarges (VADs) are a validated model of the affe

98 zations during shock (VDSs) and vocalization afterdischarges (VADs) was challenged by the intrathecal

99 ations during shock (VDSs), and vocalization afterdischarges (VADs) when administered into the spinal

100 s during shock), and forebrain (vocalization afterdischarges, VADs) levels of the neuraxis were elici

101 ng shock, VDSs), and forebrain (vocalization afterdischarges, VADs) levels were elicited by noxious t

102 Termination of the afterdischarge was heralded by a large DC shift initiate

103 rrupted motor, sensory or language function, afterdischarges were more likely to occur at other sites

104 human infantile spasms: electrodecrement or afterdischarges were observed.