ライフサイエンスコーパス: fEPSP

1 fEPSPs evoked at the CA3-CA1 synapse presented larger am

2 s of baclofen on the relationship between an fEPSP during the spike train and the timing of spikes pr

3 se hypotheses, we measured PS amplitudes and fEPSP slopes in CA1 pyramidal cells in hippocampal slice

4 -conotoxin GVIA inhibited both the [Zn]t and fEPSP equally, and the modulation of neurotransmitter re

5 mean amplitude and slope of the post-apneic fEPSP was significantly larger compared with the pre-apn

6 The basal fEPSP response was reduced by lowered ambient glucose, a

7 The impairments in basal fEPSPs and cognition observed in 7-month-old 5XFAD mice

8 -induced potentiation of the hippocampal CA1 fEPSP is mediated by an NMDA receptor mechanism.

9 d (PPADS, 10 micromol/L) reduced the control fEPSP amplitude in the duodenum, ileum, taenia coli, pro

10 to those measured for the EPSP [field EPSP (fEPSP)].

11 in the CA1 region during LTP of field EPSPs (fEPSPs) and that two structurally unrelated PI3-kinase i

12 We recorded the field EPSPs (fEPSPs) evoked at the CA3-CA1 synapse during the perform

13 gage presynaptic inhibition and field EPSPs (fEPSPs) in hippocampal slices to monitor synaptic output

14 The lack of effect on evoked fEPSPs in these pathways is also consistent with diabete

15 Input/Output curves constructed from fEPSP data indicated that CNN-males, but not females, ha

16 rnation all showed at least 40% increases in fEPSP slope following tetanus at a slice temperature of

17 Hexamethonium (100 micromol/L) inhibited fEPSPs in the gastric corpus by 98% +/- 1% (n = 31) and

18 teralized trials, the AMPA receptor-mediated fEPSP is enhanced in the trained aPC at 48 h.

19 l from CIE treatment, NMDA-receptor-mediated fEPSPs were augmented relative to age-matched controls.

20 aracterize the P2-receptor subtype mediating fEPSPs.

21 Noncholinergic fEPSPs were concentration-dependently (1-30 micromol/L)

22 ed that the hSyn-HM3D-mediated depression of fEPSP appears to be driven by presynaptic activation of

23 The enhancement of fEPSP PPF by PREGS did not result from an increase of De

24 , whereas the hSyn-HM4D-mediated increase of fEPSP is induced by a reduction in GABAA receptor functi

25 after high-frequency stimulation, an LTP of fEPSP was seen.

26 mM) resulted in a dose-related reduction of fEPSP amplitudes (up to 52% reduction) in both hippocamp

27 mV, the amplitude (25 +/- 1 mV; n = 307) of fEPSPs was similar along the gut.

28 The amplitudes of fEPSPs recorded from the hippocampus ipsilateral to the

29 t, GR 125487, caused comparable decreases of fEPSPs in both tissues.

30 ic stimuli evoked two to five populations of fEPSPs, one to three of which were at threshold for acti

31 The initial slope of fEPSPs was used to investigate changes in synaptic stren

32 the field excitatory postsynaptic potential (fEPSP) coordinately, strongly indicating that zinc is co

33 A1) field excitatory postsynaptic potential (fEPSP) response to cornu ammonis region 3 (CA3) stimulat

34 in field excitatory post-synaptic potential (fEPSP) slope in area CA1 following tetanic stimulation o

35 n field excitatory post-synaptic potentials (fEPSP) in slices from 60-day animals, although ingenol,

36 d field excitatory post-synaptic potentials (fEPSP), and slice nicotinamide adenine dinucleotide (NAD

37 aneously with postsynaptic field potentials (fEPSPs) to investigate the mechanism of neurosteroid enh

38 ed field excitatory postsynaptic potentials (fEPSPs) and paired pulse facilitation (PPF) in KO and co

39 to fast excitatory postsynaptic potentials (fEPSPs) in myenteric neurons but the subunit composition

40 ome fast excitatory postsynaptic potentials (fEPSPs) in myenteric neurons of guinea pig ileum.

41 ked fast excitatory postsynaptic potentials (fEPSPs) in myenteric S neurons were evaluated, and the d

42 ed field excitatory postsynaptic potentials (fEPSPs) in the CA1 region of hippocampal slices prepared

43 Field excitatory postsynaptic potentials (fEPSPs) or population spikes (PSs) were recorded from th

44 ed field excitatory postsynaptic potentials (fEPSPs) recorded from hippocampal CA1 neurons was examin

45 nic fast excitatory postsynaptic potentials (fEPSPs) that were graded in amplitude, subthreshold for

46 Field excitatory postsynaptic potentials (fEPSPs) were recorded from either the dentate gyrus (DG)

47 Field excitatory postsynaptic potentials (fEPSPs) were recorded from the CA1 stratum radiatum foll

48 Field excitatory postsynaptic potentials (fEPSPs) were recorded in the CA1 region in slices from y

49 field extracellular postsynaptic potentials (fEPSPs), which depended on fiber pathway and time postin

50 campal field excitatory synaptic potentials (fEPSPs) showed that prenatal exposure to Ro61-8048 incre

51 Field excitatory post-synaptic potentials (fEPSPs) were recorded in stratum radiatum of hippocampal

52 s investigate the distribution of purinergic fEPSPs along the length of the gut and characterize the

53 phate (1 micromol/L) also reduced purinergic fEPSPs.

54 The pharmacology of the purinergic fEPSPs was investigated in detail in the ileum.

55 d the mGlu2/3 agonist LY354740, also reduced fEPSPs (up to 80% reduction).

56 Post-tetanus fEPSP slopes increased more than 100% in hippocampal sli

57 rain and the timing of spikes preceding that fEPSP, a relationship that we refer to as the history de

58 We found that fEPSPs induced by NMDA receptor activation were unaltere

59 The fEPSP slope was measured for 60 min after tetanus.

60 , neither 0.1 nor 1 mM melatonin altered the fEPSP, whereas both concentrations only slightly reduced

61 LTP, while 1 mM melatonin also depressed the fEPSP.

62 Zn]t closely resembles that measured for the fEPSP.

63 tic mechanisms underlying the changes in the fEPSP.

64 G-IV) induced a significant reduction of the fEPSP amplitude in control rats, but not in chronic epil

65 The greater susceptibility of the fEPSP in the ipsilateral hippocampus to systemic hypoxia

66 his effect strengthens the dependence of the fEPSP on the first ISI preceding it.

67 tion, cold exposed rats exhibited LTP of the fEPSP slope and population spike of similar magnitude an

68 locked the apnea-induced potentiation of the fEPSP.

69 -CPT), blunted the hypoxic depression of the fEPSP.

70 , there was no stress-specific effect on the fEPSP slope or population spike and no effect on paired-

71 hibition of the evoked population spike, the fEPSP and the intracellularly recorded EPSP.

72 The fEPSPs recorded from S neurons from P2X2-/- mice were un

73 The fEPSPs recorded from S neurons in tissues from P2X2+/+ m

74 ) inhibitor, H89, but H89 did not affect the fEPSPs in control tissue.

75 channels with iberiotoxin did not alter the fEPSPs in inflamed tissue, but increased the fEPSPs in c

76 fEPSPs in inflamed tissue, but increased the fEPSPs in control tissue to the amplitude detected in in

77 ea resulted in a maximal potentiation of the fEPSPs at 1 to 3 min after the termination of each episo

78 ly more depressed with hypoxia than were the fEPSPs recorded from the contralateral hippocampus.

79 lycemia in our slice model, assessed through fEPSP, LTP, and NADH responses, replicate closely the in

80 In inflamed tissue, fEPSPs were reduced to control levels by the protein kin

81 a greater maximum for Hill function fits to fEPSP versus DeltaF/F(0) during the second of paired res

82 that P2X2 homomeric receptors contribute to fEPSPs in neural pathways underlying peristalsis studied

83 the Hill function fits to DeltaF/F(0) versus fEPSP data.