ライフサイエンスコーパス: depotentiation

1 and (4) real tbTUS followed by real cTBS150 (depotentiation).

2 triatum, but also for its reversal, synaptic depotentiation.

3 mechanisms are related to metaplasticity or depotentiation.

4 olecular mechanisms underlying this specific depotentiation.

5 ssion (LTD), and Rap2 has been implicated in depotentiation.

6 large Na(+) currents displaying the typical depotentiation.

7 somewhat resistant to the process of Ca(2+) depotentiation.

8 at Orai3 channels undergo a lesser degree of depotentiation.

9 AMPA-Rs with long cytoplasmic termini during depotentiation.

10 asing the duration of TPS did not cause more depotentiation.

11 nsistent with homeostatic metaplasticity and depotentiation.

12 rotects potentiated synapses from subsequent depotentiation.

13 itric oxide synthase, unlike homosynaptic SC depotentiation.

14 ZIP induced depotentiation (a cellular substrate of memory erasure)

15 2) potentiation can be partially reversed by depotentiation (a second and distinctive form of neuropl

16 mory, altered responses to rewards, hampered depotentiation, a form of excitatory synaptic plasticity

17 D1/D5 agonists greatly reduced depotentiation, an effect that was inhibited by a D1/D5

18 of LTP in the hippocampus and indicate that depotentiation and LTD operate through somewhat differen

19 contributes significantly to TA-mediated SC depotentiation and the depotentiation resulting from blo

20 oforms of calcineurin, we have examined LTD, depotentiation, and LTP in mice lacking the predominant

21 role for Ras-ERK signaling in striatal LTP, depotentiation, and LTP restored after L-DOPA treatment

22 ibility of LTP to reversal and the degree of depotentiation are time-dependent.

23 ase in adult Tg2576 restores LTP but impairs depotentiation as shown in aged Tg2576.

24 rm, is required for long-term depression and depotentiation, as well as the late phase of long-term p

25 drug-induced dopamine responses and point to depotentiation at corticostriatal synapses as a possible

26 er induction but produces progressively less depotentiation at longer delays, until it has no longer

27 n potentials results in a robust and lasting depotentiation at these same synapses.

28 tion produced an almost complete and lasting depotentiation but had increasingly less impact at longe

29 ted that AMPA receptor facilitation promotes depotentiation by enhancing an active process triggered

30 of astrocytic Ca(2+) in preventing synaptic depotentiation by limiting repetitive dendritic activity

31 Depotentiation by NRG-1beta is blocked by two structural

32 This synaptic reset, or depotentiation, by DSI was blocked by the serotonin rece

33 itive dendritic Ca(2+) activity and synaptic depotentiation caused by the reduction of astrocytic Ca(

34 Adenosine-mediated SC depotentiation does not involve activation of c-Jun N-te

35 This depotentiation does not require NMDA receptors, group I

36 ) causes reversal of long-term potentiation (depotentiation, DP) and long-term depression (LTD), both

37 Reducing astrocytic Ca(2+) led to synaptic depotentiation during motor training and subsequent impa

38 enhanced long-term potentiation and impaired depotentiation ex vivo.

39 Long-term depotentiation exhibits many features congruent with tho

40 Additionally, the difference between depotentiation from Ca(2+) and Ba(2+) or Mg(2+) solution

41 DA receptor-dependent forms of LTP, LTD, and depotentiation in visual cortex.

42 timulation produced long-term depression and depotentiation in wild-type mice but failed to produce l

43 TA-induced SC depotentiation involves complex signaling including dopa

44 Rather, adenosine-induced depotentiation is inhibited by specific antagonists of p

45 ral functions governing synaptic plasticity; depotentiation is the reversal of long-term potentiation

46 A-dependent long-term potentiation/long-term depotentiation (LTP/LTD) could result in an experience-d

47 p38 subtypes, it appears that TA-induced SC depotentiation most likely involves p38 MAPK beta.

48 Notably, synaptic depotentiation occurred on a fraction of dendrites with

49 hich, when disrupted, results in a selective depotentiation of CS-evoked neural responses in the LA i

50 th enhanced long-term depression and blunted depotentiation of long-term potentiation at the Schaffer

51 In contrast, thapsigargin did not block depotentiation of LTP by 1 Hz LFS, suggesting that LTP c

52 NMDARs, adenosine A(1) receptors, and PP1 in depotentiation of LTP caused by low-frequency stimulatio

53 mutation or GIRK channel blockade abolishes depotentiation of LTP, demonstrating that GIRK channels

54 before the cued seeking test and found that depotentiation of PL -> PVT synaptic activity significan

55 me-dependent attenuation of mGluR2/3-induced depotentiation of previously induced LTP.

56 rease of ERK phosphorylation and the loss of depotentiation of synaptic plasticity induced by the D1

57 Moreover, optogenetically induced depotentiation of the CS-specific auditory pathways to t

58 d negative affective states are prevented by depotentiation of VH to NAcmSh synapses, restoring Kir2.

59 strating that GIRK channels are critical for depotentiation, one form of excitatory synaptic plastici

60 nce of (1) extracellularly recorded LTP, (2) depotentiation or LTD, and (3) paired-pulse facilitation

61 reverse conditioning-related changes (e.g., depotentiation) or induce plasticity at inhibitory synap

62 al synapses but did not affect potentiation, depotentiation, or mGluR-dependent LTD.

63 erbated propensity toward hippocampal-evoked depotentiation plasticity.

64 LTP-like plasticity can be abolished using a depotentiation protocol (DePo) consisting of brief conti

65 of long-term potentiation elicited by a 5 Hz depotentiation protocol.

66 Our model makes a link from depotentiation protocols in vitro to behavioral results

67 Depotentiation refers to reversal of LTP by a subsequent

68 The present results indicate that TA-induced depotentiation requires intact inputs from entorhinal co

69 Notably, in vivo optogenetic depotentiation restores normal transmission at these syn

70 tly to TA-mediated SC depotentiation and the depotentiation resulting from block of adenosine transpo

71 28 degrees C; potentiation was muted, while depotentiation (the reversal of the potentiation) remain

72 stigated whether D1/D5 receptors also affect depotentiation, the reversal of LTP by low-frequency sti

73 ion (LTP) and long-term depression (LTD) and depotentiation, three forms of synaptic plasticity in th

74 examining long-term depression and long-term depotentiation through direct electrical stimulation of

75 al process and allowed TPS to produce robust depotentiation up to 30 min after LTP induction.

76 ansmission following fear conditioning and a depotentiation upon fear extinction, BDNF(Met/Met) mice

77 cortex and that adenosine ultimately drives depotentiation via activation of p38 MAPK.

78 Depotentiation was abolished completely whereas neither

79 Depotentiation was much more robust in the mutant, and o

80 ntiation at LA synapses, and the ZIP-induced depotentiation was prevented by a GSK-3beta inhibitor, 6

81 ty, such as long-term potentiation (LTP) and depotentiation, was investigated.

82 To better understand the drug-induced depotentiation, we replicated these in vivo findings usi

83 at cocaine-primed reinstatement and synaptic depotentiation were disrupted by inhibiting AMPAR intern

84 That is, both potentiation and depotentiation were readily evoked at 28 degrees C; pote

85 caine-primed reinstatement and corresponding depotentiation, whereas infusion of the mGluR5 agonist C