ライフサイエンスコーパス: depotentiation

1 mechanisms are related to metaplasticity or depotentiation.

2 olecular mechanisms underlying this specific depotentiation.

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

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

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

6 at Orai3 channels undergo a lesser degree of depotentiation.

7 AMPA-Rs with long cytoplasmic termini during depotentiation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

26 This depotentiation does not require NMDA receptors, group I

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

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

29 Long-term depotentiation exhibits many features congruent with tho

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 Depotentiation refers to reversal of LTP by a subsequent

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

51 28 degrees C; potentiation was muted, while depotentiation (the reversal of the potentiation) remain

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

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

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

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

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

57 Depotentiation was abolished completely whereas neither

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

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

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

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