ライフサイエンスコーパス: aniracetam

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1 logical potentiation of AMPAR activity using aniracetam.

2 confirming a postsynaptic site of action of aniracetam.

3 and a corresponding structure of GluA3 with aniracetam.

4 differential modulation by cyclothiazide and aniracetam.

5 2 S1S2 ligand-binding domain in complex with aniracetam [1-(4-methoxybenzoyl)-2-pyrrolidinone] or CX6

6 th nootropics, oxiracetam (10-1000 mg/kg) or aniracetam (10-100 mg/kg), and N-methyl-D-Aspartate (NMD

7 The modulatory influence of aniracetam, a drug which reversibly modifies the kinetic

8 Aniracetam, a modulator of AMPA receptors that reduces d

9 ed deactivation, and imparted sensitivity to aniracetam, an AMPA receptor-selective positive modulato

10 ts from kinetic analysis are consistent with aniracetam and cyclothiazide acting via distinct mechani

11 vation and desensitization by cyclothiazide, aniracetam, and thiocyanate.

12 Nefiracetam at 1 nM and aniracetam at 0.1 nM reversibly potentiated alpha 4 beta

13 Aniracetam binds to a symmetrical site at the center of

14 e waveform distortions introduced by LTP and aniracetam could be corrected by uniform stretching of t

15 antal-content conditions, the evoked EPSC in aniracetam decayed with a time course intermediate betwe

16 ifferential sensitivity to cyclothiazide and aniracetam depends on a single amino acid, Ser (flip) an

17 However, the binding sites for piracetam and aniracetam differ considerably.

18 In the presence of aniracetam, evoked excitatory synaptic currents (EPSCs)

19 Although nefiracetam and aniracetam inhibited alpha 7-type currents only weakly,

20 out to determine if the altered response to aniracetam is sufficiently persistent to be a plausible

21 the nature of the change responsible for the aniracetam/LTP interaction was explored with waveform an

22 ory currents and postsynaptic spiking to the aniracetam/LTP interaction were investigated with infusi

23 The mechanism of action of aniracetam on alpha-amino-3-hydroxy-5-methyl-4-isoxazole

24 e the mechanism of action of nefiracetam and aniracetam on neuronal nicotinic acetylcholine receptors

25 LTP reduced the effect of aniracetam on the amplitude but increased its effect on

26 No effect of aniracetam on the NMDA component of the EPSC was seen, c

27 losteric modulators (e.g., cyclothiazide and aniracetam) preferentially affect the flip (i) or flop (

28 Aniracetam's effects on receptor deactivation saturated

29 agonist, and kinetic modeling indicated that aniracetam slows both the rate of channel closing, and t

30 When desensitization was reduced with aniracetam, steady-state EPSC amplitudes during trains w

31 te receptors was blocked by cyclothiazide or aniracetam, the BDNF potentiation of the synaptic respon

32 results show that, unlike cyclothiazide and aniracetam, the residues that confer splice variant diff

33 However, this effect of aniracetam was absent when release probability was lower

34 The LTP-induced change in the effect of aniracetam was extremely stable in that it was still evi

35 ssion and patch desensitization prevented by aniracetam, we conclude that significant desensitization

36 effects of 30 mg/kg oxiracetam and 100 mg/kg aniracetam were inhibited by the (+/-)-alpha-amino-3-hyd

37 olidine allosteric modulators, piracetam and aniracetam, were among the first of this class of drugs

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