ライフサイエンスコーパス: flurazepam

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1 tes inhibitory effects of the benzodiazepine flurazepam.

2 : 226 pS, P<0.01) and S-L-M (control 998 pS, flurazepam: 179 pS, P<0.01) stimulation, as well as the

3 rons following both SO-SP (control: 1058 pS, flurazepam: 226 pS, P<0.01) and S-L-M (control 998 pS, f

4 The application of flurazepam (30 microM, n = 7; 50 microM, n = 4) prolonge

5 00 nM) but insensitive to the benzodiazepine flurazepam (5 microM).

6 epam: 580 pS, P>0.05; S-L-M: control 595 pS, flurazepam: 527 pS, P>0.05).

7 epam-treated neurons (SO-SP: control 588 pS, flurazepam: 580 pS, P>0.05; S-L-M: control 595 pS, flura

8 ), pentobarbital (allosteric modulator), and flurazepam (allosteric modulator).

9 ronal GABAA receptors, IGABA was enhanced by flurazepam and relatively unaffected by redox reagents.

10 Flurazepam and zolpidem significantly slowed covalent mo

11 and [(3)H]EBOB binding, including midazolam, flurazepam, avermectin Ba1, baclofen, isoguvacine, and p

12 proaches, we show that treatment with the BZ flurazepam decreases GABA(A)R surface levels and the eff

13 Together, these data suggest that flurazepam exposure enhances degradation of alpha2 subun

14 uctance, although the benzodiazepine ligands flurazepam, flumazenil, and methyl-6,7-dimethoxy-4 ethyl

15 ssess the effects of withdrawal from chronic flurazepam (FRZ) treatment on the function of synaptic G

16 Flurazepam (FZP) withdrawal is associated with increased

17 y oral administration of the benzodiazepine, flurazepam (FZP).

18 at the BZD site, and the presence of GABA or flurazepam had no effect on its accessibility, indicatin

19 tor surface levels, strongly suggesting that flurazepam increases lysosomal degradation of GABA(A)Rs.

20 Treatment with leupeptin restored flurazepam lowered receptor surface levels, strongly sug

21 Chronic exposure to pregnanolone, GABA, flurazepam or pentobarbital induces complete uncoupling

22 The presence of flurazepam or the BZD-site antagonist flumazenil (Ro15-1

23 regnan-20-one (pregnanolone), pentobarbital, flurazepam, or GABA, then tested for enhancement of [3H]

24 slices were prepared from rats administered flurazepam orally for 1 week, 2 days after ending drug t

25 Cs were insensitive to low concentrations of flurazepam, providing a pharmacological confirmation of

26 a1R131C changed accessibility in response to flurazepam, providing structural evidence that residues

27 the abilities of eszopiclone, zolpidem, and flurazepam to potentiate I(GABA).

28 nsfer, and thus Cl(-) flux, was unchanged in flurazepam-treated neurons (SO-SP: control 588 pS, flura

29 ificant reduction in synaptic-conductance in flurazepam-treated neurons following both SO-SP (control

30 dent with decreased GABA(A)R surface levels, flurazepam treatment reduced miniature inhibitory postsy

31 Chronic flurazepam treatment substantially impairs the function

32 containing GABA(A)Rs occurred within 24 h of flurazepam treatment, whereas GABA(A)Rs incorporating al

33 ytosis and insertion rates were unchanged by flurazepam treatment.

34 9) in the modulation of I(GABA) by positive (flurazepam, zolpidem) and negative [3-carbomethoxy-4-eth

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