戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
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 s used to treat insomnia (zolpidem (ZOL) and flurazepam) and postpartum depression (the neurosteroid
12 and [(3)H]EBOB binding, including midazolam, flurazepam, avermectin Ba1, baclofen, isoguvacine, and p
13 proaches, we show that treatment with the BZ flurazepam decreases GABA(A)R surface levels and the eff
14            Together, these data suggest that flurazepam exposure enhances degradation of alpha2 subun
15 uctance, although the benzodiazepine ligands flurazepam, flumazenil, and methyl-6,7-dimethoxy-4 ethyl
16 ssess the effects of withdrawal from chronic flurazepam (FRZ) treatment on the function of synaptic G
17                                              Flurazepam (FZP) withdrawal is associated with increased
18 y oral administration of the benzodiazepine, flurazepam (FZP).
19 at the BZD site, and the presence of GABA or flurazepam had no effect on its accessibility, indicatin
20 tor surface levels, strongly suggesting that flurazepam increases lysosomal degradation of GABA(A)Rs.
21            Treatment with leupeptin restored flurazepam lowered receptor surface levels, strongly sug
22      Chronic exposure to pregnanolone, GABA, flurazepam or pentobarbital induces complete uncoupling
23                              The presence of flurazepam or the BZD-site antagonist flumazenil (Ro15-1
24 regnan-20-one (pregnanolone), pentobarbital, flurazepam, or GABA, then tested for enhancement of [3H]
25  slices were prepared from rats administered flurazepam orally for 1 week, 2 days after ending drug t
26 Cs were insensitive to low concentrations of flurazepam, providing a pharmacological confirmation of
27 a1R131C changed accessibility in response to flurazepam, providing structural evidence that residues
28  the abilities of eszopiclone, zolpidem, and flurazepam to potentiate I(GABA).
29 nsfer, and thus Cl(-) flux, was unchanged in flurazepam-treated neurons (SO-SP: control 588 pS, flura
30 ificant reduction in synaptic-conductance in flurazepam-treated neurons following both SO-SP (control
31 dent with decreased GABA(A)R surface levels, flurazepam treatment reduced miniature inhibitory postsy
32                                      Chronic flurazepam treatment substantially impairs the function
33 containing GABA(A)Rs occurred within 24 h of flurazepam treatment, whereas GABA(A)Rs incorporating al
34 ytosis and insertion rates were unchanged by flurazepam treatment.
35 9) in the modulation of I(GABA) by positive (flurazepam, zolpidem) and negative [3-carbomethoxy-4-eth