ライフサイエンスコーパス: flunitrazepam

1 from the requirements of classic BZDs (e.g., flunitrazepam).

2 ion, as evidenced by decreased binding of H3-flunitrazepam.

3 ne and were potentiated by pentobarbital and flunitrazepam.

4 n the binding affinity of the benzodiazepine flunitrazepam.

5 only the tau(slow) component is affected by flunitrazepam.

6 nt was detectable, except in the presence of flunitrazepam.

7 tive to allosteric activation by ethanol and flunitrazepam.

8 ioligands was unaffected by incorporation of flunitrazepam.

9 GABA and potently decreased the response to flunitrazepam.

10 nd subsequent mole-equivalent challenge with flunitrazepam.

11 (propofol, 3 microM) and the benzodiazepine flunitrazepam (1 microM) potentiated GABA-evoked current

12 The benzodiazepine flunitrazepam (1 microM) slowed deactivation at a holdin

13 AME did not affect the modulation of the [3H]flunitrazepam (2 nM) or [35S]TBPS (4 nM) binding by the

14 eroid, on the binding characteristics of [3H]flunitrazepam (2 nM), [3H]muscimol (5 nM), and 4 nM [35S

15 e GABAAR, as measured by potentiation of [3H]flunitrazepam ([3H]FNZ) binding.

16 e binding of [35S]TBPS (44% inhibition), [3H]flunitrazepam (41% enhancement), and [3H]muscimol (< 10%

17 [3H]flunitrazepam a benzodiazepine agonist, and [35S]t-butyl

18 ly is important for high-affinity binding by flunitrazepam (a strong positive modulator) but also pla

19 was measured by the addition of GABA to [3H]flunitrazepam and [35S]TBPS binding assays.

20 specific [35S]TBPS binding and enhancing [3H]flunitrazepam and [3H]muscimol binding 95% and 69% above

21 pha-ol-20-one potentiated the binding of [3H]flunitrazepam and [3H]muscimol in all the rat brain regi

22 d using frontal affinity chromatography with flunitrazepam and diazepam (GABA(A) receptor) and MK-801

23 xpectedly, we found that the benzodiazepines flunitrazepam and diazepam enhanced extrasynaptic inhibi

24 obe further the mechanism and orientation of flunitrazepam and other ligands in the BZ binding site.

25 ions, the binding level of [3H]muscimol, [3H]flunitrazepam, and [35S]TBPS to coated vesicles represen

26 oexponential decay phase and is modulated by flunitrazepam, and the other has a decay phase that is b

27 ed gamma-aminobutyric acid or [(3)H]-labeled flunitrazepam, and tolerance did not develop during a 5-

28 ity was measured by in vitro test with [(3)H]flunitrazepam as radioligand in which allopregnanolone a

29 increase in the maximal potentiation of [3H]flunitrazepam as well as [3H]muscimol binding (Emax) in

30 DHM competitively inhibited BZ-site [(3)H]flunitrazepam binding (IC(50), 4.36 muM), suggesting DHM

31 creased the immunoprecipitation of the [(3)H]flunitrazepam binding activity for GABA(A) receptor asse

32 s of the SAR data suggests dependence of the flunitrazepam binding activity on the hydrophobic-hydrop

33 gamma2 region Met-57-Ile-62 is important for flunitrazepam binding and that, in particular, gamma2 Me

34 observed in the degree of stimulation of [3H]flunitrazepam binding by 3alpha-OH-DHP among medullary b

35 Stimulation of [3H]flunitrazepam binding by 3alpha-OH-DHP in nuclei involve

36 otency of ammonium tartrate in enhancing [3H]flunitrazepam binding by 63%.

37 THDOC and increased the enhancement of [(3)H]flunitrazepam binding by GABA and THDOC in the dentate g

38 Coated vesicles showed a single [3H]flunitrazepam binding site with a KD value (12 nM) which

39 utant alpha1 polypeptides did not form [(3)H]flunitrazepam binding sites though wild-type alpha1 poly

40 :1 molar ratio the amount assembled into [3H]flunitrazepam binding sites.

41 nor SR95531 had a significant effect on [3H]flunitrazepam binding to CCVs, indicating that the allos

42 Inhibition of [3H]flunitrazepam binding to cerebellar membranes with imida

43 ncentrations (500-2500 microM) decreased [3H]flunitrazepam binding to control levels.

44 clophosphorothionate ([(35)S]TBPS) and [(3)H]flunitrazepam binding to GABA(A) receptors using in vitr

45 ical alpha 5 selective ligand) inhibited [3H]flunitrazepam binding to hippocampal membranes with high

46 ese compounds (5, 6, 8, and 9) inhibited [3H]flunitrazepam binding to recombinant alpha 5 beta 2 gamm

47 For [3H]flunitrazepam binding to synaptic membranes, GABA gave a

48 [3H]Flunitrazepam binding to the benzodiazepine receptor was

49 Stimulation of [3H]flunitrazepam binding to the GABA(A) receptor by two pro

50 [3H]Flunitrazepam binding was enhanced by 3alpha-OH-DHP in e

51 he ammonium tartrate-induced increase in [3H]flunitrazepam binding was manifested as a 50% decrease i

52 m autoradiographic technique to localize [3H]flunitrazepam binding, the subregional and laminar distr

53 creased after extinction training, as did H3-flunitrazepam binding.

54 A-gated current and GABA potentiation of [3H]flunitrazepam binding.

55 the BZ site after photoincorporation of [3H]flunitrazepam confirmed that binding of other radioligan

56 wing application of the benzodiazepine (BDZ) Flunitrazepam (Flu, 1 microM).

57 To address this concept, a flunitrazepam hapten was synthesized and employed in the

58 Previous photolabeling studies with [(3)H]flunitrazepam identified a primary site of incorporation

59 units from cerebellar granule cells enhanced flunitrazepam-induced potentiation of GABA-activated cur

60 Not only was flunitrazepam-induced sedation prevented but immunizatio

61 Photoincorporation of flunitrazepam into a single population of GABAA receptor

62 ceptor binding in the LC measured with [(3)H]flunitrazepam is not altered in subjects with depressive

63 tyrate; gamma-butyrolactone, 1,4-butanediol, flunitrazepam, ketamine, and nitrites.

64 Anti-flunitrazepam mAb RCA3A3 ( K d,app = 200 nM) was tested

65 y derivatized with the entire, unfragmented, flunitrazepam molecule, which undergoes a conformational

66 ligand, the coupling can either be positive (flunitrazepam), negative (Ro15-4513), or neutral (flumaz

67 ptor agonist baclofen blocks ethanol but not flunitrazepam or pentobarbital potentiation of GABA(A) I

68 Because the major site of flunitrazepam photoincorporation has been shown to be Hi

69 ARs confirmed that, at subsaturating [GABA], flunitrazepam potentiates alpha6/delta subunit-containin

70 tant 25-32 Hz tremor, which is aggravated by flunitrazepam, reduced rotarod performance, and reduced

71 GABARs, the number of binding sites for [3H]flunitrazepam relative to wild-type receptors was decrea

72 GABA ([3H]muscimol), and benzodiazepine ([3H]flunitrazepam) site ligands.

73 kedly alter the affinities of ligands (e.g., flunitrazepam) that are not subtype-selective.

74 sterically modulated specific binding of [3H]flunitrazepam to differentiated P19 cells.

75 s evaluated by studying the binding of [(3)H]flunitrazepam to GABA(A) receptors at three anatomically

76 also allosterically enhanced the binding of flunitrazepam to mammalian brain GABAA receptors.

77 However, their response to flunitrazepam was not altered, suggesting that PKCdelta

78 )gamma(2) receptors, whereas the efficacy of flunitrazepam was similar at all three receptor isoforms

79 Using (3)H-muscimol and (3)H-flunitrazepam we could determine whether the number (B(m

80 l moiety, analogous to the 5-phenyl group of flunitrazepam, which are proposed to overlap and interac

81 s of the gamma2 subunit bind the classic BZD flunitrazepam with wild-type affinity, zolpidem affinity