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1 from the requirements of classic BZDs (e.g., flunitrazepam).
2 nd subsequent mole-equivalent challenge with flunitrazepam.
3 ion, as evidenced by decreased binding of H3-flunitrazepam.
4 ne and were potentiated by pentobarbital and flunitrazepam.
5 n the binding affinity of the benzodiazepine flunitrazepam.
6  only the tau(slow) component is affected by flunitrazepam.
7 nt was detectable, except in the presence of flunitrazepam.
8 drogel droplets (GluHD) for the detection of flunitrazepam.
9 tive to allosteric activation by ethanol and flunitrazepam.
10 ioligands was unaffected by incorporation of flunitrazepam.
11  GABA and potently decreased the response to flunitrazepam.
12  (propofol, 3 microM) and the benzodiazepine flunitrazepam (1 microM) potentiated GABA-evoked current
13                           The benzodiazepine flunitrazepam (1 microM) slowed deactivation at a holdin
14 AME did not affect the modulation of the [3H]flunitrazepam (2 nM) or [35S]TBPS (4 nM) binding by the
15 eroid, on the binding characteristics of [3H]flunitrazepam (2 nM), [3H]muscimol (5 nM), and 4 nM [35S
16 e GABAAR, as measured by potentiation of [3H]flunitrazepam ([3H]FNZ) binding.
17 e binding of [35S]TBPS (44% inhibition), [3H]flunitrazepam (41% enhancement), and [3H]muscimol (< 10%
18                                          [3H]flunitrazepam a benzodiazepine agonist, and [35S]t-butyl
19 ly is important for high-affinity binding by flunitrazepam (a strong positive modulator) but also pla
20                                              Flunitrazepam, also known as "Rohypnol" or "Rophy" among
21  was measured by the addition of GABA to [3H]flunitrazepam and [35S]TBPS binding assays.
22 specific [35S]TBPS binding and enhancing [3H]flunitrazepam and [3H]muscimol binding 95% and 69% above
23 pha-ol-20-one potentiated the binding of [3H]flunitrazepam and [3H]muscimol in all the rat brain regi
24 d using frontal affinity chromatography with flunitrazepam and diazepam (GABA(A) receptor) and MK-801
25 xpectedly, we found that the benzodiazepines flunitrazepam and diazepam enhanced extrasynaptic inhibi
26 obe further the mechanism and orientation of flunitrazepam and other ligands in the BZ binding site.
27 of the sensor for point-of-need screening of flunitrazepam and suggest that GOx/GluHD-FeSPC holds pro
28 ions, the binding level of [3H]muscimol, [3H]flunitrazepam, and [35S]TBPS to coated vesicles represen
29 oexponential decay phase and is modulated by flunitrazepam, and the other has a decay phase that is b
30 ed gamma-aminobutyric acid or [(3)H]-labeled flunitrazepam, and tolerance did not develop during a 5-
31 ity was measured by in vitro test with [(3)H]flunitrazepam as radioligand in which allopregnanolone a
32  increase in the maximal potentiation of [3H]flunitrazepam as well as [3H]muscimol binding (Emax) in
33  the electro reduction of the nitro group of flunitrazepam at ca. -0.71 to -0.78 V vs. Ag printed pse
34    DHM competitively inhibited BZ-site [(3)H]flunitrazepam binding (IC(50), 4.36 muM), suggesting DHM
35 creased the immunoprecipitation of the [(3)H]flunitrazepam binding activity for GABA(A) receptor asse
36 s of the SAR data suggests dependence of the flunitrazepam binding activity on the hydrophobic-hydrop
37 gamma2 region Met-57-Ile-62 is important for flunitrazepam binding and that, in particular, gamma2 Me
38 observed in the degree of stimulation of [3H]flunitrazepam binding by 3alpha-OH-DHP among medullary b
39                           Stimulation of [3H]flunitrazepam binding by 3alpha-OH-DHP in nuclei involve
40 otency of ammonium tartrate in enhancing [3H]flunitrazepam binding by 63%.
41 THDOC and increased the enhancement of [(3)H]flunitrazepam binding by GABA and THDOC in the dentate g
42          Coated vesicles showed a single [3H]flunitrazepam binding site with a KD value (12 nM) which
43 utant alpha1 polypeptides did not form [(3)H]flunitrazepam binding sites though wild-type alpha1 poly
44 :1 molar ratio the amount assembled into [3H]flunitrazepam binding sites.
45  nor SR95531 had a significant effect on [3H]flunitrazepam binding to CCVs, indicating that the allos
46                            Inhibition of [3H]flunitrazepam binding to cerebellar membranes with imida
47 ncentrations (500-2500 microM) decreased [3H]flunitrazepam binding to control levels.
48 clophosphorothionate ([(35)S]TBPS) and [(3)H]flunitrazepam binding to GABA(A) receptors using in vitr
49 ical alpha 5 selective ligand) inhibited [3H]flunitrazepam binding to hippocampal membranes with high
50 ese compounds (5, 6, 8, and 9) inhibited [3H]flunitrazepam binding to recombinant alpha 5 beta 2 gamm
51                                      For [3H]flunitrazepam binding to synaptic membranes, GABA gave a
52                                          [3H]Flunitrazepam binding to the benzodiazepine receptor was
53                           Stimulation of [3H]flunitrazepam binding to the GABA(A) receptor by two pro
54                                          [3H]Flunitrazepam binding was enhanced by 3alpha-OH-DHP in e
55 he ammonium tartrate-induced increase in [3H]flunitrazepam binding was manifested as a 50% decrease i
56 m autoradiographic technique to localize [3H]flunitrazepam binding, the subregional and laminar distr
57 creased after extinction training, as did H3-flunitrazepam binding.
58 A-gated current and GABA potentiation of [3H]flunitrazepam binding.
59  the BZ site after photoincorporation of [3H]flunitrazepam confirmed that binding of other radioligan
60                   The oxygen interference on flunitrazepam detection was alleviated by dissolving an
61 A solution of 4 mg of clonazepam and 2 mg of flunitrazepam, each dissolved in 50 mL of ultrapure wate
62 wing application of the benzodiazepine (BDZ) Flunitrazepam (Flu, 1 microM).
63                   To address this concept, a flunitrazepam hapten was synthesized and employed in the
64    Previous photolabeling studies with [(3)H]flunitrazepam identified a primary site of incorporation
65 units from cerebellar granule cells enhanced flunitrazepam-induced potentiation of GABA-activated cur
66                                 Not only was flunitrazepam-induced sedation prevented but immunizatio
67     The findings suggest that clonazepam and flunitrazepam influence C. vicina morphology, particular
68                        Photoincorporation of flunitrazepam into a single population of GABAA receptor
69 ceptor binding in the LC measured with [(3)H]flunitrazepam is not altered in subjects with depressive
70 tyrate; gamma-butyrolactone, 1,4-butanediol, flunitrazepam, ketamine, and nitrites.
71                                         Anti-flunitrazepam mAb RCA3A3 ( K d,app = 200 nM) was tested
72 y derivatized with the entire, unfragmented, flunitrazepam molecule, which undergoes a conformational
73 ligand, the coupling can either be positive (flunitrazepam), negative (Ro15-4513), or neutral (flumaz
74 y investigated the effects of clonazepam and flunitrazepam on the development cycle of Calliphora vic
75 ptor agonist baclofen blocks ethanol but not flunitrazepam or pentobarbital potentiation of GABA(A) I
76                    Because the major site of flunitrazepam photoincorporation has been shown to be Hi
77 ARs confirmed that, at subsaturating [GABA], flunitrazepam potentiates alpha6/delta subunit-containin
78 tant 25-32 Hz tremor, which is aggravated by flunitrazepam, reduced rotarod performance, and reduced
79  GABARs, the number of binding sites for [3H]flunitrazepam relative to wild-type receptors was decrea
80  multianalyte self-testing of the main DRDs (flunitrazepam, scopolamine, ketamine) and paracetamol vi
81 GABA ([3H]muscimol), and benzodiazepine ([3H]flunitrazepam) site ligands.
82 kedly alter the affinities of ligands (e.g., flunitrazepam) that are not subtype-selective.
83 ed to the drop-volume (~60 muL) detection of flunitrazepam to a wide range of untreated and undiluted
84 sterically modulated specific binding of [3H]flunitrazepam to differentiated P19 cells.
85 s evaluated by studying the binding of [(3)H]flunitrazepam to GABA(A) receptors at three anatomically
86  also allosterically enhanced the binding of flunitrazepam to mammalian brain GABAA receptors.
87                   However, their response to flunitrazepam was not altered, suggesting that PKCdelta
88 )gamma(2) receptors, whereas the efficacy of flunitrazepam was similar at all three receptor isoforms
89                 Using (3)H-muscimol and (3)H-flunitrazepam we could determine whether the number (B(m
90                     Due to these attributes, flunitrazepam, when is surreptitiously administered to a
91 l moiety, analogous to the 5-phenyl group of flunitrazepam, which are proposed to overlap and interac
92 s of the gamma2 subunit bind the classic BZD flunitrazepam with wild-type affinity, zolpidem affinity