ライフサイエンスコーパス: TBPS

1 TBPS binding was competitively inhibited by bilobalide i

2 ere was a graded spatial distribution of 35S-TBPS binding; the most dense labeling was in the dorsome

3 Thus, in the IC, the distribution of 35S-TBPS was complementary to that of 3H-strychnine.

4 ribution of GABAA receptors labeled with 35S-TBPS and glycine receptors labeled with 3H-strychnine, G

5 dition of GABA to [3H]flunitrazepam and [35S]TBPS binding assays.

6 were correlated with neurotoxicity and [35S]TBPS displacement, but not with anticonvulsant activity.

7 of [3H]muscimol, [3H]flunitrazepam, and [35S]TBPS to coated vesicles represented 12.3 +/- 1.8%, 7.9 +

8 ([35S]t-butylbicyclophosphorothionate, [35S]TBPS), GABA ([3H]muscimol), and benzodiazepine ([3H]flun

9 to be partial agonists as indicated by [35S]TBPS and Cl- current ratios.

10 to be partial agonists as indicated by [35S]TBPS and Cl- current ratios.

11 s were partial agonists as indicated by [35S]TBPS and Cl- current ratios.

12 r, confirming the results obtained from [35S]TBPS binding.

13 Co 2-1970 inhibited [35S]TBPS binding with limited efficacy (39-65% inhibition) i

14 alpha, 5 alpha-P 57-fold for inhibiting [35S]TBPS binding to alpha 1 beta 1 gamma 2L receptors.

15 on, show limited efficacy in inhibiting [35S]TBPS binding.

16 efficacy for modulating the binding of [35S]TBPS (44% inhibition), [3H]flunitrazepam (41% enhancemen

17 se, i.e., it potentiated the binding of [35S]TBPS at lower concentrations (<=100 nM) and inhibited th

18 was a significant higher inhibition of [35S]TBPS binding (-Emax) by 5alpha-pregnan-3alpha-ol-20-one

19 ined by their potency for inhibition of [35S]TBPS binding in rat brain membranes.

20 potency of 7 nM based on inhibition of [35S]TBPS binding.

21 ed 36Cl(-) influx and GABA reduction of [35S]TBPS binding.

22 a-sterols tested are full inhibitors of [35S]TBPS binding.

23 a-series as determined by inhibition of [35S]TBPS binding.

24 tion of the [3H]flunitrazepam (2 nM) or [35S]TBPS (4 nM) binding by the neurosteroid in any of the br

25 teroid site, inhibiting 96% of specific [35S]TBPS binding and enhancing [3H]flunitrazepam and [3H]mus

26 ewise, GABA displaced nearly all of the [35S]TBPS binding to synaptic membranes but had no effect on

27 of episodic GABA application, picrotoxin and TBPS blocked (by 91 +/- 3% and 85 +/- 5%, respectively)

28 rotoxin and t-butylbicyclophosphorothionate (TBPS) are GABA(A) receptor (GABA(A)R) open channel block

29 sed was 35S-t-butylbicyclophosphorothionate (TBPS) for GABAB receptors, 3H-GABA was used as a ligand

30 d 4 nM [35S]t-butylbicyclophosphorothionate (TBPS) in cerebral cortex, cerebellum, and hippocampus of

31 t, and [35S]t-butylbiocyclophosphorthionate (TBPS), a ligand for GABAA receptor channels.

32 aused a 35% reduction of current blockade by TBPS and reduced [(35)S]TBPS binding by 25%.

33 mma2 receptors exhibited reduced blockade by TBPS current compared to wild-type receptors.

34 From TBPS shift and Cl- current assays, the in vitro efficacy

35 3 beta-substituted derivatives of 2 inhibit TBPS via a single class of binding sites.

36 spontaneous gating reduces accessibility of TBPS to its binding site.

37 The GABA-dependent component of TBPS blockade accounts for the stimulation of [(35)S]TBP

38 GABA application during picrotoxin or TBPS administration enhanced alpha1beta2gamma2 receptor

39 current blockade by TBPS and reduced [(35)S]TBPS binding by 25%.

40 he negative modulation of hippocampal [(35)S]TBPS binding by both GABA and THDOC and increased the en

41 (A)R function and the three phases of [(35)S]TBPS binding seen in the absence and the presence of GAB

42 However, picrotoxin displaceable [(35)S]TBPS binding to alpha1beta2gamma2 GABA(A)Rs occurs in th

43 ckade accounts for the stimulation of [(35)S]TBPS binding to alpha1beta2gamma2 receptors seen with GA

44 inistration to mice and inhibition of [(35)S]TBPS binding to rat whole brain membranes, were compared

45 onal differences in the modulation of [(35)S]TBPS binding, particularly between strata radiatum and s

46 steady-state desensitization reduced [(35)S]TBPS binding.

47 in the GABA-dependent stimulation of [(35)S]TBPS binding.

48 eased binding of the caged-convulsant [(35)S]TBPS to GABA(A) receptors.

49 35)S]t-butylbicyclophosphorothionate ([(35)S]TBPS) and [(3)H]flunitrazepam binding to GABA(A) recepto

50 ors directly, we measured binding of [(35)S]-TBPS to rat cortical membranes.