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1  independent, suggesting bupropion is not an open channel blocker.
2 n-channel noise, as expected for a fast-type open channel blocker.
3  involve the voltage-dependent release of an open channel blocker.
4  tail of the beta4 subunit acts as a classic open-channel blocker.
5 les are known to inhibit the PD by acting as open channel blockers.
6 onate (TBPS) are GABA(A) receptor (GABA(A)R) open channel blockers.
7  has been generally assumed that they act as open-channel blockers.
8 ine, and philanthotoxin are weakly permeable open-channel blockers.
9 out a prepulse was completely blocked by the open channel blocker, (+)-5-methyl-10,11-dihydro-5H-dibe
10 ore, and this is also the site at which many open channel blockers affect Kv channels.
11                                        Using open channel blockers as tool compounds and a combinatio
12 that polyamines do not only act as classical open channel blockers as was previously thought.
13                  Both Kvbeta subunits act as open channel blockers at physiological membrane potentia
14  suggested that quinidine acts as a cationic open-channel blocker at a site in the internal mouth of
15  these data suggest that amiloride and other open channel blockers bind to sites revealed during the
16 ridine derivative quinacrine act directly as open channel blockers, but can act indirectly as well.
17                                           An open-channel blocker can protect several of these cystei
18                               We studied the open-channel blockers disopyramide and flecainide, and t
19             Chlorisondamine, an irreversible open channel blocker for nnAChRs, caused a time-dependen
20 he activation gate in the VSD is unknown and open channel blockers for VSDs have not yet been identif
21 several D1 ligands act as voltage-dependent, open-channel blockers for NMDA receptors, regardless of
22 nto the future design of kinetically tunable open-channel blockers for the AChR.
23 ive magnitude of the dissociation rate of an open-channel blocker from the open but blocked channel (
24 -dependent phosphorylation, inhibited by the open-channel blocker glibenclamide.
25           However, quinacrine, a fluorescent open-channel blocker, has been recently shown to bind to
26     Our results suggest that PhTX acts as an open channel blocker; however, provided that the toxin r
27 receptors exhibits the characteristics of an open-channel blocker: (i) no competition with agonists,
28 using MK-801, an N-methyl-D-aspartate (NMDA) open channel blocker, implicates glutamate receptors in
29                             Experiments with open channel blockers indicate that the potentiation inv
30         Modelling Mg2+ as an impermeant fast open channel blocker indicated that external Mg2+ blocke
31         Modelling Ni2+ as an impermeant slow open channel blocker indicated that Ni2+ blocked the por
32     Moving the positive charge also restored open-channel blocker interactions that are lost in K95Q.
33 e tolbutamide because weak (i.e., fast-type) open channel blockers introduce brief events into multic
34                                   Other NMDA open channel blockers ketamine and memantine showed a si
35 nsitized state, suggesting that at least one open-channel blocker might act allosterically outside th
36 y synaptic activation in the presence of the open channel blocker MK-801 did not impair the AP5-sensi
37 rge transfer in the presence of NMDA and the open channel blocker MK-801, indicating an increased num
38 uring block of NMDA-elicited currents by the open channel blocker MK-801, indicating increased number
39 g the rate of block of NMDA receptors by the open channel blocker MK-801, we confirmed that the initi
40 anced charge transfer in the presence of the open channel blocker MK-801.
41 ns using fast-application techniques and the open channel blocker MK-801.
42 rs on cultured hippocampal neurons using the open-channel blockers (+)-MK-801 and ketamine to tag syn
43 cts as a relatively non-discriminatory rapid open channel blocker of all types of high voltage-activa
44 Using the rate of EPSC block by IEM-1460, an open channel blocker of Ca(2+)-permeable AMPARs, we prop
45                            Using a selective open channel blocker of CP-AMPARs, IEM-1460, we estimate
46        Exposure to 10 or 25 uM ivabradine-an open channel blocker of HCNs-for 24 h resulted in a dose
47                               Ketamine is an open channel blocker of ionotropic glutamatergic N-Methy
48  Dofetilide acts as a slow-onset/slow-offset open channel blocker of this current at nanomolar concen
49       This suggests that glibenclamide is an open-channel blocker of CFTR.
50 Argiope lobata, is a potent but nonselective open-channel blocker of ionotropic glutamate (iGlu) rece
51         KV beta subunits also function as an open-channel blocker of KV channels.
52              The effects of the irreversible open-channel blocker of N-methyl-D-aspartate receptors,
53  We conclude that PhTX-343 mainly acts as an open-channel blocker of nAChRs with strong subtype selec
54 ine toxins from spiders and wasps are potent open-channel blockers of ionotropic glutamate (iGlu) rec
55 CMS include cholinergic agonists, long-lived open-channel blockers of the acetylcholine receptor ion
56                                              Open-channel blockers of the nicotinic acetylcholine rec
57 sis approaches, we identified citrate as an "open channel blocker" of AtALMT9 and used this tool to e
58 ribe a class of small molecules which act as open channel blockers on the Hv1 VSD and find that a hig
59 d to exhibit differential sensitivity to the open channel blockers phencyclidine and dizolcipine (MK-
60 ogenous neurotransmitter L-glutamate and the open-channel blocker picrotoxin.
61  a partial agonist, but can be blocked by an open channel blocker, picrotoxin.
62            Thus, beta4 may be the endogenous open-channel blocker responsible for resurgent kinetics.
63  channels are dilating, and as a consequence open channel blockers such as amiloride are allowed deep
64 f ketamine not shared by other NMDA receptor open-channel blockers such as memantine and represent pr
65 ibition; this effect was largely occluded by open-channel blockers, suggesting that lidocaine binding
66  are clinically useful NMDA receptor (NMDAR) open channel blockers that inhibit NMDARs with similar p
67  by MK801 (dizocilpine hydrogen maleate), an open channel blocker, this potentiation was attributable
68                 Treatment with quinidine, an open-channel blocker used to treat the human disorder, r
69 ubstituted cysteine accessibility method and open channel blockers, we found that the M3 segment form
70           Because alcohols apparently act as open-channel blockers, we infer from our results that mo
71 petitive NMDA antagonists, more specifically open channel blockers, which may be alternatives to high
72 interpreted as deoxycholic acid acting as an open-channel blocker, which may relate to deoxycholic ac
73 potential and/or Memantine, an NMDA receptor open channel blocker, would reduce noise-induced loss of