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 r the application of (+)-tubocurarine and/or gabazine.
2 ed with high and low doses of picrotoxin and gabazine.
3 n(2+), akin to the GABAA receptor antagonist gabazine.
4 neurons treated with the GABA(A) antagonist, gabazine.
5  this was reversed by the GABA(A) antagonist gabazine.
6 reversibly blocked by the GABA(A) antagonist gabazine.
7  to ketamine, by contrast, was unaffected by gabazine.
8 nsitive to antagonism of GABA receptors with gabazine (10 uM) and CGP52432 (2.5 uM) but was blocked b
9 on model of epileptiform activity (10 microM gabazine + 10 microM CGP55845) was occluded by the SK ch
10 y abolished by the GABAA receptor antagonist gabazine (5 muM).
11 e duration of single Put stimulation induced gabazine (a GABA(A) antagonist)-sensitive responses diff
12 MT neurons and contrast them with effects of gabazine, a GABA(A) receptor blocker.
13              In line with this, we show that gabazine, a GABA-A receptor antagonist, is antihyperalge
14                                              Gabazine, a gamma-aminobutyric acid type A (GABA(A)) rec
15     Specific blockade of synaptic IPSCs with gabazine also reduced ISI variability, but only in OT ne
16 etrazol or combined application of 10 microM gabazine and 10 microM CGP55845.
17 ta are consistent with a model in which both gabazine and bicuculline act as allosteric inhibitors of
18 axon based on the actions of focally applied gabazine and GABA near this region.
19 unds are based on the competitive antagonist gabazine and incorporate a variety of photoactive groups
20 endent tonic currents that were resistant to gabazine and inhibited by bicuculline.
21 1 KO in primary sensory neurons (Grin1-cKO), gabazine and strychnine did not affect mEPSC frequency b
22  chloride conductance that is insensitive to gabazine and to picrotoxin and thus not mediated by conv
23 A(A)-R antagonists bicuculline and SR-95531 (gabazine) and increased in frequency and duration by GAB
24 duced than with the non-selective antagonist gabazine, and both were blocked by atropine.
25 e blocked by the GABA(A) receptor antagonist gabazine, and exhibit short-term depression when tested
26 ropic glutamate receptor 5 (mGluR5) prevents gabazine- and strychnine-induced increases in NMDAR-medi
27                     By contrast, exposure to gabazine (antagonist), or knockdown of the GABA-syntheti
28    In all cases, decreases in the CSI during gabazine application were accompanied by an increase in
29 nt with a role for GABAA receptors; however, gabazine, at a concentration that abolished miniature GA
30 e novel synaptic responses were abolished by gabazine, bicuculline, and picrotoxin, three structurall
31 ether the injected (intraperitoneal) dose of gabazine blocked GABAergic inhibitory transmission, we e
32 onversely, the high affinity GABA(A) blocker gabazine blocked I(phasic) without affecting I(tonic).
33         Both types of events were blocked by gabazine, but only outward currents were significantly a
34 , GABA(A)R agonist (muscimol) or antagonist (gabazine), cell proliferation and differentiation into a
35 rtion of IPSPs and EPSPs between control and gabazine conditions.
36               These currents were blocked by gabazine, confirming that they were GABA(A) receptor-med
37 ron firing with the use of GABA-A antagonist gabazine decimated its occurrence.
38 ity by intraocular injections of muscimol or gabazine during this period did not alter the developmen
39                                              Gabazine equally increased neuronal activity, but it wid
40 fferent conditions: control, after gabazine, gabazine followed by strychnine, and strychnine alone.
41 rt a study on the structural determinants of gabazine for binding to (i) the orthosteric binding site
42 ss four different conditions: control, after gabazine, gabazine followed by strychnine, and strychnin
43                         Focal application of gabazine (GBZ) (50 microM) revealed the presence of a 20
44 eration of nuclear Ca(2+) signals induced by gabazine (GBZ) addition, glutamate uncaging in the dendr
45  antagonists bicuculline-methiodide (Bic) or GABAZINE (GBZ) and the chloride channel blocker picrotox
46  that partial blockage of GABAA receptors by gabazine (GBZ) application (10 mum, a concentration that
47                      Moreover, the effect of gabazine (GBZ), a GABA antagonist, was also studied on t
48 born cells survived up to 1 month in the UVN-gabazine group whereas the astroglial population increas
49 left IN and the left MCP, were injected with gabazine (GZ) into the IN to produce SLRs followed by an
50                                     Although gabazine had negligible efficacy as an inhibitor of prop
51 hereas blockade of muscle GABAA receptors by gabazine had opposite effects.
52                         PeF stimulation with gabazine increased blood pressure, phrenic nerve dischar
53                                     Finally, gabazine increased noise correlation of simultaneously r
54                             GABAA antagonist gabazine infusions into the PVN facilitate meningeal-evo
55 cited by 50 microM taurine were abolished by gabazine, insensitive to midazolam, and partially blocke
56                                              Gabazine insensitivity of the rho1 GABACR was highly dep
57                 These results highlight that gabazine interacts with the high-affinity GHB and orthos
58 tion of a GABA(A) antagonist (bicuculline or gabazine) into the CVLM dramatically attenuated the symp
59                                        Thus, gabazine is a competitive antagonist with negligible neg
60             The GABA(A) antagonist SR-95531 (gabazine) is known to block glycine receptors, albeit wi
61 t gabazine or by an injection of an NBQX/CPP/gabazine mixture into the GPe.
62                         Furthermore, neither gabazine nor bicuculline competes for binding at the ste
63 s were recorded after adding strychnine with gabazine or administering strychnine alone, suggesting a
64 application of the GABAA receptor antagonist gabazine or by an injection of an NBQX/CPP/gabazine mixt
65           Blockade of GABA(A) receptors with gabazine or glycine receptors with strychnine potentiate
66 han that in the presence of pentobarbital or gabazine or in resting receptors.
67 demonstrates that, in the presence of either gabazine or picrotoxin (GABA receptor antagonists), many
68 d depolarization persists in the presence of gabazine or tetrodotoxin, indicating a direct action.
69 ry postsynaptic currents, and are blocked by gabazine or tetrodotoxin, indicating an indirect action.
70                     Furthermore, intrathecal gabazine- or strychnine-induced nociceptive hypersensiti
71                                              Gabazine produced an approximately parallel upward shift
72 tal from wild-type GABAA receptors; however, gabazine produced only a partial block of response pento
73 ific competitive GABA(A) antagonist SR95531 (gabazine) reduces phasic inhibition in hippocampal granu
74 ng spontaneous GABAergic synaptic input with gabazine reproduced the effects of silencing PV(+) neuro
75 spontaneously active GABAA receptors mediate gabazine-resistant tonic currents in pyramidal neurons.
76                           Propofol activated gabazine-resistant, bicuculline-sensitive currents when
77 ductance as GABA-activated channels and were gabazine-resistant.
78         In contrast, GABA(A)R blockade using gabazine resulted in a significant decrease in SSA.
79 ted GABAA receptors in pyramidal neurons are gabazine-sensitive, it follows that tonic currents are n
80 57S) gamma 2L subunits, both bicuculline and gabazine showed weak agonist activity and actually poten
81 c IPSPs could be recorded in the presence of gabazine, showing the efficacy of gabazine treatment.
82                                     Although gabazine significantly reduced response reliability, ACh
83 on of alpha(1)H101C located at the BZD-site, gabazine (SR-95531, a GABA binding site antagonist) decr
84 o report opposing effects of bicuculline and gabazine, such that bicuculline surprisingly activated n
85 ic GABA(A)R with intracellular picrotoxin or gabazine, suggesting that Nxph1 is able to recruit or st
86 ining (beta3gamma2) GABAA receptors, whereas gabazine suppressed spontaneous activity in these recept
87 ttenuated by the GABA(A) receptor antagonist gabazine (systemically administered).
88  GABA, mediate tonic current; the failure of gabazine to block tonic current reflects a lack of negat
89                Treatment with bicuculline or gabazine to enhance neuronal activity promotes recruitme
90 resence of gabazine, showing the efficacy of gabazine treatment.
91                               Bicuculline or gabazine (two competitive antagonists of GABA binding) r
92 d the negative efficacies of bicuculline and gabazine using the general anesthetic propofol to direct
93 for the tuberomammillary nucleus (TMN): when gabazine was microinjected directly into the TMN, it att
94 of neurons, GABA(A)R blockers bicuculline or gabazine were applied in addition to iGluR blockers.
95 the competitive GABA(A)R antagonist SR95531 (gabazine), which at high concentrations acts as a partia
96  they affected by the GABAA receptor blocker gabazine, which would be expected if they were polysynap
97 oapplication of GABA or muscimol, but not of gabazine, with MTSES prevented the effect, suggesting th
98  modulation of ccRTN neurons persisted after gabazine without a change in pattern.