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1 s blocked by the GABA(A) receptor antagonist bicuculline methiodide.
2 gamma-aminobutyric acid (GABA)A antagonist, bicuculline methiodide.
3 ol/side), or the GABA(A) receptor antagonist bicuculline methiodide (12.5 pmol/side) before being sub
5 ivity in NL neurons and can be eliminated by bicuculline methiodide, a potent antagonist for GABAA re
6 a dose-dependent fashion by muscimol, GABA, bicuculline methiodide, and bicuculline (in order of pot
7 clamide plus the GABA(A) receptor antagonist bicuculline methiodide (BIC) before performance of a hyp
8 atively, application of the GABAA antagonist bicuculline methiodide (BIC) shortened expirations and c
9 nfusions of the GABA(A) receptor antagonist, bicuculline methiodide (BIC), in nine freely moving maca
10 s blocked by competitive GABA(A) antagonists bicuculline-methiodide (Bic) or GABAZINE (GBZ) and the c
11 llularly and to apply the GABA(A) antagonist bicuculline methiodide (BICM) into the vicinity of the c
12 ) and selective GABA(A) receptor antagonist, bicuculline methiodide (BMI) (100 ng), were administered
13 rats were challenged with microinjections of bicuculline methiodide (BMI) (25 ng) or vehicle (artific
14 injection of the GABA(A) receptor antagonist bicuculline methiodide (BMI) 10 pmol (100 nl)(-1) into t
15 inistration of the GABAA receptor antagonist bicuculline methiodide (BMI) also cause rapid enlargemen
16 c synaptic currents, which are eliminated by bicuculline methiodide (BMI) but not glutamate receptor
17 at by blockade of local GABAA receptors with bicuculline methiodide (BMI) elicits cardiovascular chan
18 injection of the GABA(A) receptor antagonist bicuculline methiodide (BMI) into the RP evoked increase
19 n of the DMH by unilateral microinjection of bicuculline methiodide (BMI) on Fos expression in select
20 hibition in spatial tuning, we iontophoresed bicuculline methiodide (BMI) onto functionally character
21 tical and brief arterial infusions of either bicuculline methiodide (BMI) or 4-aminopyridine (4AP).
22 roinjection of the GABAA receptor antagonist bicuculline methiodide (BMI) or the E A A receptor agoni
23 istration of the GABA(A) receptor antagonist bicuculline methiodide (BMI) resulted in increased plasm
26 stimulation of the PVN by microinjection of bicuculline methiodide (BMI), a gamma-aminobutyric acid
27 e GABA(A) receptor antagonists picrotoxin or bicuculline methiodide (BMI), and had longer decay time
30 luid (aCSF; 100 nl) or the GABAA antagonist, bicuculline methiodide (BMI; 50 pmol in 100 nl) and thei
31 diffusion of the GABA(A) receptor antagonist bicuculline methiodide from the tip of a glass recording
34 when locally administered concurrently with bicuculline methiodide, had no further effect on the fir
40 of -77 mV and were blocked by application of bicuculline methiodide or picrotoxin, indicating that th
41 and fluoxetine, whereas the GABAA antagonist bicuculline methiodide potentiated the effect of CRH and
42 ic acid type A (GABA(A)) receptor antagonist bicuculline methiodide within the dentate gyrus abolishe
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