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1 [D1/D2/D3/D4] and two adrenergic [alpha1 and alpha2] receptors).
2 d kinase) activity via adrenergic alpha1 and alpha2 receptors.
3 he generation of platelets that lack surface alpha2 receptors.
4  of this modulation was due to activation of alpha2 receptors.
5 ell as dopamine D2 and adrenergic alpha1 and alpha2 receptors.
6 rog, i.c.v.), suggesting a mediator role for alpha(2) receptors.
7 findings to indicate that both alpha(1)- and alpha(2)-receptor activation can influence collateral ci
8 n of the alpha1-receptor depolarized whereas alpha2-receptor activation hyperpolarized these neurons
9 nhibitor rapamycin as well as the adrenergic alpha2 receptor agonist clonidine.
10 noradrenergic-receptor antagonists, or of an alpha2-receptor agonist, into the bed nucleus of the str
11                           Interestingly, the alpha2 receptor agonists had no effect on the high K(+)
12 se-dependent manner by brimonidine and other alpha2 receptor agonists, such as medetomidine.
13                Blockade of alpha1 but not of alpha2 receptors also reduced the numbers of S-phase nuc
14 hrine reduced activity at both alpha(1)- and alpha(2)-receptors and enhanced activity at beta(1)- and
15 d and assayed for their affinity at both the alpha2-receptor and the 5-HT uptake site.
16                                          The alpha(2) receptor antagonist, yohimbine (3 microg/microl
17 istered either: (1) saline (sham) or (2) the alpha2-receptor antagonist, RX821002 HCl (2-[2-(2-Methox
18 detomidine was completely blocked by classic alpha2 receptor antagonists, such as yohimbine, rauwolsc
19 mpounds such as 22, 26, 45, and 53 displayed alpha(2) receptor binding in the 10-20 nM range and also
20                   Inhibiting alpha1, but not alpha2, receptors blocked the evoked responses.
21 ol, one group of animals was pretreated with alpha2-receptor blocker, yohimbine, before injection of
22 ng compounds retaining high affinity for the alpha2-receptor but lacking affinity for the 5-HT uptake
23 apamycin along with activation of adrenergic alpha2 receptors by clonidine represents a double-hit to
24 at changes in T, volumes of song nuclei, and alpha(2) receptor densities might regulate seasonal chan
25 1A but lower N-methyl-D-aspartate (NMDA) and alpha2 receptor densities.
26 gly, the ethanol-evoked reduction in the NTS alpha(2)-receptor density in SHRs may explain reported f
27 d with alpha(1)-receptor activation, whereas alpha(2)-receptors exert minimal effects in this task.
28 ed distinctive ventral subdivisions; 2) high alpha2 receptor expression, which rendered distinctive a
29 entify ligand-dependent removal of activated alpha2 receptors from the cell surface as a mechanism by
30  indicating that nimodipine acts through the alpha2 receptor-G(alphai)-coupled pathway.
31       In contrast, blockade of noradrenergic-alpha2 receptors had no effect.
32 indicates alpha(1)-receptors impair, whereas alpha(2)-receptors improve, working memory.
33                 Most importantly, inhibiting alpha(2) receptors in the presence of alpha(1) inhibitio
34 differential involvement of alpha(1)- versus alpha(2)-receptors in these processes.
35                     The levels of cerebellar alpha2 receptors in aggressive AD patients were slightly
36 sed (by approximately 70%) concentrations of alpha2 receptors in the cerebellar cortex compared with
37 nd observed to possess high affinity for the alpha2-receptor (K(i) = 6.71 nM) and the 5-HT uptake sit
38                           We report that the alpha2 receptor-mediated inhibition of presynaptic Ca(2+
39 indings provide the first direct evidence of alpha2 receptor-mediated modulation of L-type Ca(2+) cha
40                                          The alpha2-receptor-mediated current in LSI neurons displaye
41 rat locus ceruleus prolonged the duration of alpha2-receptor-mediated IPSCs even when reuptake was in
42 s precludes definitive classification of the alpha2-receptor-mediated responses into different subtyp
43 t astrocytic laminin, by binding to integrin alpha2 receptor, prevents pericyte differentiation from
44 onsiveness, or is selective for alpha(1)- or alpha(2)-receptors remains unclear.
45 o distinguish between the alpha1, alpha2 and alpha2* receptor responses.
46 nociception (40 microg, i.c.v.), supraspinal alpha(2) receptors seem to mediate the antinociceptive e
47 lcholine receptors; noradrenergic alpha1 and alpha2 receptors; serotonergic 5-HT1A receptors; dopamin
48 ha1-receptor or activation of the inhibitory alpha2-receptor significantly attenuated the analgesia i
49      Similarly, vasoconstrictor responses to alpha(2)-receptor stimulation were blunted during exerci
50 ction, that this involves both alpha(1)- and alpha(2)-receptor subtypes, and that this is graded with
51 chniques to compare the ability of the three alpha2-receptor subtypes to undergo agonist-mediated int
52 udy was to evaluate the GABA(A) alpha(1) and alpha(2) receptor subunit mRNA and protein expression in
53 s in the inhibitory gamma-amino butyric acid alpha2 receptor subunit (GABRA2) gene.
54 ate analysis showed that GABARAP and GABA(A) alpha2 receptor subunit gene expression levels and GAP s
55 elative distribution of GABA(A) alpha(1) and alpha(2) receptor subunits protein or mRNA expression wa
56 he expression levels of GABA(A) alpha(1) and alpha(2) receptor subunits were analyzed using quantitat
57 re, although improgan shows some affinity at alpha(2) receptors, this drug does not act directly at t
58 t this brimonidine effect is mediated by the alpha2 receptor through a reduction of intracellular cAM
59 s insulin secretion by modulating adrenergic alpha2 receptors through the mTOR pathway.
60                    We found that alpha1- and alpha2-receptors were colocalized in the majority of a c
61 nt pooling of noradrenaline activated distal alpha2-receptors, which prolonged the duration of alpha2

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