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1  site ligand with binding selectivity at the alpha1 receptor.
2 minals were composed of dispersed, homomeric alpha1 receptors.
3 gns with the differential involvement of PFC alpha1 receptors.
4  reduced sensitivity to protons in homomeric alpha1 receptors.
5 atter is mediated in part through adrenergic alpha1 receptors.
6 ed by methoxamine, suggesting involvement of alpha1 receptors.
7 ization mediated by norepinephrine acting on alpha1 receptors.
8 l involvement of noradrenergic alpha2 versus alpha1 receptors.
9 irect coupling to adenylate cyclase, whereas alpha1-receptors act indirectly by influencing the beta-
10 tors and by pertussis toxin, suggesting that alpha1 receptors activate PI 3-kinase via a pertussis to
11 ors activates PI 3-kinase in HVSMCs and that alpha1 receptor-activated PI 3-kinase is associated with
12 hese results demonstrate that stimulation of alpha1 receptors activates PI 3-kinase in HVSMCs and tha
13  motor activity elicited by cocaine involves alpha1 receptor activation within the ventral midbrain.
14 ase activation was blocked by antagonists of alpha1 receptors and by pertussis toxin, suggesting that
15 rotonin depletor), prazosin (PRAZ, selective alpha1-receptor antagonist), WAY-100635 (selective serot
16 endent mechanism, and that these CRF1 and NE alpha1 receptors are highly colocalized on presumptive e
17                                              alpha1-Receptor blockade resulted in a small decrease in
18 were inhibited by prazosin (10(-6) mol/L, an alpha1-receptor blocker).
19 receptor-associated protein, and the glycine-alpha1 receptor can also be observed.
20 tion, cooperative signaling through M(1) and alpha1 receptors could function to induce long-term chan
21                            Activation of the alpha1-receptor depolarized whereas alpha2-receptor acti
22                                         MPOA alpha1-receptors exert similar wake-promoting actions.
23 of BAT membranes and recombinant alpha1a and alpha1d receptors expressed in COS-7 cells demonstrated
24   Notable examples include 1) high GABAA and alpha1 receptor expression, which rendered distinctive v
25 t converted picrotoxin inhibition of glycine alpha1 receptors from non-use-facilitated to use-facilit
26 , these peptides increased expression of the alpha1D receptor gene with no change in expression of th
27 may shed light on the different roles of the alpha1 receptors in mediating the neuromodulatory effect
28 ine stimulation of DNA synthesis mediated by alpha1 receptors in serum-limited conditions.
29 emes and found that alpha3 channels resemble alpha1 receptors in their high maximum open probability
30 st that insulin/IGF-I regulate expression of alpha1 receptors in VSMCs and potentially enhance the ef
31                                 Blocking the alpha1-receptor in these cells significantly reduced the
32 that noradrenergic systems operating through alpha1-receptors in the neuronal chain leading to the LH
33                                Activation of alpha1 receptors increases dopaminergic neuron burst fir
34 tion of either muscarinic M(1) or adrenergic alpha1 receptors induces activity- and NMDA receptor-dep
35 ard substrate, which primarily expresses the alpha1-receptor isoform.
36                            Results show that alpha1-receptors located within MS exert wake-promoting
37  The current study examines the influence of alpha1-receptors located within MS on sleep-wake state.
38 ne signaling pathways by which activation of alpha1 receptors may induce mitogenesis in HVSMCs, we ha
39                   Norepinephrine elicited an alpha1 receptor-mediated direct depolarization in 23% of
40  in 42% of the magnocellular neurons, was an alpha1 receptor-mediated increase in the frequency of EP
41 by local opioid application, suggesting that alpha1-receptor-mediated synaptic inputs in these primar
42                       These suggest that the alpha1 receptor mediates the TH effects in brain.
43             The distributions of alpha1B and alpha1D receptor mRNA expression in rat brain have been
44                  Increased expression of the alpha1D receptor mRNA was inhibited by the receptor tyro
45             Both insulin and IGF-I increased alpha1 receptor number; also, these peptides increased e
46 gesting a facilitative presynaptic action at alpha1 receptors on GABAergic axons that innervate hypoc
47 d the net effect of coactivation of M(1) and alpha1 receptors on the magnitude of LTD induced.
48                                     However, alpha1 receptors only contributed to MPH-induced improve
49                   Blockade of the excitatory alpha1-receptor or activation of the inhibitory alpha2-r
50  mRNA in BAT but did not alter expression of alpha1d receptors or mRNA.
51                                 In wild type alpha1 receptors, PTX inhibited glycine-gated Cl(minus s
52  contrasts with the impairing actions of PFC alpha1 receptors reported previously for working memory.
53 ce mitogenesis in HVSMCs, we have found that alpha1 receptor stimulated-DNA synthesis and activation
54       To determine directly if activation of alpha1 receptors stimulated PI 3-kinase, in vitro assays
55             These pathways may contribute to alpha1 receptor-stimulated mitogenic responses including
56 ha1-adrenergic receptor number; however, the alpha1 receptor subtype involved and the mechanism of up
57 t these peptides increased expression of the alpha1D receptor subtype in these cells.
58                               At least three alpha1 receptor subtypes have been identified by molecul
59 ic to layer 5; we found increased numbers of alpha1 receptor subunit-containing GABAergic synapses de
60                                         GABA alpha1 receptor subunits are significantly down-regulate
61  We find that amygdala-specific reduction of alpha1 receptor subunits does not affect mRNA or protein
62 (A) receptors and PKCgamma regulates GABA(A) alpha1 receptor trafficking after ethanol exposure.
63 or IGF-I for various times and expression of alpha1 receptors was detected using [3H]prazosin binding
64                  Moreover, activation of PFC alpha1 receptors was sufficient to improve sustained att
65 unctionally distinct postsynaptic sites from alpha1-receptors, we conclude that only a subset of all
66  and is inhibited by analgesic opioids, only alpha1-receptors were present.
67 ssible to decrease the cutoff in the glycine alpha1 receptor, whereas mutation of Ile-307 and/or Trp-
68 conclude noradrenaline activates ventricular alpha1-receptors, which are specifically coupled via PKC