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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 n of the alpha1-receptor depolarized whereas alpha2-receptor activation hyperpolarized these neurons
7           Dexmedetomidine (DEX), a selective alpha2 receptor (adra2a) agonist, is an important drug u
8 nhibitor rapamycin as well as the adrenergic alpha2 receptor agonist clonidine.
9 tested whether developmental exposure to the alpha2 receptor agonist guanfacine, which is commonly us
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 d and assayed for their affinity at both the alpha2-receptor and the 5-HT uptake site.
15 istered either: (1) saline (sham) or (2) the alpha2-receptor antagonist, RX821002 HCl (2-[2-(2-Methox
16 detomidine was completely blocked by classic alpha2 receptor antagonists, such as yohimbine, rauwolsc
17                   Inhibiting alpha1, but not alpha2, receptors blocked the evoked responses.
18 ol, one group of animals was pretreated with alpha2-receptor blocker, yohimbine, before injection of
19 ng compounds retaining high affinity for the alpha2-receptor but lacking affinity for the 5-HT uptake
20 apamycin along with activation of adrenergic alpha2 receptors by clonidine represents a double-hit to
21 1A but lower N-methyl-D-aspartate (NMDA) and alpha2 receptor densities.
22 ed distinctive ventral subdivisions; 2) high alpha2 receptor expression, which rendered distinctive a
23 entify ligand-dependent removal of activated alpha2 receptors from the cell surface as a mechanism by
24  indicating that nimodipine acts through the alpha2 receptor-G(alphai)-coupled pathway.
25       In contrast, blockade of noradrenergic-alpha2 receptors had no effect.
26                     The levels of cerebellar alpha2 receptors in aggressive AD patients were slightly
27 sed (by approximately 70%) concentrations of alpha2 receptors in the cerebellar cortex compared with
28 nd observed to possess high affinity for the alpha2-receptor (K(i) = 6.71 nM) and the 5-HT uptake sit
29 vel strategy combining a conditional GABA(A) alpha2 receptor knockout mouse with optogenetics.
30                           We report that the alpha2 receptor-mediated inhibition of presynaptic Ca(2+
31 indings provide the first direct evidence of alpha2 receptor-mediated modulation of L-type Ca(2+) cha
32                                          The alpha2-receptor-mediated current in LSI neurons displaye
33 rat locus ceruleus prolonged the duration of alpha2-receptor-mediated IPSCs even when reuptake was in
34 s precludes definitive classification of the alpha2-receptor-mediated responses into different subtyp
35 t astrocytic laminin, by binding to integrin alpha2 receptor, prevents pericyte differentiation from
36 o distinguish between the alpha1, alpha2 and alpha2* receptor responses.
37 lcholine receptors; noradrenergic alpha1 and alpha2 receptors; serotonergic 5-HT1A receptors; dopamin
38 ha1-receptor or activation of the inhibitory alpha2-receptor significantly attenuated the analgesia i
39 chniques to compare the ability of the three alpha2-receptor subtypes to undergo agonist-mediated int
40 s in the inhibitory gamma-amino butyric acid alpha2 receptor subunit (GABRA2) gene.
41 ate analysis showed that GABARAP and GABA(A) alpha2 receptor subunit gene expression levels and GAP s
42 acting on the same population of channels as alpha2 receptors, suggesting close apposition of both re
43 t this brimonidine effect is mediated by the alpha2 receptor through a reduction of intracellular cAM
44 s insulin secretion by modulating adrenergic alpha2 receptors through the mTOR pathway.
45                    We found that alpha1- and alpha2-receptors were colocalized in the majority of a c
46 nt pooling of noradrenaline activated distal alpha2-receptors, which prolonged the duration of alpha2