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1 site ligand with binding selectivity at the alpha1 receptor.
2 minals were composed of dispersed, homomeric alpha1 receptors.
3 reduced sensitivity to protons in homomeric alpha1 receptors.
4 atter is mediated in part through adrenergic alpha1 receptors.
5 ed by methoxamine, suggesting involvement of alpha1 receptors.
6 ization mediated by norepinephrine acting on alpha1 receptors.
7 l involvement of noradrenergic alpha2 versus alpha1 receptors.
8 irect coupling to adenylate cyclase, whereas alpha1-receptors act indirectly by influencing the beta-
9 tors and by pertussis toxin, suggesting that alpha1 receptors activate PI 3-kinase via a pertussis to
10 ors activates PI 3-kinase in HVSMCs and that alpha1 receptor-activated PI 3-kinase is associated with
11 hese results demonstrate that stimulation of alpha1 receptors activates PI 3-kinase in HVSMCs and tha
12 motor activity elicited by cocaine involves alpha1 receptor activation within the ventral midbrain.
13 ase activation was blocked by antagonists of alpha1 receptors and by pertussis toxin, suggesting that
14 rotonin depletor), prazosin (PRAZ, selective alpha1-receptor antagonist), WAY-100635 (selective serot
15 endent mechanism, and that these CRF1 and NE alpha1 receptors are highly colocalized on presumptive e
19 tion, cooperative signaling through M(1) and alpha1 receptors could function to induce long-term chan
22 of BAT membranes and recombinant alpha1a and alpha1d receptors expressed in COS-7 cells demonstrated
23 Notable examples include 1) high GABAA and alpha1 receptor expression, which rendered distinctive v
24 t converted picrotoxin inhibition of glycine alpha1 receptors from non-use-facilitated to use-facilit
25 , these peptides increased expression of the alpha1D receptor gene with no change in expression of th
26 may shed light on the different roles of the alpha1 receptors in mediating the neuromodulatory effect
28 emes and found that alpha3 channels resemble alpha1 receptors in their high maximum open probability
29 st that insulin/IGF-I regulate expression of alpha1 receptors in VSMCs and potentially enhance the ef
31 that noradrenergic systems operating through alpha1-receptors in the neuronal chain leading to the LH
33 tion of either muscarinic M(1) or adrenergic alpha1 receptors induces activity- and NMDA receptor-dep
36 The current study examines the influence of alpha1-receptors located within MS on sleep-wake state.
37 ne signaling pathways by which activation of alpha1 receptors may induce mitogenesis in HVSMCs, we ha
39 in 42% of the magnocellular neurons, was an alpha1 receptor-mediated increase in the frequency of EP
40 by local opioid application, suggesting that alpha1-receptor-mediated synaptic inputs in these primar
45 gesting a facilitative presynaptic action at alpha1 receptors on GABAergic axons that innervate hypoc
50 ce mitogenesis in HVSMCs, we have found that alpha1 receptor stimulated-DNA synthesis and activation
53 ha1-adrenergic receptor number; however, the alpha1 receptor subtype involved and the mechanism of up
56 ic to layer 5; we found increased numbers of alpha1 receptor subunit-containing GABAergic synapses de
58 We find that amygdala-specific reduction of alpha1 receptor subunits does not affect mRNA or protein
60 or IGF-I for various times and expression of alpha1 receptors was detected using [3H]prazosin binding
61 unctionally distinct postsynaptic sites from alpha1-receptors, we conclude that only a subset of all
63 ssible to decrease the cutoff in the glycine alpha1 receptor, whereas mutation of Ile-307 and/or Trp-
64 conclude noradrenaline activates ventricular alpha1-receptors, which are specifically coupled via PKC
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