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1  site ligand with binding selectivity at the alpha1 receptor.
2 l involvement of noradrenergic alpha2 versus alpha1 receptors.
3 minals were composed of dispersed, homomeric alpha1 receptors.
4 gns with the differential involvement of PFC alpha1 receptors.
5  reduced sensitivity to protons in homomeric alpha1 receptors.
6 atter is mediated in part through adrenergic alpha1 receptors.
7 ed by methoxamine, suggesting involvement of alpha1 receptors.
8 ization mediated by norepinephrine acting on alpha1 receptors.
9 n this report also had high affinity for the alpha(1) receptor.
10 old selectivity over 5-HT(1A) and adrenergic alpha(1) receptors.
11 irect coupling to adenylate cyclase, whereas alpha1-receptors act indirectly by influencing the beta-
12 tors and by pertussis toxin, suggesting that alpha1 receptors activate PI 3-kinase via a pertussis to
13 ors activates PI 3-kinase in HVSMCs and that alpha1 receptor-activated PI 3-kinase is associated with
14 hese results demonstrate that stimulation of alpha1 receptors activates PI 3-kinase in HVSMCs and tha
15 t, attentional set shifting is improved with alpha(1)-receptor activation, whereas alpha(2)-receptors
16  motor activity elicited by cocaine involves alpha1 receptor activation within the ventral midbrain.
17 ed in a substantial decrease in affinity for alpha(1) receptors and reduction in inhibition of K(+) c
18  effect, retains the ability to inhibit both alpha(1)-receptor and RyR2, thereby suppressing contract
19 ase activation was blocked by antagonists of alpha1 receptors and by pertussis toxin, suggesting that
20                                 Prazosin, an alpha(1) receptor antagonist, reduced moderate alcohol i
21 rotonin depletor), prazosin (PRAZ, selective alpha1-receptor antagonist), WAY-100635 (selective serot
22 h vascular and lower urinary tract tone, and alpha(1) receptor antagonists such as terazosin (1b) are
23 endent mechanism, and that these CRF1 and NE alpha1 receptors are highly colocalized on presumptive e
24 ment in sustained attention was abolished by alpha(1)-receptor blockade.
25                                              alpha1-Receptor blockade resulted in a small decrease in
26 were inhibited by prazosin (10(-6) mol/L, an alpha1-receptor blocker).
27 receptor-associated protein, and the glycine-alpha1 receptor can also be observed.
28 FNE were due largely due to activation of LC alpha(1)-receptors consistent with the known greater den
29                              Aff have robust alpha(1)-receptor contraction and beta(1)-receptor dilat
30 tion, cooperative signaling through M(1) and alpha1 receptors could function to induce long-term chan
31                            Activation of the alpha1-receptor depolarized whereas alpha2-receptor acti
32  we observed similar levels of expression of alpha(1) receptor-encoding mRNA across the subregions of
33                                         MPOA alpha1-receptors exert similar wake-promoting actions.
34 ngly and in combination to wild-type glycine alpha(1) receptors expressed in Xenopus laevis oocytes.
35   Notable examples include 1) high GABAA and alpha1 receptor expression, which rendered distinctive v
36 t converted picrotoxin inhibition of glycine alpha1 receptors from non-use-facilitated to use-facilit
37                     Prior research indicates alpha(1)-receptors impair, whereas alpha(2)-receptors im
38 may shed light on the different roles of the alpha1 receptors in mediating the neuromodulatory effect
39 ine stimulation of DNA synthesis mediated by alpha1 receptors in serum-limited conditions.
40 emes and found that alpha3 channels resemble alpha1 receptors in their high maximum open probability
41 st that insulin/IGF-I regulate expression of alpha1 receptors in VSMCs and potentially enhance the ef
42                                 Blocking the alpha1-receptor in these cells significantly reduced the
43 that noradrenergic systems operating through alpha1-receptors in the neuronal chain leading to the LH
44                                Activation of alpha1 receptors increases dopaminergic neuron burst fir
45 tion of either muscarinic M(1) or adrenergic alpha1 receptors induces activity- and NMDA receptor-dep
46 ard substrate, which primarily expresses the alpha1-receptor isoform.
47                            Results show that alpha1-receptors located within MS exert wake-promoting
48  The current study examines the influence of alpha1-receptors located within MS on sleep-wake state.
49 ne signaling pathways by which activation of alpha1 receptors may induce mitogenesis in HVSMCs, we ha
50                   Norepinephrine elicited an alpha1 receptor-mediated direct depolarization in 23% of
51  in 42% of the magnocellular neurons, was an alpha1 receptor-mediated increase in the frequency of EP
52 by local opioid application, suggesting that alpha1-receptor-mediated synaptic inputs in these primar
53                       These suggest that the alpha1 receptor mediates the TH effects in brain.
54             Both insulin and IGF-I increased alpha1 receptor number; also, these peptides increased e
55                  It is hypothesized that the alpha(1)-receptors of the mouse LC are strongly activate
56 tors on afferent nociceptors and stimulatory alpha(1)-receptors on inhibitory peptidergic interneuron
57 gesting a facilitative presynaptic action at alpha1 receptors on GABAergic axons that innervate hypoc
58 d the net effect of coactivation of M(1) and alpha1 receptors on the magnitude of LTD induced.
59                                     However, alpha1 receptors only contributed to MPH-induced improve
60                   Blockade of the excitatory alpha1-receptor or activation of the inhibitory alpha2-r
61                                We found that alpha(1) receptors potentiate CeA GABAergic (gamma-amino
62 g tasks, additional studies examined whether alpha(1)-receptors promote sustained attention, similar
63                                 In wild type alpha1 receptors, PTX inhibited glycine-gated Cl(minus s
64  contrasts with the impairing actions of PFC alpha1 receptors reported previously for working memory.
65 ce mitogenesis in HVSMCs, we have found that alpha1 receptor stimulated-DNA synthesis and activation
66       To determine directly if activation of alpha1 receptors stimulated PI 3-kinase, in vitro assays
67             These pathways may contribute to alpha1 receptor-stimulated mitogenic responses including
68  Forearm vasoconstrictor responses to direct alpha(1)-receptor stimulation were blunted during exerci
69 ha1-adrenergic receptor number; however, the alpha1 receptor subtype involved and the mechanism of up
70                               At least three alpha1 receptor subtypes have been identified by molecul
71 ic to layer 5; we found increased numbers of alpha1 receptor subunit-containing GABAergic synapses de
72 the effects of a progressive loss of GABA(A) alpha(1)-receptor subunits and up-regulation of alpha(2/
73                                         GABA alpha1 receptor subunits are significantly down-regulate
74  We find that amygdala-specific reduction of alpha1 receptor subunits does not affect mRNA or protein
75 (A) receptors and PKCgamma regulates GABA(A) alpha1 receptor trafficking after ethanol exposure.
76 or IGF-I for various times and expression of alpha1 receptors was detected using [3H]prazosin binding
77                  Moreover, activation of PFC alpha1 receptors was sufficient to improve sustained att
78 unctionally distinct postsynaptic sites from alpha1-receptors, we conclude that only a subset of all
79  and is inhibited by analgesic opioids, only alpha1-receptors were present.
80 ssible to decrease the cutoff in the glycine alpha1 receptor, whereas mutation of Ile-307 and/or Trp-
81 conclude noradrenaline activates ventricular alpha1-receptors, which are specifically coupled via PKC