ライフサイエンスコーパス: alpha(1) receptor

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 l involvement of noradrenergic alpha2 versus alpha1 receptors.

7 ization mediated by norepinephrine acting on alpha1 receptors.

8 n this report also had high affinity for the alpha(1) receptor.

9 old selectivity over 5-HT(1A) and adrenergic alpha(1) receptors.

10 irect coupling to adenylate cyclase, whereas alpha1-receptors act indirectly by influencing the beta-

11 tors and by pertussis toxin, suggesting that alpha1 receptors activate PI 3-kinase via a pertussis to

12 ors activates PI 3-kinase in HVSMCs and that alpha1 receptor-activated PI 3-kinase is associated with

13 hese results demonstrate that stimulation of alpha1 receptors activates PI 3-kinase in HVSMCs and tha

14 t, attentional set shifting is improved with alpha(1)-receptor activation, whereas alpha(2)-receptors

15 motor activity elicited by cocaine involves alpha1 receptor activation within the ventral midbrain.

16 ed in a substantial decrease in affinity for alpha(1) receptors and reduction in inhibition of K(+) c

17 ase activation was blocked by antagonists of alpha1 receptors and by pertussis toxin, suggesting that

18 rotonin depletor), prazosin (PRAZ, selective alpha1-receptor antagonist), WAY-100635 (selective serot

19 h vascular and lower urinary tract tone, and alpha(1) receptor antagonists such as terazosin (1b) are

20 endent mechanism, and that these CRF1 and NE alpha1 receptors are highly colocalized on presumptive e

21 ment in sustained attention was abolished by alpha(1)-receptor blockade.

22 alpha1-Receptor blockade resulted in a small decrease in

23 were inhibited by prazosin (10(-6) mol/L, an alpha1-receptor blocker).

24 receptor-associated protein, and the glycine-alpha1 receptor can also be observed.

25 FNE were due largely due to activation of LC alpha(1)-receptors consistent with the known greater den

26 Aff have robust alpha(1)-receptor contraction and beta(1)-receptor dilat

27 tion, cooperative signaling through M(1) and alpha1 receptors could function to induce long-term chan

28 Activation of the alpha1-receptor depolarized whereas alpha2-receptor acti

29 MPOA alpha1-receptors exert similar wake-promoting actions.

30 ngly and in combination to wild-type glycine alpha(1) receptors expressed in Xenopus laevis oocytes.

31 Notable examples include 1) high GABAA and alpha1 receptor expression, which rendered distinctive v

32 t converted picrotoxin inhibition of glycine alpha1 receptors from non-use-facilitated to use-facilit

33 Prior research indicates alpha(1)-receptors impair, whereas alpha(2)-receptors im

34 may shed light on the different roles of the alpha1 receptors in mediating the neuromodulatory effect

35 ine stimulation of DNA synthesis mediated by alpha1 receptors in serum-limited conditions.

36 emes and found that alpha3 channels resemble alpha1 receptors in their high maximum open probability

37 st that insulin/IGF-I regulate expression of alpha1 receptors in VSMCs and potentially enhance the ef

38 Blocking the alpha1-receptor in these cells significantly reduced the

39 that noradrenergic systems operating through alpha1-receptors in the neuronal chain leading to the LH

40 Activation of alpha1 receptors increases dopaminergic neuron burst fir

41 tion of either muscarinic M(1) or adrenergic alpha1 receptors induces activity- and NMDA receptor-dep

42 ard substrate, which primarily expresses the alpha1-receptor isoform.

43 Results show that alpha1-receptors located within MS exert wake-promoting

44 The current study examines the influence of alpha1-receptors located within MS on sleep-wake state.

45 ne signaling pathways by which activation of alpha1 receptors may induce mitogenesis in HVSMCs, we ha

46 Norepinephrine elicited an alpha1 receptor-mediated direct depolarization in 23% of

47 in 42% of the magnocellular neurons, was an alpha1 receptor-mediated increase in the frequency of EP

48 by local opioid application, suggesting that alpha1-receptor-mediated synaptic inputs in these primar

49 These suggest that the alpha1 receptor mediates the TH effects in brain.

50 Both insulin and IGF-I increased alpha1 receptor number; also, these peptides increased e

51 It is hypothesized that the alpha(1)-receptors of the mouse LC are strongly activate

52 tors on afferent nociceptors and stimulatory alpha(1)-receptors on inhibitory peptidergic interneuron

53 gesting a facilitative presynaptic action at alpha1 receptors on GABAergic axons that innervate hypoc

54 d the net effect of coactivation of M(1) and alpha1 receptors on the magnitude of LTD induced.

55 Blockade of the excitatory alpha1-receptor or activation of the inhibitory alpha2-r

56 g tasks, additional studies examined whether alpha(1)-receptors promote sustained attention, similar

57 In wild type alpha1 receptors, PTX inhibited glycine-gated Cl(minus s

58 ce mitogenesis in HVSMCs, we have found that alpha1 receptor stimulated-DNA synthesis and activation

59 To determine directly if activation of alpha1 receptors stimulated PI 3-kinase, in vitro assays

60 These pathways may contribute to alpha1 receptor-stimulated mitogenic responses including

61 Forearm vasoconstrictor responses to direct alpha(1)-receptor stimulation were blunted during exerci

62 ha1-adrenergic receptor number; however, the alpha1 receptor subtype involved and the mechanism of up

63 At least three alpha1 receptor subtypes have been identified by molecul

64 ic to layer 5; we found increased numbers of alpha1 receptor subunit-containing GABAergic synapses de

65 GABA alpha1 receptor subunits are significantly down-regulate

66 We find that amygdala-specific reduction of alpha1 receptor subunits does not affect mRNA or protein

67 (A) receptors and PKCgamma regulates GABA(A) alpha1 receptor trafficking after ethanol exposure.

68 or IGF-I for various times and expression of alpha1 receptors was detected using [3H]prazosin binding

69 unctionally distinct postsynaptic sites from alpha1-receptors, we conclude that only a subset of all

70 and is inhibited by analgesic opioids, only alpha1-receptors were present.

71 ssible to decrease the cutoff in the glycine alpha1 receptor, whereas mutation of Ile-307 and/or Trp-

72 conclude noradrenaline activates ventricular alpha1-receptors, which are specifically coupled via PKC