ライフサイエンスコーパス: etorphine

1 n cortex and thalamus, with the exception of etorphine.

2 rally distinct opioid alkaloids morphine and etorphine.

3 are exposed to saturating concentrations of etorphine.

4 detectable within 10 min in the presence of etorphine.

5 ta-endorphin(1-27) prevents these effects of etorphine.

6 y efficacious agonists, such as fentanyl and etorphine.

7 Cotreatment with a subanalgesic dose of etorphine (10 ng/kg) was equally effective as NTX in enh

8 Mice were treated for 7 days with etorphine (200 microg/kg/day infusion) or morphine (40 m

9 endocytosis in the presence of alkaloid drug etorphine, a potent agonist of mu, delta, and kappa opio

10 the presence of peptide (DADLE) or alkaloid (etorphine) agonist.

11 In contrast, agonists such as etorphine and fentanyl activated ERKs in a beta-arrestin

12 Although both etorphine and morphine effectively activate the mu OR, o

13 Therefore, we examined etorphine and morphine effects on regulation of GRK-2 an

14 sibility that unequal receptor regulation by etorphine and morphine might be due to differential regu

15 Both etorphine and morphine produced significant tolerance (E

16 ns) as well as by the alkaloid agonist drugs etorphine and morphine.

17 ephalin (ME), [D-Ser2,Leu5,Thr6]-enkephalin, etorphine, and [D-Ala2,N-Me-Phe4,Gly-ol5]enkephalin incr

18 sts conducted over a 192-h period, morphine, etorphine, and buprenorphine administered before elicita

19 the hypothesis that the mu-opioids morphine, etorphine, and buprenorphine would produce significant s

20 hr and the nonselective opioids levorphanol, etorphine, and ethylketocyclazocine were found to desens

21 ng and desensitization were observed: 1) ME, etorphine, and methadone resulted in both receptor desen

22 one after long-term treatment with morphine, etorphine, and methadone, three agonists reported to hav

23 the opioid antagonist naloxone, the agonist etorphine, and other hydrophobic ligands enhanced cell s

24 peritoneal injection of the alkaloid agonist etorphine, and this process was blocked by the antagonis

25 l for G protein-dependent signaling, such as etorphine- and morphine-mediated inhibition of adenylyl

26 ression of GRIN1 resulted in the increase in etorphine- and non-morphine-induced neurite outgrowth in

27 In addition to the potent agonist action of etorphine at mu-, delta- and kappa-inhibitory opioid rec

28 zed after activation by the alkaloid agonist etorphine but not after activation by morphine.

29 cated within the lipid raft domains, whereas etorphine, but not morphine, induced the translocation o

30 Enkephalins and etorphine cause opioid receptors to internalize rapidly

31 Neither U50,488H nor etorphine caused down-regulation of the rat kappa-opioid

32 lls treated with 10 microM concentrations of etorphine, DAMGO, beta-endorphin, morphine, and butorpha

33 Etorphine decreased spinal muOR density by approximately

34 ficant down-regulation of the hkor, although etorphine did not.

35 Individual opiates, such as morphine and etorphine, differ both in their ability to promote physi

36 In the presence of Ba2+, pM-nM etorphine elicited dose-dependent increases, instead of

37 Morphine and etorphine elicited quantitatively similar chemotaxis, bu

38 orphine effectively activate the mu OR, only etorphine elicits robust mu OR phosphorylation followed

39 The ultra-potent opioid analgesic, etorphine, elicits naloxone-reversible, dose-dependent i

40 full agonists sufentanil, dihydroetorphine, etorphine, etonitazine, and [D-Ala2, MePhe4, Glyol5]enke

41 down-regulation by full agonists; DAMGO and etorphine exhibited approximately 80% internalization, w

42 lation and receptor desensitization, whereas etorphine, fentanyl, and [D-Ala2,N-Me-Phe4,Gly5-ol]-enke

43 Phosphorylation blockage made etorphine, fentanyl, and DAMGO function as morphine in t

44 verexpressing dominant-negative GRK2 enabled etorphine, fentanyl, and DAMGO to activate PKCepsilon.

45 ng Ser363, Thr370 and Ser375 to Ala) enabled etorphine, fentanyl, and DAMGO to use the PKCepsilon pat

46 tion in the affinity of [3H]diprenorphine or etorphine for the receptor or the potency of etorphine t

47 binding in membranes with the rank order of etorphine > DAMGO = beta-endorphin > morphine > butorpha

48 ds examined, efficacy decreased in the order etorphine >> morphine > fentanyl = oxymorphine > butorph

49 Higher concentrations of etorphine (> nM) not only increased gK but, in addition,

50 rast to minimal neurite outgrowth induced by etorphine in control neuroblastoma N2A cells, overexpres

51 ronic treatment with extremely high doses of etorphine in vivo.

52 sence of Ba2+ However, low concentrations of etorphine, in contrast to all other opioids tested, decr

53 Etorphine increased ( approximately 70%) DYN-2 protein a

54 Both morphine and etorphine induce tolerance; however, only etorphine prod

55 quantitatively similar chemotaxis, but only etorphine induced receptor internalization.

56 t alter the magnitude of either morphine- or etorphine-induced adenylyl cyclase superactivation.

57 Etorphine-induced desensitization of cell surface recept

58 Etorphine-induced down-regulation evoked an elevation of

59 ioid receptor is not an obligatory event for etorphine-induced down-regulation of the receptor.

60 horylation, whereas beta-arrestin-dependent, etorphine-induced ERK phosphorylation required MOR to tr

61 ernalization, but it partially inhibited the etorphine-induced MOR endocytosis.

62 The etorphine-induced MOR translocation required the dissoci

63 The magnitude of etorphine-induced phosphorylation of this mutant recepto

64 betaFNA significantly increased the rate of etorphine-induced receptor desensitization.

65 raperitoneal injection of the opiate agonist etorphine, intense MOR-IR was present in vesicle-like st

66 Etorphine is an non-selective opioid receptor agonist wi

67 sely, beta2 receptors in these cells undergo etorphine-mediated endocytosis.

68 slices with subsaturating concentrations of etorphine, methadone, oxymorphone, or beta-CNA also redu

69 Cotreatment of these neurons with pM NTX or etorphine not only results in marked enhancement of the

70 )triphosphate binding, whereas the effect of etorphine on GTP binding cannot be inhibited by naltrind

71 This weak excitatory agonist action of etorphine on non-mu-/delta-/kappa-opioid receptor functi

72 ncubation with a saturating concentration of etorphine or morphine at 37 degrees C for 30 min failed

73 nd etorphine induce tolerance; however, only etorphine produces mu-opioid receptor (muOR) down-regula

74 ethylketocyclazocine, or tifluadom, but not etorphine, promoted receptor internalization.

75 ) shift = 7.6- and 7.3-fold for morphine and etorphine, respectively).

76 tions of naloxone (NLX), naltrexone (NTX) or etorphine selectively antagonize excitatory, but not inh

77 ent with GM1 ganglioside or pertussis toxin, etorphine shows excitatory agonist action on non-mu-/del

78 or the clinical use of ultra-low-dose NTX or etorphine so as to increase the antinociceptive potency

79 potent inhibitory APD-shortening effects of etorphine still occur in DRG neurons tested in the prese

80 e same mutant exhibits naltrindole-sensitive etorphine-stimulated [35S]guanosine-5'-O-(3-thio)triphos

81 Moreover, U50,488H or etorphine stimulation of the rat kappa receptor, which d

82 ion of GRK2 or GRK2 and arrestin-2 permitted etorphine to induce down-regulation of the hkor, althoug

83 etorphine for the receptor or the potency of etorphine to inhibit forskolin-stimulated adenylyl cycla

84 ptor down-regulation associated with chronic etorphine treatment may accelerate dynamin-related activ

85 Chronic etorphine treatment resulted in a time-dependent down-re

86 de of adenylyl cyclase superactivation after etorphine treatment was identical to that observed with

87 imilar to that of wild type MOR after 4 h of etorphine treatment.

88 kephalin-Thr, [D-Ala2,D-Leu5]enkephalin, and etorphine treatments also caused a pronounced internaliz

89 In addition, etorphine, which did not promote human kappa receptor in