ライフサイエンスコーパス: endomorphin

1 the opioids released by veratridine were not endomorphins.

2 ost selective endogenous MOR ligands are the endomorphins.

3 Endomorphin 1 (10, 30, 100 nmol/kg) administered intrave

4 endogenous mu-opioid receptor (MOR) agonists endomorphin 1 (EM1) and 2 (EM2) were tested for their ca

5 n, the endogenous kappa receptor agonist) or endomorphin 1 (EM1, the endogenous mu receptor agonist)

6 The distributions of endomorphin 1 (Tyr-Pro-Trp-Phe-NH2; EM1) and endomorphin

7 (POMC), the precursor to beta-endorphin, and endomorphin 1 and 2 on sectioned rat forebrain revealed

8 Endomorphin 1 and 2 were below the detection limit of th

9 dia and attenuated the hypotensive effect of endomorphin 1.

10 ed the bradycardia and hypotension caused by endomorphin 1.

11 tment, whereas a few agonists, in particular endomorphins 1 and 2, display apparent bias toward arres

12 The endogenous opioid peptide endomorphin-1 (1) was modified by attachment of lactose

13 affinity mu opioid receptor (MOR) agonists, endomorphin-1 (E-1) and -2 (E-2), modulate ASIC currents

14 Light microscopic studies have shown that endomorphin-1 (EM-1) -containing fibers are distributed

15 tracerebroventricular (i.c.v.) injections of endomorphin-1 (EM-1) and endomorphin-2 (EM-2) in the rat

16 morphine and the endogenous opioid peptides, endomorphin-1 (EM-1) and endomorphin-2 (EM-2), on mu opi

17 Endomorphin-1 (EM-1) is a recently isolated endogenous p

18 The present study examined the effect of endomorphin-1 (EM1), an endogenous opioid with a high af

19 Endomorphin-1 (EM1), in contrast to several other mu opi

20 A series of diastereoisomers of endomorphin-1 (EM1, Tyr(1)-Pro(2)-Trp(3)-Phe(4)-NH(2)) h

21 Endomorphin-1 (Tyr-Pro-Trp-Phe-NH(2); EM1) and endomorph

22 and isolation from brain of such a peptide, endomorphin-1 (Tyr-Pro-Trp-Phe-NH2), which has a high af

23 Endomorphin-1 and -2 (EM1, EM2) are endogenous opioids w

24 We suggested that the endomorphins (endomorphin-1 and -2) might be biased toward arrestin re

25 Therefore, because the potencies of endomorphin-1 and endomorphin-2 to elicit internalizatio

26 inuous exposure of the cloned mu receptor to endomorphin-1 did not diminish the subsequent ability of

27 g-Phe, and the putatively endogenous peptide endomorphin-1 displayed particularly distinct bias profi

28 g the 60 min of observation, indicating that endomorphin-1 does not induce rapid desensitization of t

29 Bilateral administration of endomorphin-1 in the globus pallidus of rats induced oro

30 u-opioid receptors, the behavioral effect of endomorphin-1 in the globus pallidus was blocked by the

31 have investigated the behavioral effects of endomorphin-1 in the globus pallidus, a brain region tha

32 Infusion of endomorphin-1 internalized MOR.

33 provides no support for the hypothesis that endomorphin-1 modulates the consolidation of conditioned

34 hat the highly selective mu receptor agonist endomorphin-1 modulates the expression of conditioned de

35 vation induced by the endogenous MOR agonist endomorphin-1, and a cross-antagonism, by which a MOR an

36 in the rat VTA induced by local infusion of endomorphin-1, demonstrating a key role of MOR-Gal1R het

37 Gly-N-Met-Phe-glycinol-enkephalin (DAMGO) or endomorphin-1, into the medial preoptic nucleus attenuat

38 riene E4, Lysopc(20:4), 5-methoxytryptamine, Endomorphin-1, Lysopc(20:3)) were good prediction for th

39 We find that the magnitude of spinal endomorphin 2 (EM2) antinociception not only varies with

40 endomorphin 1 (Tyr-Pro-Trp-Phe-NH2; EM1) and endomorphin 2 (Tyr-Pro-Phe-Phe-NH2; EM2) in the rat cent

41 ously showed that intrathecal application of endomorphin 2 [EM2; the highly specific endogenous mu-op

42 The effects of endomorphin 2 were qualitatively similar.

43 maximally effective concentration), but not endomorphin-2 (0.6 mM; an endogenous ligand for micro -o

44 austively stereodiversified library based on endomorphin-2 (1) to discover mu opioid receptor (MOR) l

45 previously reported that microinjections of endomorphin-2 (E-2; an endogenous mu-receptor agonist) i

46 d-Pro2-endomorphin-2 (ED50=0.05 microg) was more potent than en

47 in-2 (ED50=0.05 microg) was more potent than endomorphin-2 (ED50=30 microg) in significantly increasi

48 functional domains of the endogenous opioid endomorphin-2 (EM-2) and the tachykinin SP, respectively

49 c.v.) injections of endomorphin-1 (EM-1) and endomorphin-2 (EM-2) in the rat brain to determine the s

50 us opioid peptides, endomorphin-1 (EM-1) and endomorphin-2 (EM-2), on mu opioid receptor (MOR) intern

51 activity of a constrained cyclic analogue of endomorphin-2 (EM-2: Tyr-Pro-Phe-Phe-NH(2)) and related

52 Endomorphin-2 (EM-2: Tyr-Pro-Phe-Phe-NH(2)) is an endoge

53 We show that endomorphin-2 (EM2), an arrestin-biased ligand for micro

54 re and after systemic administration of EM1, endomorphin-2 (EM2), DAMGO, and morphine in the consciou

55 domorphin-1 (Tyr-Pro-Trp-Phe-NH(2); EM1) and endomorphin-2 (Tyr-Pro-Phe-Phe-NH(2); EM2) have been loc

56 immunoreactive for the endogenous MOR ligand endomorphin-2 (Tyr-Pro-Phe-Phe-NH2) (EM-2) have been rep

57 A second peptide, endomorphin-2 (Tyr-Pro-Phe-Phe-NH2), which differs by on

58 The tetrapeptide, endomorphin-2 (Tyr-Pro-Phe-PheNH2) possesses high affini

59 -Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO) and endomorphin-2 activated inwardly rectifying K(+) current

60 or l-Pro, a more metabolically-stable d-Pro2-endomorphin-2 analog should produce longer analgesic act

61 e exists for functional interactions between endomorphin-2 and MOR1.

62 ercising muscle and evoke a pressor reflex), endomorphin-2 and naloxone resulted in a significantly g

63 A small proportion of these endomorphin-2 axons contained MOR1, but many of the dend

64 ts by [N-Phe(1)]-nociceptin-(1-13)-NH(2) and endomorphin-2 by naloxone, was not due to some nonspecif

65 el of pharmacological agonism confirmed that endomorphin-2 had a much lower operational efficacy for

66 idase IV plays a role in the inactivation of endomorphin-2 in vivo, and thereby modulates its central

67 However, endomorphin-2 induced faster desensitization of the K(+)

68 anatomical data support the hypothesis that endomorphin-2 is a ligand for MORs in the trigeminal dor

69 Together, these results indicate that endomorphin-2 is an arrestin-biased agonist at MOPr and

70 Endomorphin-2 is present in high density in the spinal a

71 sia elicited by either endomorphin-2, d-Pro2-endomorphin-2 or Ala-Pyrrolidonyl-2-nitrile returned aft

72 d MOR1, but many of the dendritic targets of endomorphin-2 terminals contained MOR1.

73 , because the potencies of endomorphin-1 and endomorphin-2 to elicit internalization were unaffected

74 ason for this is likely to be the ability of endomorphin-2 to induce greater phosphorylation of MOPr

75 cells stably expressing MOPr, the ability of endomorphin-2 to induce phosphorylation of Ser375 in the

76 We confirmed the localization of endomorphin-2 to unmyelinated axons and axon terminals i

77 Consistent with previous studies, endomorphin-2 was contained primarily in dense core vesi

78 The present study found that endomorphin-2 was degraded approximately twice as fast t

79 , by dipeptidyl peptidase IV, whereas d-Pro2-endomorphin-2 was totally resistant to this enzyme's act

80 If endomorphin-2 were an endogenous ligand for the MOR1, we

81 slices with a micro-opioid receptor agonist (endomorphin-2, 100 nM).

82 , N-MePhe(4), Gly-ol(5)]-enkephalin (DAMGO), endomorphin-2, and morphine in rat and mouse locus coeru

83 ail-flick test, analgesia elicited by either endomorphin-2, d-Pro2-endomorphin-2 or Ala-Pyrrolidonyl-

84 ia, and potentiated the analgesic actions of endomorphin-2, particularly on the tail-flick test.

85 estigated this phenomenon in more detail for endomorphin-2, using endogenous MOPr in rat brain as wel

86 , has been described which should potentiate endomorphin-2-induced analgesia.

87 ociceptin, while it did block the effects of endomorphin-2.

88 The naturally occurring endomorphins are also released by primary afferents unde

89 The endomorphins are endogenous opioids with high affinity a

90 Endomorphins are endogenous peptides that have high affi

91 Endomorphins are opioid tetrapeptides that have high aff

92 The endomorphins are recently discovered endogenous agonists

93 It was concluded that the endomorphins attenuated the HCVR only in large doses, we

94 hese findings have uncovered a novel role of endomorphins by which the opioids can enhance the lactic

95 The results support the idea that some endomorphin-containing neurons in the hypothalamus proje

96 study demonstrates that, like morphine, the endomorphins down-regulate mu opioid receptors in a dose

97 Endomorphins (EM-1 and EM-2) are selective, high affinit

98 We suggested that the endomorphins (endomorphin-1 and -2) might be biased towa

99 These results suggest a novel role for endomorphins in modulating ASIC function to effect lacti

100 examined the modulation of ASIC currents by endomorphins in sensory neurons from rats with freely pe

101 The endomorphin-mediated potentiation was a result of a left

102 t-enkephalin and alpha-neoendorphin, but not endomorphins or beta-endorphin.

103 The neuroanatomical results suggest that endomorphins participate in modulating nociceptive and a

104 Endomorphins potentiated sustained ASIC currents in both

105 Endomorphins produce analgesia; however, their role in o

106 eflexively increases mean arterial pressure; endomorphin release is also increased under inflammatory

107 The endomorphins represent a novel group of endogenous opioi

108 ne, while administration of APETx2 inhibited endomorphin's enhancing effect in both groups.

109 summary, EA may induce release of endogenous endomorphins that activate mu opioid receptors in GABAne

110 Thus, endogenous enkephalins and endomorphins, thought to be released during noxious peri

111 morphin (DERM), deltorphin (DELT), TIPP, and endomorphin were conjugated to BODIPY TR or Alexa Fluor