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 zation of the mu-selective endogenous opioid endomorphin-1 (EM-1) via an array of nuclear magnetic re

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

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

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

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

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

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

25 neurons were enhanced by naturally occurring endomorphin-1 and -2 opioid peptides, indicating a role

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

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

28 (3)S)Tyr and -Trp were incorporated into the endomorphin-1 chain (EM-1) and into model tripeptides by

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

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

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

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

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

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

35 Infusion of endomorphin-1 internalized MOR.

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

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

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

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

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

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

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

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

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

45 The effects of endomorphin 2 were qualitatively similar.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 lates, including enalaprilat, perindoprilat, endomorphin-2 and isoniazid, and subjected to biological

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

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

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

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

69 The endomorphin-2 derivative displayed increased activity at

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

86 f bilorphin and the strongly arrestin-biased endomorphin-2 with the MOPr indicate distinct receptor i

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

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

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

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

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

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

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

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

95 The endomorphins are endogenous opioids with high affinity a

96 Endomorphins are endogenous peptides that have high affi

97 Endomorphins are opioid tetrapeptides that have high aff

98 The endomorphins are recently discovered endogenous agonists

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

100 (i) complexes, including beta-endorphin- and endomorphin-bound muOR, deltorphin-bound deltaOR, dynorp

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

102 odeled exposure to opiates (u-opioid agonist endomorphin), cannabinoids (WIN 55,212-2), alcohol (etha

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

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

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

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

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

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

109 was immunolocalized in cells that express an endomorphin-like peptide implicated in cell signaling an

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

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

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

113 Endomorphins potentiated sustained ASIC currents in both

114 Endomorphins produce analgesia; however, their role in o

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

116 The endomorphins represent a novel group of endogenous opioi

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

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

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

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