ライフサイエンスコーパス: DPDPE

1 DPDPE also produced excitatory or biphasic effects.

2 DPDPE attenuated the contrast effect when injected befor

3 DPDPE had little effect on evoked EPSCs.

4 DPDPE had no effect.

5 DPDPE moved the receptor C-tail away from the Gbetagamma

6 DPDPE-induced feeding in the accumbens was significantly

7 DPDPE-induced inhibition was completely blocked by the d

8 ntially all 3H-[D-Pen2,D-Pen5]enkephalin (3H-DPDPE) and 3H-[D-Ala2,D-Glu4]deltorphin (3H-deltorphin-2

9 sponse as well as on brain receptors for [3H]DPDPE were also determined.

10 AR differences in whole-brain homogenate [3H]DPDPE and/or [3H]DELT, but paradoxically not [3H]DAMGO,

11 The delta opioid ligands, [3H]DPDPE (delta 1) and [3H]DSLET (delta 2) were used in qua

12 ng of [3H][d-Ala2]deltorphin II, but not [3H]DPDPE, was also observed in CXBK mice.

13 with deltorphin II decreased the Bmax of [3H]DPDPE by 76 and 87%, respectively.

14 2 or 4 days decreased density (Bmax) of [3H]DPDPE to bind to brain homogenates by 77 and 76%, respec

15 deltorphin II had no effect on the Kd of [3H]DPDPE to bind to brain membranes.

16 of delta 1-opioid receptors labeled with [3H]DPDPE.

17 delta-receptor agonist, enkephalin D-pen2,5 (DPDPE), was without effect on control or on axotomized c

18 by morphine for DOP-/- c.f. WT neurons and a DPDPE-induced decrease of IPSC frequency revealed a role

19 In addition, DPDPE increased BDNF mRNA expression, as measured by in

20 he kappa-agonist U50488 or the delta-agonist DPDPE, was reversed by the mu antagonist CTOP.

21 ith the MOR agonist DAMGO or the DOR agonist DPDPE decreased RGS4 protein by approximately 60% accomp

22 Intra-VTA microinjection of the DOR agonist DPDPE decreases drinking, particularly in low-drinking a

23 The delta opioid receptor (DOR) agonist DPDPE decreases ethanol (EtOH) consumption when injected

24 0488 (3 microM) and the delta opioid agonist DPDPE (1 microM) had no effect.

25 ta-opioid G-protein coupled receptor agonist DPDPE, which reproducibly exhibits subpicomolar binding

26 88H, and the selective delta-opioid agonist, DPDPE.

27 ouse strains, the delta 1 selective agonist, DPDPE, inhibited the A2a-activated adenylyl cyclase but

28 the kappa agonist U50,488 or delta agonists DPDPE or Deltorphin II.

29 GO) and two different delta-opioid agonists (DPDPE or 2-methyl-4a alpha-(3-hydroxyphenyl)-1,2,3,4,4a,

30 hether a variety of peptidic delta agonists, DPDPE, JOM-13, a systemically active derivative of DPDPE

31 er, antinociception induced by U-50,488H and DPDPE was not modified by noribogaine (10-40 mg/kg).

32 nkephalin, PL017 (a mu-receptor agonist) and DPDPE (a delta-receptor agonist) to the ganglion side of

33 ME, DAMGO and DPDPE increased the paired-pulse ratio of IPSCs.

34 This action of DAMGO and DPDPE was attenuated selectively by mu- and delta-opioid

35 Ba2+ current inhibitions by both DAMGO and DPDPE were completely reversed by depolarizing (to > 50

36 The inhibitory actions of DAMGO and DPDPE were reversed by naloxone and/or 7-benzylidenenalt

37 3H]bremazocine (in the presence of DAMGO and DPDPE) respectively.

38 of mu- and delta-opioid agonists (DAMGO and DPDPE, respectively) on GABAergic interneurons in stratu

39 11.5 until birth were treated with DAMGO and DPDPE, respectively, and the ability of these drugs to i

40 ist, antagonized the effect of both DELT and DPDPE.

41 Furthermore, the LPA- and DPDPE-mediated PLC-beta3 phosphorylation was additive an

42 Both DAMGO (1 microM) and DPDPE (1 microM) reversibly inhibited Ba2+ currents (by

43 By comparison, DAMGO, morphine, and DPDPE were found to yield ED50 values of 0.14, 2.4, and

44 d by morphine (60 nmol), DAMGO (1 nmol), and DPDPE (100 nmol), but not by the kappa agonist trans-(1S

45 9593 weakly depressed the EPSC while OFQ and DPDPE had no effect.

46 A time- and DPDPE concentration-dependent and naloxone-reversible in

47 appa- and delta-opioid receptors (U69593 and DPDPE) failed to hyperpolarize RMTg neurons.

48 two antisense probes targeting exon 3 block DPDPE analgesia.

49 /spinal antinociceptive interaction for both DPDPE and DELT were synergistic in all nociceptive tests

50 Activation of the PLC-beta3 by DPDPE was one of the prerequisites for agonist-mediated

51 riments revealed that DOR internalization by DPDPE and SNC-80 was similar, but only DPDPE induced rec

52 increase in BDNF mRNA expression produced by DPDPE were blocked by the delta antagonist naltrindole.

53 on the recovery from contrast was reduced by DPDPE injections administered before nonreinforced presh

54 Binding studies of SL-3111 and [p-ClPhe4]DPDPE on the cloned wild-type and mutated human delta-op

55 s, as well as the synthetic analogues DAMGO, DPDPE, deltorphin and U50488H all were similarly attenua

56 ng micro (DAMGO), kappa (U50488), and Delta (DPDPE) opioid receptor agonists 48 hrs after infection.

57 agonist microinjections [mu (DAMGO), delta (DPDPE), or kappa (U50488H)] and constructed anatomical m

58 ved with the mu agonist DAMGO but not delta (DPDPE) or kappa (U69593) agonists.

59 not phosphorylated in the presence of either DPDPE or LPA.

60 oid agonists, D-pen(2), D-phe(5) enkephalin (DPDPE), and kappa agonist, U50 488, all significantly de

61 D-Penicillamine(2,5)-enkephalin (DPDPE) is a potent opioid peptide that exhibits a high s

62 selective agonist, [D-Pen(2,5)] enkephalin (DPDPE; 1 microM), in combination, manifest a striking fa

63 mpetition with [(3)H][D-Pen(2,5)]enkephalin (DPDPE) for delta-opioid receptors.

64 ta(1) agonist [D-Pen(2),D-Pen(5)]enkephalin (DPDPE) or delta(2) agonist [D-Ala(2),Glu(4)]deltorphin (

65 eceptor with agonist [d-Pen(2,5)]enkephalin (DPDPE) resulted in the rapid phosphorylation of the rece

66 ability of [d-Pen(2), d-Pen(5)]-enkephalin (DPDPE) to inhibit forskolin-stimulated intracellular cAM

67 , delta(1) ([D-Pen(2), D-Pen(5)]-enkephalin (DPDPE)) or delta(2) ([D-Ala(2), Glu(4)]-deltorphin (Delt

68 a-selective agonist [D-Pen(2,5)]-enkephalin (DPDPE), but not by the kappa-selective agonist (+)-(5 al

69 nced the potency of [D-Pen(2,5)]-enkephalin (DPDPE), decreased the potency of [D-Ala(2),D-Leu(5)]-enk

70 OR)-selective agonist [D-Pen2,5] enkephalin (DPDPE) to regulate cAMP levels in spinal cord.

71 ol]enkephalin (DAMGO), [d-Pen2,5]enkephalin (DPDPE), and [d-Ala2]deltorphin II (DELT), selective mu,

72 ioid receptor agonist, [D-Pen2,5]enkephalin (DPDPE), reduced the NMDA-evoked responses of 90% of NS n

73 by the delta agonist [D-Phe2,5]-enkephalin (DPDPE) (1 microM).

74 ioid receptor agonist [D-Pen2,5]-enkephalin (DPDPE) principally inhibited excitatory transmission in

75 lta 1-receptor agonist [D-Pen2,5]enkephalin (DPDPE; 0.05-2 mg/kg), the delta 2-receptor agonist [D-Al

76 onist [D-Ala2-,N-Me-Phe4,Gly-ol] enkephalin (DPDPE; 24 microg/kg).

77 the spinal level, [D-Pen2,D-Pen5]enkephalin (DPDPE) acts also acts through delta2 receptors and all t

78 ability of 24-hr [D-Pen2,D-Pen5]enkephalin (DPDPE) treatment to internalize and down-regulate DORs e

79 ne, U-50,488H and [D-Pen2,D-Pen5]enkephalin (DPDPE) which are mu- kappa- and delta-opioid receptor ag

80 rly (i.c.v.) with [D-Pen2,D-Pen5]enkephalin (DPDPE), a delta 1-opioid receptor agonist (20 micrograms

81 ne, U-50,488H and [D-Pen2,D-Pen5]enkephalin (DPDPE), which are mu-, kappa- and delta-opioid receptor

82 elective agonist [D-Pen2, D-Pen5]enkephalin (DPDPE).

83 halin (DAMGO) and [D-Pen2,D-Pen5]enkephalin (DPDPE).

84 a delta-specific ([D-Pen2,D-Pen5]enkephalin (DPDPE); 0, 30, 50, 62, or 70 nmol), mu-specific ([D-Ala2

85 -selective ligands [D-Pen2,Pen5]-enkephalin (DPDPE) and deltorphin II (1 microM) did not.

86 penicillamine, 5-D-penicillamine]enkephalin (DPDPE) had no effect on these behaviors.

87 D-Ala(2),N-Me-Phe(4),Gly-ol(5)]-enkephalin), DPDPE ([D-Pen2,5]-enkephalin) and bremazocine (in the pr

88 receptor (3H-[D-Pen(2), D-Pen(5)]enkephalin, DPDPE) binding.

89 9 and 139 +/- 5%, respectively; furthermore, DPDPE and deltorphin II (1 microM) inhibited Ca2+ curren

90 drophobic character of the D-Pen residues in DPDPE, which has been found to be extremely important fo

91 of the delta-opioid-selective peptide ligand DPDPE.

92 beta arr1(-/-) MEFs and beta arr2(-/-) MEFs, DPDPE-induced DOR desensitization was significantly redu

93 administration of either DAMGO (2.5 microg), DPDPE (5 microg) or Deltorphin (5 microg).

94 neurons with CTAP followed by brief (10-min) DPDPE exposure.

95 In other neurons, DPDPE also produced facilitation, or inhibition followed

96 efore administration of 400 ng DAMGO, 100 ng DPDPE or 20 microg dynorphin significantly reduced the a

97 microM) and OFQ (100 nM to 1 microM) but not DPDPE (1 microM) were found to depress the amplitude of

98 inhibit [3H]cAMP production, the ability of DPDPE to down-regulate this mutant receptor after 24-hr

99 The inhibitory action of DPDPE was dose dependent (IC50 = 1.6 nM) and was attenua

100 Central administration of DPDPE (delta-selective agonist) and U-50488 (kappa-selec

101 Intraventricular administration of DPDPE also reduced the frequency of paw withdrawal (FPW)

102 JOM-13, a systemically active derivative of DPDPE, deltorphin II, and H-Dmt-Tic-NH-CH2-Bid could pro

103 Galpha(o), rescued the short-term effect of DPDPE after pertussis toxin treatment.

104 In vivo, nor-BNI enhanced the effect of DPDPE and decreased the effect of SNC80 to inhibit PGE(2

105 body augmented the antinociceptive effect of DPDPE in vivo, and the DOR-KOR heteromer agonist 6'-GNTI

106 The effect of DPDPE was specific to PLC-beta3; the betagamma-insensiti

107 /kg), which failed to reverse the effects of DPDPE in 100% (4/4) of neurons, effectively antagonized

108 The effects of DPDPE were antagonized by 7-benzylidenenaltrexone (BNTX,

109 With the exception of DPDPE in the hot plate test, isobolographic analysis rev

110 in DOR likewise resulted in the inability of DPDPE to inhibit [3H]cAMP production, the ability of DPD

111 administered EtOH, although the magnitude of DPDPE-induced inhibition correlated with behavioral meas

112 and beta-arrestin 2 accelerated the rate of DPDPE- but not DAMGO-induced receptor desensitization.

113 altrindole (5'-GNTI) reduced the response of DPDPE both in cultured neurons and in vivo.

114 and has a binding profile similar to that of DPDPE but different from that of (+)-4-[((alphaR)-alpha(

115 on by DPDPE and SNC-80 was similar, but only DPDPE induced recycling.

116 , including mu opioid (DAMGO), delta opioid (DPDPE), GABA(B) (baclofen), cannabinoid CB(1) (WIN 55,21

117 s of the selective delta1 and delta2 opioids DPDPE and [d-Ala2]deltorphin II, respectively, CXBK mice

118 given prior to the injection of U-50,488H or DPDPE did not modify the development of tolerance to the

119 iception of morphine but not of U-50,488H or DPDPE.

120 ociceptive actions of morphine, U-50,488H or DPDPE.

121 , s.c.), U-50,488H (15 or 25 mg/kg, i.p.) or DPDPE (10 microg/mouse, i.c.v.) produced antinociception

122 mg/kg, s.c.), U-50,488H (25 mg/kg, i.p.) or DPDPE (20 microg/mouse, i.c.v.) twice a day for 4 days.

123 Pharmaceutical opioids, in particular DPDPE, did not affect viral replication.

124 that in VTA brain slices from drinking rats DPDPE presynaptically inhibits GABA(A) receptor mediated

125 Retained DPDPE analgesia is also demonstrated upon formalin testi

126 nduced motor impairment have the most robust DPDPE-induced inhibition of GABAAR IPSCs in VTA neurons.

127 tion of kappa- (U69 593) or delta-selective (DPDPE) opioid receptor agonists did not affect IBa.

128 he mu-selective (DAMGO) and delta-selective (DPDPE) opioid receptor agonists, mimicked the effect of

129 Specifically, DPDPE-induced inhibition correlated with predrinking mea

130 rs and all the antisense probes block spinal DPDPE analgesia.

131 ptors responsible for spinal and supraspinal DPDPE analgesia can be discriminated at the molecular le

132 Coincidently, after long-term DPDPE treatment, pertussis toxin treatment eliminated th

133 Here, we demonstrated that DPDPE-induced rapid receptor desensitization, as measure

134 We previously showed that DPDPE inhibition of GABAA receptor-mediated inhibitory p

135 The DPDPE-imprinted polymer showed a broad structure-activit

136 The DPDPE-induced inhibition of excitatory transmission beca

137 8-15 cells with calphostin C could block the DPDPE effect.

138 pholipase C inhibitor U73122 could block the DPDPE effect.

139 ylated, with Ser(363) being critical for the DPDPE-induced phosphorylation of the receptor.

140 e ligands and are in good agreement with the DPDPE-delta opioid receptor "template" model.

141 d delta-opioid peptide ligand [(2S, 3R)-TMT1]DPDPE, a series of small organic peptide mimetic compoun

142 In addition to DPDPE, lysophosphatidic acid (LPA) stimulated the PLC-be

143 DAMGO, modest differences in sensitivity to DPDPE, and no differences in sensitivity to DELT.

144 phine-induced loss of the multiplicative VIP-DPDPE interaction, it does not alter the associated chan

145 nt study investigates whether or not the VIP-DPDPE facilitation of cAMP formation is subject to toler

146 The VIP-DPDPE facilitative interaction was also eliminated by ph

147 or VIP6-28, respectively antagonized the VIP-DPDPE facilitative interaction, as did pertussis toxin t

148 Chronic morphine exposure abolishes the VIP-DPDPE facilitative interaction, consistent with its rele

149 is required for the manifestation of the VIP-DPDPE facilitative interaction, its relevance to opioid

150 of protein kinase C (PKC) reinstates the VIP-DPDPE multiplicative interaction characteristic of opioi

151 tization following exposure to SNC-80, while DPDPE promoted transient receptor interaction with betaa

152 Treatment of mice with DPDPE for 2 or 4 days decreased density (Bmax) of [3H]DP

153 Treatment of mice with DPDPE for 2 or 4 days decreased its analgesic response b

154 lerance that was absent in mice treated with DPDPE.