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1                                              DADLE reduced cAMP production by 70% (IC50 of approximat
2 d with sham-EA using a delta-opioid agonist, DADLE, decreased BP (n = 6).
3             Co-application of nociceptin and DADLE to neurons that were responsive to both agonists,
4 ot affect the efficacy of VGCC inhibition by DADLE.
5 a containing 1 mg/kg D-Ala2-Leu5-enkaphalin (DADLE), which mimics natural hibernation, or preperfusio
6 DOR agonist [d-Ala(2), d-Leu(5)]-enkephalin (DADLE) caused a decrease in the membrane abundance of DO
7 e potency of [D-Ala(2),D-Leu(5)]-enkephalin (DADLE), and decreased the potency and efficacy of 4-[(R)
8        Exposure to D-Ala2-E-Leu5 enkephalin (DADLE) (1 microM) for 30 min completely desensitized NG1
9 s in response to D-Ala2, D-Leu5, enkephalin (DADLE).
10 ic AMP (cAMP) and [D-Ala2,D-Leu5]enkephalin (DADLE) inhibition of forskolin-stimulated cAMP productio
11  deltorphin and [D-Ala2, D-Leu5]-enkephalin (DADLE), elevated [Ca2+]i, measured by flow cytofluoromet
12 ephalin (DAMGO), [D-Ala2,D-Leu5]-enkephalin (DADLE), trans-(+/-)-3,4-dichloro-N-methyl-N-(2-[1-pyrrol
13 ceptor agonist, [D-ala2, D-leu5]-enkephalin (DADLE), while a minority of cells (approximately 30%) we
14  the agonist D-alanine-5-leucine-enkephalin (DADLE) in wild-type and T149A mutant-expressing clones.
15    In contrast, [D-pen2, L-Pen5] enkephalin (DADLE, 1.0 nmol), a delta-opioid selective agonist, and
16                        ARPE-19 cells express DADLE uptake activity that is inhibited by small peptide
17                                 Furthermore, DADLE hearts demonstrated better histological ultrastruc
18 nkephalin analogue, Try-D-Ala-Gly-Phe-D-Leu (DADLE).
19  with BK resulted in more than twice as many DADLE responsive neurons (54%) but did not affect the ef
20 ion of delta-opioid receptors with 10 microM DADLE reduced glutamate-induced injury by almost half as
21            Desensitization induced by 100 nM DADLE was overcome by a higher concentration of DADLE (1
22  and pertussis toxin inhibited the action of DADLE.
23 LE was overcome by a higher concentration of DADLE (100 microM).
24                                The effect of DADLE (1 microM) was blocked by the mu-antagonist D-Phe-
25 reatment on the maximum inhibitory effect of DADLE on forskolin-stimulated cAMP formation following b
26                  Additionally, the effect of DADLE on forskolin-stimulated cAMP production was determ
27 ochemical properties, the cyclic prodrugs of DADLE, [Ala2,D-Leu5]-Enk, [D-Ala2,Leu5]-Enk, and [Ala2,L
28 t important factor to manipulate the rate of DADLE release and, thus, the pharmacological activity; p
29  the parent peptide to assure the release of DADLE by specific enzymes.
30 d gradually over 25 min following washout of DADLE.
31 y the uptake of the synthetic opioid peptide DADLE ((H-Tyr-D-Ala-Gly-Phe-D-Leu-OH) and by its suscept
32  (OMCA) cyclic prodrug of the opioid peptide DADLE ([D-Ala2,D-Leu5]-Enk, H-Tyr-D-Ala-Gly-Phe-D-Leu-OH
33 alization either in the presence of peptide (DADLE) or alkaloid (etorphine) agonist.
34 ses H8 (1 microM) for 45 min did not prevent DADLE-induced desensitization.
35 tely desensitized NG108-15 cells to a second DADLE-induced response.
36 w substantial down-regulation upon long term DADLE treatment.
37        Patch-clamp experiments revealed that DADLE inhibited voltage-gated Ca(2+) channels (VGCCs) in
38                                          The DADLE IC50 was unaffected by ethanol treatment.
39  receptor antagonist, completely blocked the DADLE protective effect.
40 d bradykinin failed to cross-desensitize the DADLE-evoked response, although both agonists mobilized
41 MP (0.1 mM) for 30 min did not influence the DADLE-induced increases in [CA2+]i.
42 ure to PdBu (1 microM) failed to prevent the DADLE-induced desensitization in NG108-15 cells.
43 y 30%) were selectively responsive either to DADLE or to nociceptin, but not both.
44  surface upon prolonged exposure (2-48 h) to DADLE.
45 and 5) delta-opioid receptor activation with DADLE increased GABA(A)Ralpha and GlyRalpha1 density in
46 consumption were significantly improved with DADLE pretreatment vs. all groups after storage and refl
47 cs natural hibernation, or preperfusion with DADLE, administered for 15 min at 2 mmol, 25 min prior t
48 emonstrates that hibernation protection with DADLE is beneficial for prolonged cardiac storage.

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