1                                  Exposure to D-Ala(2)-D-Leu(5) enkephalin (100 nM) for 90 s induced i

2 lective agonists [D-Pen2,D-Pen5]enkephalin, [D-Ala2,D-Leu5]enkephalin, and [D-Ser2,Leu5]enkephalin-Th

3 n5]enkephalin, [D-Ser2,Leu5]enkephalin-Thr, [D-Ala2,D-Leu5]enkephalin, and etorphine treatments also

4 e delta opioid receptor, exposure to 100 nM [D-Ala2,D-Leu5]enkephalin causes internalization of the r

5 , treatment of neurons with the DOR agonist [d-Ala(2), d-Leu(5)]-enkephalin (DADLE) caused a decrease

6 nkephalin (DPDPE), decreased the potency of [D-Ala(2),D-Leu(5)]-enkephalin (DADLE), and decreased the

7 ilar decreases in cAMP levels in response to D-Ala2, D-Leu5, enkephalin (DADLE).

8            The DOR agonists, deltorphin and [D-Ala2, D-Leu5]-enkephalin (DADLE), elevated [Ca2+]i, me

9 ptin and the delta-opioid receptor agonist, [D-ala2, D-leu5]-enkephalin (DADLE), while a minority of

10   [D-Ala2,Phe4,Gly5-ol]-enkephalin (DAMGO), [D-Ala2,D-Leu5]-enkephalin (DADLE), trans-(+/-)-3,4-dichl

11 thanol consumption on cyclic AMP (cAMP) and [D-Ala2,D-Leu5]enkephalin (DADLE) inhibition of forskolin

12  binds Gbetagamma (QEHA, 1 mM) decreased the D-Ala(2)-D-Leu(5) enkephalin-evoked response.

13 s of DOR agonists ([D-Pen2,5]-enkephalin or [D-Ala2, D-Leu5]-enkephalin) on BK (10 microm)/prostaglad

14                                 Addition of [D-Ala2, D-Leu5]-enkephalin or [D-Pen2,D-Pen5]-enkephalin