ライフサイエンスコーパス: SKF-38393

1 ,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol (SKF 38393).

2 line secretion was recorded as low as 500 nM SKF 38393.

3 n calcium transients elicited by the agonist SKF-38393.

4 ed for at least 36 d after repeated doses of SKF-38393.

5 e immediate-early genes c-fos and zif 268 by SKF-38393.

6 lateral intra-PFC infusions of a D1 agonist (SKF 38393; 0.23 microg/side) and antagonist (SCH 23390;

7 gonist and antagonist drugs: Agonists: (+/-)-SKF 38393 ((+/-)-1-phenyl-2,3,4, 5-tetrahydro-(1H)-3-ben

8 Injection of either the D1 agonist SKF 38393 (10 mg/kg) or the D2 antagonist spiperone (0.6

9 ia caused by a dopamine D1 receptor agonist, SKF 38393 (10 mg/kg, s.c.), indicating that it reduces h

10 The selective dopamine D1 receptor agonists SKF 38393 (10 microM) and SKF 81297A (10 microM), but no

11 The D1-like dopamine receptor agonist SKF 38393 (10 microM) depressed the outward IPSC by 43 %

12 ion of the dopamine (DA) D1 receptor agonist SKF-38393 (10 microM) at 2DIV for 3 h also increased (+1

13 The dopamine D1 agonist (SKF-38393, 12.5 mg/kg day) had no significant effect on

14 eated treatment with the D1-receptor agonist SKF-38393 (2 mg/kg/day, 3-14 days) was used to increase

15 he partial D1-dopamine (DA) receptor agonist SKF-38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-

16 als, whilst the dopamine D1 receptor agonist SKF 38393 (30 mg/kg, i.p.) was inactive; however, both d

17 It has been shown that dopamine and SKF 38393, a D1-like receptor agonist, caused inhibition

18 SKF 38393, a selective D1 agonist, had little or no effe

19 To test this, the effects of the D1 agonist SKF 38393 and D2/3 agonist quinelorane were examined on

20 larly, Na,K-ATPase activity was inhibited by SKF 38393 and PDBu in adult but not in old rats.

21 higher in old compared with adult rats, and SKF 38393 and PDBu stimulated PKC activity in adult but

22 The present study demonstrated that SKF 38393 and PDBu, a phorbol ester and protein kinase C

23 Both SKF 38393 and quinelorane stimulated the expression of C

24 ain areas; prazosin, yohimbine, amphetamine, SKF 38393 and SCH 23390 had no effects on cataplexy.

25 Pharmacological analyses, using D1 agonists (SKF 38393 and SKF 81297), a D1 antagonist (SCH 23390), a

26 mixture of the dopamine D1 receptor agonist SKF 38393 and the D2 agonist quinpirole (SKF/Quin) incre

27 raperitoneal administration of selective D1 (SKF 38393) and D2 (quinelorane) dopaminergic receptor ag

28 at least 21 days after repeated dosing with SKF-38393, and were not accompanied by markers of neurod

29 SKF-38393 blocked the MPTP-induced depletion of glutathi

30 SKF-38393, but not, quinpirole significantly reversed th

31 of their rotational response to levodopa or SKF 38393 challenge, but prolonged the duration of quinp

32 receptor (MOR).D1LR stimulation with agonist SKF 38393 concentration-dependently depressed C-fiber-ev

33 mine and subsequent treatment with levodopa, SKF 38393 (D1-preferring dopamine agonist), or quinpirol

34 4 h following mPFC infusion of a D1 agonist (SKF 38393), D1 antagonist (SCH 23390), or a vehicle solu

35 The D1 agonist, SKF-38393, enhanced the number of exocytotic events as d

36 nutes after administration of the D1 agonist SKF 38393, Fos-LI was increased in both the PVN and cAMY

37 Activation of D1 receptors with SKF 38393 had no effect on either the total number of SS

38 SKF-38393 had no effects either on total or monoamine ox

39 Only the D(1) agonist, SKF-38393, had a significant dose-dependent inhibitory e

40 amined a dopaminergic (D1) receptor agonist, SKF-38393 HCl (SKF) for its possible neuroprotective act

41 ,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol (SKF 38393) hydrochloride into pars reticulata of substan

42 Systemic administration of SKF 38393 increased c-fos and zif268 mRNAs in the striat

43 Chronic treatment with SKF 38393 increased NR2A (p<0.0001) but decreased NR2B (

44 rom hair cells, we observed that D1R agonist SKF-38393 increased microphonic potentials, whereas D1R

45 The D1 agonist, 50 microM (+/-) SKF 38393, increased the basal rate of release from the

46 ve D1 antagonist, blocked and attenuated the SKF 38393-induced increase in Fos-LI in the PVN and cAMY

47 acid caused a dose-dependent attenuation of SKF 38393-induced rotation and partially decreased c-fos

48 , and Experiment 3 determined the effects of SKF 38393 injection into a control site.

49 Results indicated that microinjection of SKF 38393 into either the NA or the MPOA facilitates mat

50 e authors examined whether microinjection of SKF 38393 into MPOA was capable of stimulating the onset

51 Infusions of the D1 agonist SKF 38393 into the LBA had no effect.

52 Direct infusion of the D1 receptor agonist SKF-38393 into the prelimbic cortex was found to modulat

53 ncongruent performance following infusion of SKF-38393 into the prelimbic cortex.

54 hese studies are interpreted to suggest that SKF-38393 may prove a valuable drug in the treatment of

55 In adult rats, SKF 38393-mediated phosphorylation was antagonized by SC

56 The actions were neither mimicked by SKF-38393 nor antagonized by SCH-23390 (a selective D1 a

57 However, a 3-h incubation with SKF-38393 on 0DIV slice cultures did not affect PPT mRNA

58 on was mimicked by the selective D1 agonists SKF 38393 or SKF 81297-C and blocked by superfusion with

59 der the partial dopamine D1 receptor agonist SKF 38393 or the opioid antagonist naltrexone.

60 n of the D1/D5-receptor with the agonist (R)-SKF 38393 or the specific antagonist SCH 23390.

61 D1 agonist, SKF-38393 or D2 agonist, LY-171555 (also known as quinpi

62 e of either the dopamine D1 receptor agonist SKF-38393 or the D2 receptor antagonist eticlopride.

63 rrent administration of either a D1 agonist (SKF 38393) or a D1 antagonist (SCH 23390), suggesting th

64 .5 microl/side) of a D1 DA receptor agonist, SKF 38393, or a D2 DA receptor agonist, quinpirole, into

65 rect dopamine D(1) receptor agonist, N-allyl-SKF 38393; or a dopamine reuptake inhibitor, cocaine.

66 8059 or SL327, prior to each priming dose of SKF-38393, prevented the morphological changes associate

67 discernable effects of dopamine, SKF 81297A, SKF 38393, quinpirole, cocaine or amphetamine were obser

68 es were generated with cocaine, desipramine, SKF-38393, quinpirole, SCH-23390, and sulpiride.

69 ation of the ERK signaling pathway in MPC of SKF-38393-sensitized neonate-lesioned rats.

70 ,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol [SKF 38393 (SKF)] hydrochloride nor the D2 agonist (-)-qu

71 The (S, -) SKF 38393 stereoisomer was significantly less effective

72 SKF-38393-stimulated increases were completely blocked b

73 At 36 d, an additional injection of SKF-38393 to sensitized rats restored phospho-ERK to max

74 While the D1-selective agonist SKF 38393 was without effect at a dose of 0.5 nmol/side,

75 In neonate-lesioned, adult rats primed with SKF-38393, we found selective, persistent alterations in

76 Both naltrexone and SKF 38393 were found to attenuate overshadowing; however

77 Furthermore, a D1 agonist, SKF 38393, when infused into the renal artery, dose depe