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Chemical Compound Review

SKF-38393     2-phenyl-4- azabicyclo[5.4.0]undeca- 7,9,11...

Synonyms: CHEMBL286080, SureCN469578, SKF 38393, R-SK&F 38393, SKF 38393-A, ...
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Disease relevance of SKF 38393


Psychiatry related information on SKF 38393


High impact information on SKF 38393

  • Furthermore, a D1 agonist, SKF 38393, when infused into the renal artery, dose dependently increased sodium excretion in normotensive F2s (n = 3) without altering renal blood flow but was inactive in hypertensive F2s (n = 21) [11].
  • Bilateral infusion of SKF 38393 (7.5 microg/side), a D1/D5 receptor agonist, into the CA1 region of the dorsal hippocampus, enhanced retention of a step-down inhibitory avoidance when given 3 or 6 h, but not immediately (0 h) or 9 h, after training [12].
  • Separate administration of a high dose of a selective D1 (SKF 38393; 20 mg/kg) or D2 (quinpirole; 3 mg/kg) agonist induced Fos-like immunoreactivity in few neurons, whereas combined administration of the D1 and D2 agonists produced patches of intensely stained immunoreactive nuclei in the caudate-putamen [13].
  • The relief from GABAergic inhibition could be reproduced with SKF-38393, a dopamine D1 receptor agonist, and with forskolin, an adenylyl cyclase activator, suggesting that dopamine acts through a cAMP second-messenger pathway [14].
  • In a second experiment, in animals receiving 1 mg/kg SKF-38393 either alone or in combination with 1 mg/kg quinpirole, the level of zif268 mRNA was measured with a double-labeling method in striatal neurons containing enkephalin mRNA, a marker of D2-containing neurons, and in neurons not containing enkephalin, putative D1-containing neurons [15].

Chemical compound and disease context of SKF 38393


Biological context of SKF 38393

  • Current-response curves revealed that the inhibitory responses of CPu neurons to microiontophoretic administration of both the selective D1 receptor agonist SKF-38393 and the selective D2 receptor agonist quinpirole were significantly increased in 6-OHDA-pretreated rats, suggesting up-regulation of both receptor subtypes [21].
  • In situ hybridization using cRNA probes demonstrated that a single injection of SKF 38393 on the last day of gestation induced c-fos gene expression in the fetal hamster SCN and that mRNA for the D1-dopamine receptor was present in the SCN at that time [22].
  • Injections of SKF 38393 (8 mg/kg) were given to pregnant, SCN-lesioned hamsters during the last 5 d of gestation and the phases of the offspring's wheel-running activity rhythms were measured on postnatal day 20 [22].
  • Finally, to examine the second messenger coupling characteristics of the involved D1 receptors, several membrane-permeable analogs of cAMP were tested iontophoretically in place of SKF 38393 [23].
  • The offspring from these treatment groups showed average phases that differed by 11.3 hr, demonstrating that prenatal SKF 38393 set the phase of the offspring's circadian rhythms [22].

Anatomical context of SKF 38393

  • In control (lesioned and treated chronically with saline) rats, the D1 agonist SKF 38393 (5 mg/kg, i.v.) increased 2-DG uptake in the substantia nigra pars reticulata and entopeduncular nucleus ipsilateral to the lesion by 84% and 56%, respectively [24].
  • The reduction in rotational asymmetry caused by the intranigral VM grafts was 64% for SKF 38393 (D1 agonist), 54% for apomorphine (mixed D1 and D2 agonist), and 67% for quinpirole (D2 agonist) when compared to a control spinal cord graft group [25].
  • Increased density of PV-ir GABA interneurons in the ACC at 1 day withdrawal was reproduced in rats repeatedly injected with apomorphine or with SKF-38393 [26].
  • Both dopamine and the D1-selective agonist SKF 38393 inhibited the binding of [3H]SCH 23390 to transfectant cell membranes; the binding of these agonists was sensitive to GTP [27].
  • Treatment of the cortical slices with either SKF-38393, a D1-like agonist, or PDBu, a direct activator of PKC, caused translocation of PKC-betaI from cytosol to membranes in adult but not in old rats [28].

Associations of SKF 38393 with other chemical compounds


Gene context of SKF 38393

  • The D1 agonist SKF 38393 dose-dependently increased AP-1 binding; this effect was significantly increased in reserpine-treated rats and even more markedly enhanced in denervated striatum [34].
  • In a novel environment (open-field) only the highest dose of SKF 38393 used (20 mg/kg) produced significant activation, perhaps due to a ceiling effect in GIRK2 knockout mice [35].
  • The effects of cholecystokinin (CCK) on behavioural responses to the dopamine D1 receptor agonist (+/- )SKF 38393 ((+/- )-2,3,4,5-tetrahydro-7,8- dihydroxy-1-phenyl-1H-3-benzazepine HCl) were studied in the rat [36].
  • Both responses were inhibited by CCK-8S (10-50 micrograms/kg i.p.), but the preferential CCKB receptor agonist CCK-4 (20-100 micrograms/kg i.p.) attenuated SKF 38393-induced grooming only [36].
  • Female ob/ob mice were treated daily at 1 h after light onset with the D(1)/D(2) agonists, SKF-38393 (20 mg/kg) and bromocriptine (15 mg/kg), respectively or vehicle for 2 weeks [37].

Analytical, diagnostic and therapeutic context of SKF 38393

  • In cell-attached patch recordings, bath application of SKF 38393 decreased currents as in whole-cell recordings, whereas quinpirole consistently (6/10) enhanced currents--suggesting that D2-like receptors could act through membrane delimited and non-delimited pathways [38].
  • Perfusion of the ACB for 60 min with the D1-like receptor agonist SKF 38393 (SKF, 1-100 microM) dose-dependently reduced the extracellular levels of DA in the ACB, whereas the extracellular levels of DA in the VTA were not changed [39].
  • RESULTS: We found that intravenous infusion of DA and SKF 38393 caused natriuresis and diuresis in adult rats, but this response was blunted in old rats [40].
  • Direct injection of SKF-38393 (0.5 or 1.5 micrograms/0.5 microliter), a selective D1 receptor agonist, into the striatum through a cannula secured alongside a microdialysis probe produced a rapid dose-dependent transient increase in striatal DA efflux and a more gradual reduction in efflux of DOPAC [41].
  • In contrast, in mesangial cells, enzyme assay and Western blots showed that MAO activity and protein increased by approximately 80% after 48-h incubation with the D(2)-like receptor agonist bromocriptine and quinpirole but not with the D(1)-like receptor agonist SKF-38393 [42].


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  14. Dopamine modulates GABAc receptors mediating inhibition of calcium entry into and transmitter release from bipolar cell terminals in tiger salamander retina. Wellis, D.P., Werblin, F.S. J. Neurosci. (1995) [Pubmed]
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  19. Sensitive and rapid behavioral differentiation of N-methyl-D-aspartate receptor antagonists. Ginski, M.J., Witkin, J.M. Psychopharmacology (Berl.) (1994) [Pubmed]
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  22. Entrainment of the fetal hamster circadian pacemaker by prenatal injections of the dopamine agonist SKF 38393. Viswanathan, N., Weaver, D.R., Reppert, S.M., Davis, F.C. J. Neurosci. (1994) [Pubmed]
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