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Chemical Compound Review

Eticloprida     5-chloro-3-ethyl-N-[[(2S)-1...

Synonyms: Eticlopride, Eticlopridum, CHEMBL8946, FLB-131, BSPBio_000864, ...
 
 
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Disease relevance of Eticlopride

  • However, METH-induced hyperthermia was also blocked by alphaMT and eticlopride [1].
  • The effect was counteracted by the D(2) antagonist eticlopride, pertussis toxin, the inhibitor of intracellular Ca(2+) release TMB-8, incubation in Ca(2+)-free experimental medium, and PKC desensitization obtained by chronic pretreatment with the phorbol ester TPA [2].
  • Studies in the male rat have shown that the dopamine D-2 receptor antagonists sulpiride and eticlopride, produce a dose-dependent prevention of the hypothermia induced by the D-1/D-2 receptor agonist apomorphine and the relatively selective D-2 agonist pergolide in the rat [3].
 

Psychiatry related information on Eticlopride

 

High impact information on Eticlopride

  • A dose-dependent increase in the state of phosphorylation of DARPP-32 occurred in mouse striatum after systemic administration of the D(2) receptor antagonist eticlopride (0.1-2.0 mg/kg) [8].
  • The eticlopride-induced increase in DARPP-32 phosphorylation was also decreased by pretreatment with the D(1) receptor antagonist SCH 23390 (0.125 and 0.25 mg/kg) and completely reversed by combined pretreatment with SCH 23390 (0.25 mg/kg) plus SCH 58261 (10 mg/kg) [8].
  • The neuroleptic drug eticlopride, a highly selective D(2) receptor antagonist, blocked the quinpirole-induced phosphorylation of MAPK and CREB [9].
  • In wild type mice, this induction is completely abolished by pretreatment with the D(1)-selective antagonist SCH23390, and pretreatment with the D(2)-like receptor antagonist eticlopride reduces the levels of c-fos expressed in response to D(1) receptor stimulation [10].
  • The same effect is observed using eticlopride, a selective dopamine D2 receptor antagonist [11].
 

Chemical compound and disease context of Eticlopride

 

Biological context of Eticlopride

 

Anatomical context of Eticlopride

 

Associations of Eticlopride with other chemical compounds

  • In contrast, pretreatment with the dopaminergic D1-like antagonist SCH 23390 (0.005-0.02 mg/kg) or the D2-like antagonist eticlopride (0.03-0.3 mg/kg) produced a dose-dependent attenuation of caffeine-produced reinstatement at doses that did not decrease cocaine self-administration [23].
  • Moreover, the ability of haloperidol and eticlopride to stimulate phosphorylation at both seryl residues is prevented by treatment with SL327, a compound that blocks activation of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) [24].
  • The D2 receptor antagonist eticlopride did not appear to alter the METH effect, but this was difficult to determine because eticlopride decreased NPY levels by itself [25].
  • Because the pharmacology of NMDA receptors depends on the incorporation of different NR2 subunits and NR2 subunits show regional and cellular differences in their expression in striatum, our study examined whether different NMDA receptor antagonists would have differential effects on eticlopride-induced immediate early gene expression in striatum [17].
  • Groups of rats were injected with a single dose of either isotonic saline or eticlopride (0.5 mg/kg i.p.) and killed at various time intervals ranging from 5 min to 24 h and frozen brain sections processed by in situ hybridization histochemistry [21].
 

Gene context of Eticlopride

  • Differential effects of N-methyl-D-aspartate receptor blockade on eticlopride-induced immediate early gene expression in the medial and lateral striatum [17].
  • We then examined a potential interaction of glucocorticoid receptor with central dopamine in pair bonding by treating females with i.c.v. dopamine receptor antagonists (haloperidol, SCH23390, or eticlopride) prior to peripheral administration of RU-486 [26].
  • Eticlopride-induced c-fos and zif268 mRNA expression in striatum was not blocked by H-89 [27].
  • To test whether other signaling pathways are involved in eticlopride-mediated gene induction, we also infused inhibitors of the mitogen-activated and calcium/calmodulin-dependent protein kinases into animals and then treated them with eticlopride [27].
  • Eticlopride-induced Fos occurred only in pallidal neurons projecting to the striatum, providing functional evidence for pallidostriatal cells without axon collaterals to other nuclei [28].
 

Analytical, diagnostic and therapeutic context of Eticlopride

References

  1. Methamphetamine-induced rapid decrease in dopamine transporter function: role of dopamine and hyperthermia. Metzger, R.R., Haughey, H.M., Wilkins, D.G., Gibb, J.W., Hanson, G.R., Fleckenstein, A.E. J. Pharmacol. Exp. Ther. (2000) [Pubmed]
  2. Dopamine D(2) receptor-induced COX-2-mediated production of prostaglandin E(2) in D(2)-transfected Chinese hamster ovary cells without simultaneous administration of a Ca(2+)-mobilizing agent. Hellstrand, M., Eriksson, E., Nilsson, C.L. Biochem. Pharmacol. (2002) [Pubmed]
  3. Apomorphine and pergolide induce hypothermia by stimulation of dopamine D-2 receptors. Ogren, S.O., Fuxe, K. Acta Physiol. Scand. (1988) [Pubmed]
  4. Effects of dopamine D1- or D2-like receptor antagonists on the hypermotive and discriminative stimulus effects of (+)-MDMA. Bubar, M.J., Pack, K.M., Frankel, P.S., Cunningham, K.A. Psychopharmacology (Berl.) (2004) [Pubmed]
  5. The effects of eticlopride on Morris water task performance in male and female rats neonatally treated with quinpirole. Brown, R.W., Thompson, K.N., Click, I.A., Best, R.A., Thacker, S.K., Perna, M.K. Psychopharmacology (Berl.) (2005) [Pubmed]
  6. Evaluation of DOI, 8-OH-DPAT, eticlopride and amphetamine on impulsive responding in a reaction time task in rats. Blokland, A., Sik, A., Lieben, C. Behavioural pharmacology. (2005) [Pubmed]
  7. Influence of eticlopride on cocaine- and DA D2 agonist-induced behavioral effects in rats. Ferrari, F., Giuliani, D. Pharmacol. Biochem. Behav. (1996) [Pubmed]
  8. Regulation of the phosphorylation of the dopamine- and cAMP-regulated phosphoprotein of 32 kDa in vivo by dopamine D1, dopamine D2, and adenosine A2A receptors. Svenningsson, P., Lindskog, M., Ledent, C., Parmentier, M., Greengard, P., Fredholm, B.B., Fisone, G. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  9. D(2) dopamine receptors induce mitogen-activated protein kinase and cAMP response element-binding protein phosphorylation in neurons. Yan, Z., Feng, J., Fienberg, A.A., Greengard, P. Proc. Natl. Acad. Sci. U.S.A. (1999) [Pubmed]
  10. Decreased c-fos responses to dopamine D(1) receptor agonist stimulation in mice deficient for D(3) receptors. Jung, M.Y., Schmauss, C. J. Biol. Chem. (1999) [Pubmed]
  11. Regulation of phosphorylation of the GluR1 AMPA receptor by dopamine D2 receptors. Håkansson, K., Galdi, S., Hendrick, J., Snyder, G., Greengard, P., Fisone, G. J. Neurochem. (2006) [Pubmed]
  12. Blockade of D2 dopamine receptors in the VTA induces a long-lasting enhancement of the locomotor activating effects of amphetamine. Tanabe, L.M., Suto, N., Creekmore, E., Steinmiller, C.L., Vezina, P. Behavioural pharmacology. (2004) [Pubmed]
  13. Cocaine induces conditioned place preference and increases locomotor activity in male Japanese quail. Levens, N., Akins, C.K. Pharmacol. Biochem. Behav. (2001) [Pubmed]
  14. Typical and atypical neuroleptics antagonize MK-801-induced locomotion and stereotypy in rats. Hoffman, D.C. J. Neural Transm. Gen. Sect. (1992) [Pubmed]
  15. Acute amphetamine down-regulates RGS4 mRNA and protein expression in rat forebrain: distinct roles of D1 and D2 dopamine receptors. Schwendt, M., Gold, S.J., McGinty, J.F. J. Neurochem. (2006) [Pubmed]
  16. Effect of chronic cocaine treatment on mu- and delta-opioid receptor mRNA levels in dopaminergically innervated brain regions. Azaryan, A.V., Coughlin, L.J., Búzás, B., Clock, B.J., Cox, B.M. J. Neurochem. (1996) [Pubmed]
  17. Differential effects of N-methyl-D-aspartate receptor blockade on eticlopride-induced immediate early gene expression in the medial and lateral striatum. Keefe, K.A., Adams, A.C. J. Pharmacol. Exp. Ther. (1998) [Pubmed]
  18. Dopamine D1 and D2 receptors influence dopamine transporter synthesis and degradation in the rat. Kimmel, H.L., Joyce, A.R., Carroll, F.I., Kuhar, M.J. J. Pharmacol. Exp. Ther. (2001) [Pubmed]
  19. Regulatory effects of D2 receptors in the ventral tegmental area on the mesocorticolimbic dopaminergic pathway. Chen, N.N., Pan, W.H. J. Neurochem. (2000) [Pubmed]
  20. Reduced eticlopride-induced Fos expression in caudate-putamen and globus pallidus after unilateral frontal cortex injury: relation to neglect. Vargo, J.M., Marshall, J.F. Neuroscience (1997) [Pubmed]
  21. Temporal changes in the messenger RNA levels of cellular immediate early genes and neurotransmitter/receptor genes in the rat neostriatum and substantia nigra after acute treatment with eticlopride, a dopamine D2 receptor antagonist. Sirinathsinghji, D.J., Schuligoi, R., Heavens, R.P., Dixon, A., Iversen, S.D., Hill, R.G. Neuroscience (1994) [Pubmed]
  22. Excitation by dopamine of rat subthalamic nucleus neurones in vitro-a direct action with unconventional pharmacology. Tofighy, A., Abbott, A., Centonze, D., Cooper, A.J., Noor, E., Pearce, S.M., Puntis, M., Stanford, I.M., Wigmore, M.A., Lacey, M.G. Neuroscience (2003) [Pubmed]
  23. Dopaminergic mechanism for caffeine-produced cocaine seeking in rats. Green, T.A., Schenk, S. Neuropsychopharmacology (2002) [Pubmed]
  24. Regulation of striatal tyrosine hydroxylase phosphorylation by acute and chronic haloperidol. Håkansson, K., Pozzi, L., Usiello, A., Haycock, J., Borrelli, E., Fisone, G. Eur. J. Neurosci. (2004) [Pubmed]
  25. Effects of stimulants of abuse on extrapyramidal and limbic neuropeptide Y systems. Westwood, S.C., Hanson, G.R. J. Pharmacol. Exp. Ther. (1999) [Pubmed]
  26. Glucocorticoid receptor involvement in pair bonding in female prairie voles: the effects of acute blockade and interactions with central dopamine reward systems. Curtis, J.T., Wang, Z. Neuroscience (2005) [Pubmed]
  27. Examination of the involvement of protein kinase A in D2 dopamine receptor antagonist-induced immediate early gene expression. Adams, A.C., Keefe, K.A. J. Neurochem. (2001) [Pubmed]
  28. Differing influences of dopamine agonists and antagonists on Fos expression in identified populations of globus pallidus neurons. Ruskin, D.N., Marshall, J.F. Neuroscience (1997) [Pubmed]
  29. Chronic eticlopride and dopamine denervation induce equal nonadditive increases in striatal D2 receptor density: autoradiographic evidence against the dual mechanism hypothesis. LaHoste, G.J., Marshall, J.F. Neuroscience (1991) [Pubmed]
  30. Selective stimulation of striatal dopamine receptors of the D1- or D2-class causes opposite changes of fos expression in the rat cerebral cortex. Blandini, F., Fancellu, R., Orzi, F., Conti, G., Greco, R., Tassorelli, C., Nappi, G. Eur. J. Neurosci. (2003) [Pubmed]
  31. Regional in vivo binding of the substituted benzamide [3H]eticlopride in the rat brain: evidence for selective labelling of dopamine receptors. Köhler, C., Hall, H., Gawell, L. Eur. J. Pharmacol. (1986) [Pubmed]
  32. Dopamine D2 receptors in the nucleus accumbens are important for social attachment in female prairie voles (Microtus ochrogaster). Gingrich, B., Liu, Y., Cascio, C., Wang, Z., Insel, T.R. Behav. Neurosci. (2000) [Pubmed]
  33. New fluorine-substituted analogue of eticlopride with high affinity toward dopamine D2 receptors. Watanabe, K., Fukumura, T., Sasaki, S., Maeda, M., Takehara, S. Chem. Pharm. Bull. (1991) [Pubmed]
 
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