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

• RESULTS: Both SCH 23390 and eticlopride blocked (+)-MDMA-evoked hyperactivity in a dose-related manner; the highest doses of the antagonists also effectively suppressed basal locomotor activity [4].
• The effects of eticlopride on Morris water task performance in male and female rats neonatally treated with quinpirole [5].
• Evaluation of DOI, 8-OH-DPAT, eticlopride and amphetamine on impulsive responding in a reaction time task in rats [6].
• In the second series, (-) eticlopride, at the same doses, antagonized PE elicited by various DA D2 agonists at nonstereotyping doses; when, along with PE, stereotyped behavior was induced, only the latter was inhibited by (-) eticlopride, which even increased PE [7].

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

• Rats pre-exposed to the low dose of eticlopride exhibited enhanced locomotor activity whereas those pre-exposed to the intermediate or high doses did not differ from saline pre-exposed controls, suggesting that blockade of D2 dopamine receptors in the VTA can lead to sensitized locomotor responding to AMPH [12].
• In contrast, pretreatment of eticlopride reduced cocaine-induced locomotor activity [13].
• Pretreatment with the typical neuroleptic haloperidol (0.01, 0.05, 0.1, 0.5 mg/kg SC) and the dopamine D2 receptor selective antagonist eticlopride (0.005, 0.01, 0.05 mg/kg SC) each resulted in significant and dose-dependent reductions of locomotor activity and sniffing [14].

Biological context of Eticlopride

• Further, the down-regulation of RGS4 immunoreactivity by eticlopride was robust whereas the effect of SCH23390 was blunted as compared with its effect on mRNA [15].
• Both SCH 23390 and eticlopride, selective antagonists of D1- and D2-dopamine receptors, respectively, blocked this cocaine-induced up-regulation of MOR mRNA in nucleus accumbens [16].
• Eticlopride increased immediate early gene expression in striatum, with the increase generally being greater in lateral than in medial striatum [17].
• This suppression of eticlopride-induced gene expression was significant only in the medial-central aspect of striatum [17].
• In contrast to the striatum, NPA and quinpirole increased the DAT half-life, which was blocked by eticlopride and by itself had no effect on DAT kinetics [18].

Anatomical context of Eticlopride

• Systemic administration of D(1) (SCH23390) or D(2) (eticlopride) receptor antagonists blocked amphetamine-induced locomotion but amphetamine augmented both the SCH23390-induced increase and the eticlopride-induced decrease in RGS4 mRNA in the caudate putamen [15].
• To investigate the regulatory effects of somatodendritic D2 receptors on the terminal's extracellular dopamine (DA) concentration, a D2 antagonist (eticlopride) was infused directly into the ventral tegmental area via a microdialysis probe in chloral hydrate-anesthetized rats [19].
• In the same animals, eticlopride-induced Fos in globus pallidus was also examined [20].
• In the dorsolateral neostriatum, there was an increase in proneurotensin messenger RNA 10 min after eticlopride, this increase becoming significant (P < 0.01) at 60 min [21].
• In contrast, (-)-sulpiride, eticlopride and (+)-butaclamol all abolished the D2-like receptor-mediated inhibition by dopamine of substantia nigra pars compacta neurones [22].

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

• Chronic eticlopride and dopamine denervation induce equal nonadditive increases in striatal D2 receptor density: autoradiographic evidence against the dual mechanism hypothesis [29].
• Using permanent cannulas implanted in the right striatum, Sprague-Dawley rats received intrastriatal microinfusions of SKF 38393 (D1 agonist) or quinpirole (D2 agonist) or saline (controls), combined with systemic administration of D1 antagonist SCH 23390 or D2 antagonist eticlopride or saline [30].
• Approximately 95% of the radioactivity recovered from the striatum was in the form of authentic eticlopride, as determined by thin-layer chromatography [31].
• Microinjection of the D2 antagonist eticlopride into the NAcc (but not the prelimbic cortex) blocked the formation of a partner preference in mating voles, whereas the D2 agonist quinpirole facilitated formation of a partner preference in the absence of mating [32].
• The in vitro binding affinity of this ligand toward the D2 receptor was found to be as potent as eticlopride, suggesting that the corresponding 18F-labelled compound may be useful as an in vivo radioligand for positron emission tomography [33].

References