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Chemical Compound Review

Antisedan     4-(2-ethyl-1,3-dihydroinden- 2-yl)-3H...

Synonyms: Atipamezol, Atipamezole, Atipamezolum, antipamezole, Antisedan (TN), ...
 
 
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Disease relevance of Atipamezole

 

Psychiatry related information on Atipamezole

  • The administration of atipamezole (300 micrograms/kg), a selective antagonist of alpha 2-adrenoceptors, enhanced locomotor activity compared to saline-treated rats, but these effects did not differ between the TMT group and their controls [6].
  • METHODS: Male mice were administered either prazosin, betaxolol, atipamezole, corticosterone, or repeated restraint stress prior to measurement of either nest-leaving or TST [7].
  • Although the highly selective alpha-2 receptor antagonist, atipamezole (ATI), failed to affect spatial working memory on its own, at the doses studied (0.1-0.5 mg/kg, s.c.), it dramatically enhanced the working memory deficit produced by PCP [8].
  • Conversely, atipamezole administered intrathecally, but not intracerebroventricularly, blocked the enhanced tail-flick latency response to N2O [9].
  • The present study investigated the effects of dexmedetomidine (an alpha-2 adrenoceptor agonist), atipamezole (an alpha-2 adrenoceptor antagonist) and tacrine (an inhibitor of acetylcholinesterase) on the performance of adult and aged rats in a delayed non-matching to position task assessing spatial short-term memory [10].
 

High impact information on Atipamezole

 

Chemical compound and disease context of Atipamezole

 

Biological context of Atipamezole

 

Anatomical context of Atipamezole

  • Administration of atipamezole normalised [14C]DG uptake particularly in the cerebellum and spinal cord both in sham-operated and ischemic rats and to a lesser extent in the thalamus in sham-operated rats [25].
  • 5 Atipamezole had no inhibitory effect on MAO-A or MAO-B activity in renal membranes, which speaks against the involvement of MAOs in the observed radioligand binding [26].
  • The alpha 2-adrenoceptor antagonists used were, atipamezole, which occupies both central and peripheral receptors, and L 659,066, which poorly penetrates the blood brain barrier [21].
  • Systemically administered medetomidine produced an atipamezole-reversible, dose-dependent suppressive effect on the evoked responses of nociceptive medial thalamic and spinothalamic tract neurons [27].
  • In the present paper we have shown that local infusions of NE or of the alpha2-adrenoceptor antagonist, atipamezole, in the mouse amygdala produces localized expression of fos [28].
 

Associations of Atipamezole with other chemical compounds

 

Gene context of Atipamezole

  • Phenylephrine caused ERK phosphorylation only at a concentration high enough to exert non subtype-specific effects (10 microM), and this effect was counteracted by the alpha(2)-adrenergic antagonist atipamezole [32].
  • Atipamezole (1-3 mg/kg) significantly attenuated the ethanol-induced reduction in exploratory head-dipping in a holeboard test whereas L 659,066 was only effective at a dose of 1 mg/kg, higher doses (3 and 10 mg/kg) and a lower dose (0.3 mg/kg) were ineffective [4].
  • Atipamezole was without effect on ethanol's locomotor stimulant effect in the holeboard but L 659,066 attenuated this effect at doses less than 3 mg/kg Many alpha-2 adrenoceptor ligands also have affinity for nonadrenergic imidazoline-binding sites [4].
  • Dexmedetomidine at 100 nM added to the basolateral side of the CCD reduced AVP-stimulated Pf by 95% to 100%, and the alpha-2 antagonist atipamezole reversed the inhibition [33].
  • In the arcuate, only the highest dose of atipamezole had an effect on PRL, and this was in the opposite direction from that seen in the PVN [34].
 

Analytical, diagnostic and therapeutic context of Atipamezole

  • Sedation was quickly reversed by the administration of the antagonist atipamezole after the fMRI experiment [35].
  • Atipamezole did not enhance short-term or long-term memory in either TMT or control groups [6].
  • The alpha 2-adrenoceptor antagonists idazoxan (2.5 and 20 mg/kg), atipamezole (2.5 mg/kg), and fluparoxan (10 mg/kg) increased ACh outflow by up to 250-325% of basal levels over a 3-h period following intraperitoneal injection [36].
  • Atipamezole alone did not alter background EEG, nor did it affect the clonic convulsant threshold [37].
  • Medetomidine, a new alpha 2-adrenoceptor agonist produced dose-dependent (30-100 micrograms/kg i.p.) analgesia in the formalin test in rats, and this effect was reversed by atipamezole (1 mg/kg), a new alpha 2-adrenoceptor antagonist [38].

References

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  20. Reversal of the sedative and sympatholytic effects of dexmedetomidine with a specific alpha2-adrenoceptor antagonist atipamezole: a pharmacodynamic and kinetic study in healthy volunteers. Scheinin, H., Aantaa, R., Anttila, M., Hakola, P., Helminen, A., Karhuvaara, S. Anesthesiology (1998) [Pubmed]
  21. Modulation of the hypothermic and hyperglycaemic effects of 8-OH-DPAT by alpha 2-adrenoceptor antagonists. Durcan, M.J., Wozniak, K.M., Linnoila, M. Br. J. Pharmacol. (1991) [Pubmed]
  22. Potentiation of the anti-obesity effect of the selective beta 3-adrenoceptor agonist BRL 35135 in obese Zucker rats by exercise. Santti, E., Huupponen, R., Rouru, J., Hänninen, V., Pesonen, U., Jhanwar-Uniyal, M., Koulu, M. Br. J. Pharmacol. (1994) [Pubmed]
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  25. Differentially altered cerebral metabolism in ischemic rats by alpha2-adrenoceptor blockade and its relation to improved limb-placing reactions. Barbelivien, A., Jolkkonen, J., Rutkauskaite, E., Sirviö, J., Sivenius, J. Neuropharmacology (2002) [Pubmed]
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  28. Activation of fos in mouse amygdala by local infusion of norepinephrine or atipamezole. Stone, E.A., Zhang, Y., Hiller, J.M., Simon, E.J., Hillman, D.E. Brain Res. (1997) [Pubmed]
  29. Effect of alpha2 antagonists and an agonist on EEG slowing induced by scopolamine and lesion of the nucleus basalis. Riekkinen, P., Sirviö, J., Jäkälä, P., Lammintausta, R., Riekkinen, P. Neuropharmacology (1990) [Pubmed]
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  31. Effects of atipamezole, detomidine and medetomidine on release of steroid hormones by porcine adrenocortical cells in vitro. Jager, L.P., De Graaf, G.J., Widjaja-Greefkes, H.C. Eur. J. Pharmacol. (1998) [Pubmed]
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