title: Systemic administration of atipamezole, an alpha 2-antagonist, can reduce scopolamine-induced hyperactivity in rats.
abstract: The present study investigated whether an alpha 2-adrenoceptor antagonist (atipamezole) can influence hyperactivity induced by the systemic administration of scopolamine. In the water maze (WM) task, scopolamine (scop) 0.25 mg/kg treatment significantly increased swimming speed during the acquisition phase of this task. Atipamezole (ati) 30 micrograms/kg slightly reduced swimming speed both in saline- and in scop-treated rats. Ati 300 micrograms/kg slightly reduced swimming speed in saline-treated rats, and it prevented the scop-induced increase in swimming speed, because ati300-scop treated rats swam more slowly than the saline-saline group. In addition, ati 300 micrograms/kg reduced the total distance swum in scop-treated rats during a free swim trial (the platform was removed from the pool) performed 1 day after the acquisition phase of the WM test, even though it did not affect this parameter when administered alone. In the open arena task, which assessed the ambulation of rats when the pool was covered with a solid floor, scopolamine dose-dependently increased locomotor activity. The rats ambulated more when treated with scop 0.50 mg/kg compared to vehicle treatment, whereas the effect of scop 0.25 mg/kg treatment did not reach significance. In a test investigating the effects of ati 300 micrograms/kg and scop 0.50 mg/kg given singly or combined, the rats ambulated more during both ati 300 micrograms/kg and scop 0.50 mg/kg treatments given alone, but when combined, the rats ambulated less than during scop-saline treatment even though this was more than during control (saline-saline) treatment. These results indicate that the systemic administration of an alpha 2-antagonist can reduce hyperactivity induced by scopolamine.
authors.affiliation: A.I. Virtanen Institute, University of Kuopio, Finland.
authors.forename: M
authors.initials: M
authors.lastname: Niittykoski
authors.forename: V
authors.initials: V
authors.lastname: Hakkarainen
authors.forename: T
authors.initials: T
authors.lastname: Puumala
authors.forename: R
authors.initials: R
authors.lastname: Lappalainen
authors.forename: S
authors.initials: S
authors.lastname: Ruotsalainen
authors.forename: A
authors.initials: A
authors.lastname: Haapalinna
authors.forename: J
authors.initials: J
authors.lastname: Sirviö
mesh_terms: D058669:Adrenergic alpha-2 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D006948:Hyperkinesis / Q000139:chemically induced / Q000517:prevention & control*; D007093:Imidazoles / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D018782:Maze Learning / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D018341:Receptors, Adrenergic, alpha-2 / Q000378:metabolism; D012601:Scopolamine; D013550:Swimming
chemical_list: D058669:Adrenergic alpha-2 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D007093:Imidazoles; D018341:Receptors, Adrenergic, alpha-2; C050701:atipamezole; D012601:Scopolamine