ON THE ELEVATED PLUS-MAZE THE ANXIOLYTIC-LIKE EFFECTS OF THE 5-HT1A AGONIST, 8-OH-DPAT, BUT NOT THE ANXIOGENIC-LIKE EFFECTS OF THE 5-HT1A PARTIAL AGONIST, BUSPIRONE, ARE BLOCKED BY THE 5-HT1A ANTAGONIST, WAY-100635
N. Collinson et Gr. Dawson, ON THE ELEVATED PLUS-MAZE THE ANXIOLYTIC-LIKE EFFECTS OF THE 5-HT1A AGONIST, 8-OH-DPAT, BUT NOT THE ANXIOGENIC-LIKE EFFECTS OF THE 5-HT1A PARTIAL AGONIST, BUSPIRONE, ARE BLOCKED BY THE 5-HT1A ANTAGONIST, WAY-100635, Psychopharmacology, 132(1), 1997, pp. 35-43
In the present study we evaluated the effects of the 5-HT1A receptor p
artial agonist, buspirone hydrochloride and the 5-HT1A receptor agonis
t, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) on the elevated
plus-maze. In addition, the ability of the 5-HT1A receptor antagonist
, WAY 100635, to reverse the effects of both compounds was determined.
8-OH-DPAT (0.01-0.3 mg/kg, SC) dose-dependently increased the percent
time on, and the number of entries to, the open arms of the maze. In
a second experiment, WAY 100635 (0.003-0.3 mg/kg, SC) dose-dependently
reversed the anxiolytic-like effects of 8-OH-DPAT (0.3 mg/kg, SC). In
a third experiment, buspirone (0.3-4.0 mg/kg, SC) dose-dependently de
creased the time spent on the open arms of the maze, indicating that i
t had anxiogenic-like effects. Buspirone also significantly decreased
locomotor activity, which was evident in the decreases in the distance
travelled on the open arms. closed arms and on the maze as a whole, t
he total number of arm entries and the mean speed of the animals. In c
ontrast to its effects on 8-OH-DPAT-induced behaviours in the maze, WA
Y 100635 (0.003-1.0 mg/kg SC) failed to reverse any of the effects ind
uced by buspirone. Animals treated with high doses of WAY 100635 (0.3-
1.0 mg/kg SC) alone did not significantly differ from vehicle-treated
animals on any of the measures recorded during elevated plus-maze tria
ls. These data suggest that the anxiolytic-like effects of 8-OH-DPAT,
but not the anxiogenic-like effects of buspirone, on the elevated plus
-maze are mediated via S-HT1A receptors in the CNS.