Abstract

The effect of anxiolytics, benzodiazepine (BZP), diazepam (DZP), non-BZP zopiclone (ZOP) and phénobarbital (PBT), on the proconflict effect induced by methyl-β-carboline-3-carboxylate (β-CCM) or by pentetrazol (PTZ) was investigated. The proconflict effect of β-CCM and PTZ was reduced by these anxiolytics and aminooxyacetic acid (AOAA). In addition, isoniazid produced proconflict activity. Therefore, it is suggested that anxiolytics facilitate the GABA-erglc function, causing the inhibition of the proconflict effect. Although both propyl-β-carboline-3-carboxylate (β-CCP) and Ro15-1788 did not produce proconflict activity, they reduced the proconflict effect induced by β-CCM but not by PTZ. These data clearly show that β-CCM exerts the proconflict effect through interaction with BZP receptor and that there are behavioral similarities between β-CCP and Ro15-1788. In this study, we additionally observed the time latency until the rat began to drink the water. β-CCM and PTZ prolonged this latency in a dose-dependent manner. However, AOAA could not reduce the prolonged latency induced by β-CCM and by PTZ, and anxiolytics and β-CCP could not reduce the prolonged latency induced by β-CCM. The mechanism of the prolongation of latency induced by β-CCM and PTZ seems to be different from that of the proconflict effect.

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