EFFECTS OF ETHANOL, CHLORDIAZEPOXIDE, AND MK-801 ON PERFORMANCE IN THE ELEVATED-PLUS MAZE AND ON LOCOMOTOR-ACTIVITY

Citation
He. Criswell et al., EFFECTS OF ETHANOL, CHLORDIAZEPOXIDE, AND MK-801 ON PERFORMANCE IN THE ELEVATED-PLUS MAZE AND ON LOCOMOTOR-ACTIVITY, Alcoholism, clinical and experimental research, 18(3), 1994, pp. 596-601
Citations number
40
Categorie Soggetti
Substance Abuse
ISSN journal
01456008
Volume
18
Issue
3
Year of publication
1994
Pages
596 - 601
Database
ISI
SICI code
0145-6008(1994)18:3<596:EOECAM>2.0.ZU;2-0
Abstract
The effects of ethanol, chlordiazepoxide, and MK-801 on performance in the elevated-plus maze and on activity measured in a circular activit y monitor were compared in Sprague-Dawley rats to determine whether th ese effects of ethanol could be explained by its action on either GABA B or NMDA receptors. Both ethanol and chlordiazepoxide produced an inc rease in the time spent in the open arms of the elevated plus maze and in the ratio of open arm to total arm entries, indicative of an anxio lytic action of these drugs. MK-801 did not alter either the time spen t in the open arms or the ratio of open to total arm entries. Chlordia zepoxide and MK-801 produced an increase in total arm entries that sug gested that these compounds were increasing locomotor activity. Ethano l also increased total arm entries, but the effect was not statistical ly reliable. Following habituation to an activity monitor, neither eth anol nor chlordiazepoxide increased activity in this task, whereas MK- 801 produced a robust increase in locomotion. Additionally, neither et hanol nor chlordiazepoxide blocked the MK-801 induced locomotor stimul ation. The latter finding suggests that the effects of ethanol on GABA A receptors was not blocking an increased activity level produced by i ts antagonism of NMDA. Additionally, these results indicate that the a nxiolytic and locomotor action of ethanol in rats parallel the effects of a benzodiazepine and not those of an NMDA antagonist. Finally, the se results suggest that the consequence of ethanol's antagonism of NMD A receptor function is more restricted than that produced by MK-801.