The catalase inhibitor sodium azide reduces ethanol-induced locomotor activity

The involvement of brain catalase in modulating the psychopharmacological e ffects of ethanol was investigated by examining ethanol-induced locomotor a ctivity in sodium azide-treated mice. Mice were pretreated with IP injectio ns of the catalase inhibitor sodium azide (5, 10, or 15 mg/kg) or sa line. Following this treatment, animals received IP injections of ethanol (0.0, 1 .6, 2.4, or 3.2 g/kg). Ten minutes after ethanol administration, locomotor activity was recorded during a 10-min testing period in open-field chambers . The time effect between the two treatments (0, 30, 60, or 90 min) was als o evaluated. Results indicated that sodium azide alone did not change spont aneous locomotor activity. However, this catalase inhibitor significantly r educed ethanol-induced locomotor activity when it was injected simultaneous ly or 30 min before ethanol injections. Moreover, perfused brain homogenate s of mice treated with sodium azide also showed a significant reduction of catalase activity. No differences in blood ethanol levels were observed bet ween sodium azide and saline pretreated animals. Results of an additional e xperiment showed that sodium azide (10 mg/kg, at 30 min) did not produce an effect on d-amphetamine- (2 mg/kg) or tert-butanol- (0.5 g/kg) induced loc omotor activities. A specific interaction between ethanol and sodium azide at the level of the central nervous system is suggested. These results prov ide further support for the involvement of brain catalase in ethanol-induce d behavioral effects. They also support the notion that acetaldehyde may be produced directly in the brain by catalase and that it may be an important regulator of ethanol's locomotor effects. (C) 1999 Elsevier Science Inc. A ll rights reserved.