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Z Amit

Publications and source records attributed to Z Amit.

206 records · Page 12Linked to original sources
PubMedDate not supplied

Ethanol-induced motor activity in normal and acatalasemic mice.

The role of brain catalase in modulating the psychopharmacological effects of ethanol was investigated by examining ethanol induced motor activity in normal, C3H-N, and a corresponding group of acatalasemic C3H-A, mice. Following administration of one of three doses of ethanol (0.8, 1.6, and 3.2 g/kg) or saline, mice were placed in open field chambers and locomotor and rearing activity was measured during a 10-min testing period. A significant increase in locomotor activity was recorded in both groups of mice at lower doses of ethanol, while the higher dose produced a marked depression. Normal mice demonstrated more locomotor activity than acatalasemic mice at all ethanol doses. No differences between both groups of mice were observed in rearing activity. Also, no differences in blood ethanol levels were observed between the two substrains. Brain and liver residual catalase activity in the acatalasemic mice was found to be 40% and 50%, respectively, of normal mice. Furthermore, evidence for possible involvement of the peroxidatic activity in ethanol-induced motor activity is presented. These results suggest a role for centrally formed acetaldehyde as a factor mediating some of ethanol's psychopharmacological effects.

Acetaldehyde↗
PubMedDate not supplied

Effects of 3-amino-1,2,4-triazole on brain catalase in the mediation of ethanol consumption in mice.

Research has suggested that catalase plays a role in mediating ethanol's psychopharmacological effects. It has been shown that acatalasemic (C3H-A) mice differing in the activity of this enzyme consume larger amounts of ethanol. It has also been reported that when catalase activity is pharmacologically reduced, via 3-amino-1,2,4-triazole (AT), rats reduce their intake and preference for ethanol. The present research attempted to investigate AT's effects in nonselected mice. Swiss Webster mice were randomly assigned to groups of four per cage and further assigned to either a 5%, a 10%, or a 15% ethanol exposure condition. Mice were given a choice between water and increasing 1% concentrations of ethanol starting with 2%. Following five days of baseline, mice were injected daily with either AT (0.5 g/kg) or saline for five days. Results showed that AT significantly reduced ethanol consumption across treatment, but not posttreatment days. Results could not be explained by differences in total fluid intake. These results suggest a role for brain catalase in ethanol consumption across a variety of strains and species and further support the involvement of centrally formed acetaldehyde in the mediation of ethanol's psychopharmacological effects.

Acetaldehyde↗
PubMedDate not supplied

Lack of effect of dopamine D2 blockade on ethanol intake in selected and unselected strains of rats.

Previous research has suggested that brain catecholamines may be involved in regulating ethanol intake. This study was designed to look more specifically at dopamine (DA) and whether DA D2 receptor blockade with the antagonist pimozide would alter ethanol consumption in rats. Subjects were male Maudsley Reactive and Wistar rats, the former previously shown to consume larger amounts of ethanol than the latter. Both strains were screened for ethanol intake by presentation of ethanol solutions (free choice with water) in increasing steps from 2% to 10% (v/v) on an alternate-day schedule. Following the screening period, animals were switched to a schedule of everyday presentation of the 10% (v/v) ethanol solution (free choice with water) for 10 baseline days. Animals were then divided into high and low drinking levels according to whether their mean baseline ethanol intake (g/kg) fell within +/- 0.5 SD of the mean intake of their group (Maudsley Reactives: mean = 2.55 g/kg, low drinkers < 1.63, high drinkers > 3.47; Wistars: mean = 2.17 g/kg, low drinkers < 1.53, high drinkers > 2.82). The animals were assigned to one of five treatment groups for 5 subsequent days where they received IP injections of pimozide (0.08, 0.24, or 0.48 mg/kg), tartaric acid, or saline. Following the treatment period, ethanol consumption was recorded for 5 posttreatment days. No significant differences due to treatment were observed for either intake or preference of ethanol across treatments, drinking groups, or strains. The results obtained in the present study suggested that interference in DA neurotransmission through administration of the D2 antagonist pimozide does not significantly alter ethanol consumption in either MR or Wistar animals.

Alcohol Drinking↗
PubMedDate not supplied

The regulation of alcohol consumption in rats: the role of alcohol-metabolizing enzymes-catalase and aldehyde dehydrogenase.

Aldehyde dehydrogenase (ALDH) and catalase enzymatic activities in brain were assayed and compared to measures of alcohol consumption in two groups of animals screened and maintained on free-choice alcohol access under different conditions. In the first group of Long-Evans rats screened and maintained in home cages, mean alcohol intake was 3.49 g/kg/day with a range of 1.69-5.33 g/kg/day. When alcohol intake (g/kg), total ALDH, low K(m) ALDH, and catalase activities were entered in a multiple regression, a significant correlation of r = 0.51 (p < 0.05) was obtained. In the second group of rats consisting of Long-Evans, P, and NP rats screened using a drinkometer procedure, a multiple correlation between ALDH and catalase enzyme activities and alcohol intake of r = 0.42 (p < 0.05) was obtained. There was a strong relationship between the frequency of alcohol drinking bouts and the activities of catalase and ALDH (r = 0.68, p < 0.0001). The P rats had significantly higher catalase activities than either the NP or Long-Evans rats. The results of the present study confirmed earlier reports on the role of alcohol-metabolizing enzymes in the regulation of alcohol intake. The results also highlighted the fact that the activity of these alcohol-metabolizing enzymes may play a mediating role in patterns of alcohol intake displayed by animals selected for high and low alcohol drinking and also unselected animals.

Alcohol Drinking↗
PubMedDate not supplied

The role of ethanol availability on stress-induced increases in ethanol consumption.

Exposure to stressors can increase ethanol consumption and ethanol can attenuate the behavioral and biochemical effects of stressors. This study determined whether the availability of ethanol during the period of exposure to repeated restraint alters the poststress increase in ethanol intake. Seven days of restraint increased ethanol intake on the first poststress test only in animals deprived of ethanol during the restraint period. These results indicate that the availability of ethanol during exposure to restraint can attenuate the impact of restraint on ethanol intake. Ethanol intake was also positively related to novelty-induced locomotion and restraint eliminated this relationship. However, amphetamine-induced locomotion was not altered by either restraint or EtOH intake. These results indicate that voluntary ethanol intake can attenuate the impact of restraint stress and that restraint stress can alter the influence of ethanol on novelty-induced locomotion. It is suggested that this symmetrical relationship between ethanol intake and restraint stress may be involved in an interactive manner that determines stress-induced ethanol consumption.

Alcohol Drinking↗
PubMedDate not supplied

Effect of ethanol drinking and naltrexone on subsequent drinking in rats.

The effects of several days of oral ethanol drinking paired with naltrexone (NTX) on subsequent ethanol drinking were investigated in rats. We hypothesized that repeated pairings of NTX combined with forced oral ethanol intake would extinguish ethanol drinking so that when NTX injections were terminated, voluntary oral ethanol drinking would be suppressed. Thirty-two male. Long-Evans rats were provided with alternate days of either 8% ethanol solution or water as the sole source of fluid. Intraperitoneal injections of 0, 2.5, or 5.0 mg of NTX hydrochloride were administered on the ethanol days. Following the termination of injections, rats were returned to unrestricted access to water and ethanol and 24-h measurements of fluid intake were recorded. NTX decreased ethanol intake 4 h, but not 24 h, after NTX injections. Despite the consumption of significant amounts of ethanol during NTX treatment, there was no change in voluntary oral ethanol intake patterns after NTX injections were terminated (reinstatement of voluntary ethanol drinking). Thus, NTX's reduction in ethanol intake was limited in duration and did not result in long-term extinction of ethanol drinking behavior.

Alcohol Drinking↗