Biomedical subjects

C M Aragon

Publications and source records attributed to C M Aragon.

At least 19 recordsLinked to original sources

PubMed2001

Influence of brain catalase on ethanol-induced loss of righting reflex in mice.

The effect of lead acetate and 3-amino-1, 2, 4-triazole (AT) on ethanol-induced loss of righting reflex (LORR) and brain catalase activity was studied in an attempt to confirm earlier observations on the involvement of catalase in ethanol-induced effects. Lead acetate (0 or 100 mg/kg) or AT (0 or 500 mg/kg) was injected (acutely) into mice 7 days or 5 h before testing. Other mice were exposed to drinking fluid containing 500 ppm lead acetate for 60 days. On the test day, mice received an intraperitoneal injection of ethanol (4.0 or 4.5 g/kg) and the duration of LORR was recorded. Acute lead-treated animals demonstrated a reduction in the duration of the LORR. However, both chronic administration of lead acetate and AT treatment increased the duration of ethanol-produced LORR. Furthermore, brain catalase activity in acute lead pretreated animals showed a significant induction, whereas it was reduced in chronic lead and AT treated mice. These results suggest that brain catalase activity, and by implication centrally formed acetaldehyde, may modulate ethanol-induced LORR.

Animals↗

PubMed2001

Brain catalase activity is highly correlated with ethanol-induced locomotor activity in mice.

It has been demonstrated that acute administration of lead to mice enhances brain catalase activity and ethanol-induced locomotion. These effects of lead seem to be related, since they show similar time courses and occur at similar doses. In the present study, in an attempt to further evaluate the relation between brain catalase activity and lead-induced changes in ethanol-stimulated locomotion, the interaction between lead acetate and 3-amino-1H,2,4-triazole (AT), a well-known catalase inhibitor, was assessed. In this study, lead acetate or saline was acutely injected intraperitoneally to Swiss mice at doses of 50 or 100 mg/kg 7 days before testing. On the test day, animals received an intraperitoneal injection of AT (0, 10, or 500 mg/kg). Five hours following AT treatment, ethanol (0.0 or 2.5 g/kg, ip) was injected and the animals were placed in open-field chambers, in which locomotion was measured for 10 min. Neither lead exposure nor AT administration, either alone or in combination, had any effect on spontaneous locomotor activity. AT treatment reduced ethanol-induced locomotion as well as brain catalase activity. On the other hand, ambulation and brain catalase activity were significantly increased by both doses of lead. Furthermore, AT significantly reduced the potentiation produced by lead acetate on brain catalase and on ethanol-induced locomotor activity in a dose-dependent manner. A significant correlation was found between locomotion and catalase activity across all test conditions. The results show that brain catalase activity is involved in the effects of lead acetate on ethanol-induced locomotion in mice. Thus, this study confirms the notion that brain catalase provides the molecular basis for understanding some of the mechanisms of the action of ethanol in the central nervous system.

Animals↗

PubMed2001

L-cysteine, a thiol amino acid, increases the stimulating acute effect of ethanol on locomotion.

The present study deals with the effect of L-cysteine on the acute stimulating effects of ethanol. Swiss albino mice were pretreated with 0.0, 18.75, 37.50, or 75.00 mg/kg of cysteine simultaneously, 30 or 60 min, before the administration of saline or 0.8, 1.6, 2.4, or 3.2 g/kg of ethanol at 20% vol./vol. After these treatments, mice were left in the open-field chamber for 20 min, and locomotor activity was evaluated for the last 10 min. The specificity of the effects of L-cysteine was analyzed with the use of two drugs that also induce locomotor activity--d-amphetamine and methanol. Mice received L-cysteine (37.5 mg/kg), and 30 min after this treatment d-amphetamine (2 mg/kg) or methanol (2.4 g/kg) was injected. Data showed that L-cysteine at 37.5 mg/kg was able to increase locomotion induced by 2.4 and 3.2 g/kg of ethanol when it was administered 30 min before ethanol injection. The effects of L-cysteine are specific for the stimulation of ethanol on locomotion, because L-cysteine does not alter d-amphetamine-induced locomotor activity or methanol-induced locomotion. Moreover, blood ethanol levels were not affected by L-cysteine pretreatment. Therefore, the present findings demonstrated that ethanol-induced locomotor effects are enhanced by L-cysteine, in a manner similar to that of other sulfur amino acids.

Animals↗

PubMed2000

Lead acetate potentiates brain catalase activity and enhances ethanol-induced locomotion in mice.

Several reports have demonstrated that acute lead acetate administration enhances brain catalase activity in animals. Other reports have shown a role of brain catalase in ethanol-induced behaviors. In the present study we investigated the effect of acute lead acetate on brain catalase activity and on ethanol-induced locomotion, as well as whether mice treated with different doses of lead acetate, and therefore, with enhanced brain catalase activity, exhibit an increased ethanol-induced locomotor activity. Lead acetate or saline was injected IP in Swiss mice at doses of 50, 100, 150, or 200 mg/kg. At 7 days following this treatment, ethanol (0.0, 1.5, 2.0, 2.5, or 3.0 g/kg) was injected IP, and the animals were placed in the open-field chambers. Results indicated that the locomotor activity induced by ethanol was significantly increased in the groups treated with lead acetate. Maximum ethanol-induced locomotor activity increase was found in animals treated with 100 mg/kg of lead acetate and 2.5 g/kg of ethanol. Total brain catalase activity in lead-pretreated animals also showed a significant induction, which was maximum at 100 mg/kg of lead acetate treatment. No differences in blood ethanol levels were observed among treatment groups. The fact that brain catalase and ethanol-induced locomotor activity followed a similar pattern could suggest a relationship between both lead acetate effects and also a role for brain catalase in ethanol-induced behaviors.

Animals↗

PubMed2000

Lession on the hypothalamic arcuate nucleus by estradiol valerate results in a blockade of ethanol-induced locomotion.

It has been suggested that the endogenous opioid system, especially b-endorphins (b-ep), can play a key role in the behavioral effects of ethanol. A single injection of estradiol valerate (EV) produces a neurotoxic effect on the b-endorphin cell population of the hypothalamic arcuate nucleus. In the present study we questioned whether mice pretreated with EV, exhibit any alterations in ethanol-induced behavioral effects. Female Swiss mice were pretreated with EV (2 mg/0.2 ml per mice) or vehicle and, 8 weeks later, these animals were challenged with ethanol (0.0-3.2 g/kg). Immediately after ethanol injection, mice were placed in the open field chambers and locomotor activity was assessed. EV administration did not produce any change in spontaneous locomotor activity but, conversely, blocked the locomotor activity induced by low (0.8 g/kg) and moderate (1.6 or 2.4 g/kg) doses of ethanol. Interestingly, the behavioral effects of higher doses of ethanol on locomotor activity as well as on the duration of the loss of righting reflex were unaffected by EV. Moreover, neither rota-rod performance or blood ethanol levels were affected by EV. In a second study, the effects of EV pre-treatment on caffeine- and 1-propanol-induced locomotor activity was tested. No differences were observed between groups in caffeine- or 1-propanol-induced locomotion. The results of the present study indicate that EV blocks ethanol-induced locomotor activity and that this effect can not be related with any difference in ethanol levels or nonspecific motor impairment. Furthermore, they suggest that b-ep containing neurons of the hypothalamic arcuate nucleus may play a role in some, but not all, behavioral effects of ethanol.

1-Propanol↗

PubMed2000

A psychopharmacological study of the relationship between brain catalase activity and ethanol-induced locomotor activity in mice.

OBJECTIVE: The present experiments analyze the effects of the brain catalase inhibitor 3-amino-1,2,4-triazole (AT) on the locomotor activity induced by ethanol. METHOD: In the first experiment, mice received injections of either AT (0.5 g/kg) or saline (S) 5 hours prior to an ethanol injection (0, 0.8, 1.6, 2.4, 3.2 or 4 g/kg). In the second experiment, five different groups of mice received injections of AT (0, 0.010, 0.030, 0.060, 0.125, 0.250 or 0.500 g/kg) 5 hours prior to being injected with 1.6 g/kg of ethanol. In the third experiment, six groups of mice were treated with AT (0.5 g/kg), simultaneously, 2.5, 5, 10 or 20 hours before the administration of 1.6 g/kg of ethanol. Immediately after ethanol injection, mice were placed individually in the open-field apparatus for 20 minutes. In another set of experiments, the effects of AT on brain catalase activity were studied. Animals were injected with AT at 0, 0.010, 0.030, 0.060, 0.125, 0.250 or 0.500 g/kg, and 5, 10 or 20 hours following AT treatment mice were perfused and the brain was removed. RESULTS: Pretreating mice with AT reduces ethanol-induced locomotor activity (1.6, 2.4 and 3.2 g/kg) without altering spontaneous locomotion. Pretreatment with AT (from 0.125 g/kg to 0.5 g/kg) produced a clear dose-dependent decrease of ethanol locomotion and brain catalase activity. The effect of AT was observed 5 and 10 hours after the injection of this drug, and it disappeared 20 hours following AT treatment. CONCLUSIONS: Current data showed a parallel property of AT in producing a remarkable dose- and time-dependent decrease in catalase activity and ethanol locomotion.

Amitrole↗

PubMed1999

Cyanamide reduces brain catalase and ethanol-induced locomotor activity: is there a functional link?

The present study was designed in an attempt to assess a previously suggested role of brain catalase activity in ethanol-induced behaviour by examining ethanol-induced locomotor activity in cyanamide-treated mice. Mice were pretreated with IP injections of the catalase inhibitor cyanamide (3.75, 7.5, 15, 30 or 45 mg/kg) or saline. Following this treatment, animals in each group received IP injections of ethanol (0.0, 1.6, 2.4 or 3.2 g/kg) and locomotion was recorded. Several time intervals (0, 5, 10, 15, 20 or 25 h) between the two treatments were also evaluated. Results indicated that cyanamide administration produced a dose-dependent decrease in ethanol-induced locomotor activity that depends on the time between treatments. However, cyanamide did not change spontaneous or d-amphetamine-induced locomotor activity. Moreover, an additive effect of cyanamide and another brain catalase inhibitor, 3-amino-1,2,4-triazole (AT), on the reduction of ethanol-induced locomotor activity was observed. Perfused brain homogenates of mice treated with cyanamide, AT or cyanamide+AT showed a significant reduction of brain catalase activity. The dose and time patterns of both effects were closely related and a significant correlation between them was obtained. These results suggest that cyanamide could reduce locomotor activity through its inhibition of brain catalase, giving further support to the notion that brain catalase may be an important regulator of some ethanol-induced behavioural effects.

Analysis of Variance↗

PubMed1999

The ethanol-induced open-field activity in rodents treated with isethionic acid, a central metabolite of taurine.

The effect of isethionic acid, a central metabolite of taurine, on ethanol-induced locomotor activity was investigated in rodents. Ten minutes following an (i.p.) simultaneous administration of ethanol (0.0, 1.5, 2.0, 2.5, 3.0, 3.5 g/kg) and isethionic acid (0.0, 22.5, 45.0, 90.0, 180.0 mg/kg), mice were placed in the open-field chambers and locomotor activity was measured during a ten-minute testing period. A significant interaction was found between isethionic acid and ethanol. Isethionic acid pre-treated mice (45.0, 90.0 and 180.0 mg/kg) showed a higher locomotor activity than the saline group at 2.5 and 3 g/kg of ethanol. In a second study, isethionic acid (45 mg/kg) and ethanol (1 g/kg) were simultaneously injected to rats. Ten minutes after the two treatments, rats were placed in the open-field chamber for a 30-minute period. The depressant effects that ethanol produced on rat locomotion were amplified by the same dose of isethionic acid as it affected ethanol-induced locomotion in mice (45 mg/kg). However, isethionic acid did not change the spontaneous locomotion at any of the doses tested in mice or rats. Since no differences in blood ethanol levels were detected in both mice and rats, the interaction between isethionic acid's action and ethanol-related locomotion does not seem to be due to different rates of absorption of ethanol or any other pharmacokinetic process related to ethanol levels. The current study displayed that isethionic acid, administered intraperitoneally, behaves in a similar way to its immediate precursor, taurine, by amplifying ethanol-induction of the locomotor activity.

Animals↗

PubMed1999

Methionine enhances alcohol-induced narcosis in mice.

Methionine is an essential amino acid that has been used as a therapeutic drug in some disorders. In this study we questioned whether methionine affects ethanol-induced loss of righting reflex (narcosis). One hour after IP methionine administration (60, 120, 240, 480, 720, 960, and 1280 mg/kg), mice were injected with ethanol (4.0 g/kg), and the duration of loss of righting reflex was recorded. Methionine, at the higher doses (960 and 1280 mg/ kg), significantly increased this effect on ethanol-treated animals. A time-course study revealed that methionine increased the duration of the loss of righting reflex induced by ethanol until 4 h after being injected. Because methionine did not affect blood ethanol levels, no change in peripheral alcohol can explain the observed effects. This potentiation was not specific for ethanol because methionine increased 3-methyl-1-butanol (0.6 g/kg) and 1-propanol (2.4 g/kg)-induced loss of righting reflex as well. Therefore, the results obtained in this study suggest the need for further investigation into methionine-ethanol interactions prior to the use of methionine as an agent that can be used as an antidepressant and to prevent damage to organic tissue in alcoholism.

1-Propanol↗

PubMed1999

The catalase inhibitor sodium azide reduces ethanol-induced locomotor activity.

The involvement of brain catalase in modulating the psychopharmacological effects of ethanol was investigated by examining ethanol-induced locomotor activity in sodium azide-treated mice. Mice were pretreated with i.p. injections of the catalase inhibitor sodium azide (5, 10, or 15 mg/kg) or saline. Following this treatment, animals received i.p. 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 also evaluated. Results indicated that sodium azide alone did not change spontaneous locomotor activity. However, this catalase inhibitor significantly reduced ethanol-induced locomotor activity when it was injected simultaneously or 30 min before ethanol injections. Moreover, perfused brain homogenates of mice treated with sodium azide also showed a significant reduction of catalase activity. No differences in blood ethanol levels were observed between sodium azide and saline pretreated animals. Results of an additional experiment 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 locomotor activities. A specific interaction between ethanol and sodium azide at the level of the central nervous system is suggested. These results provide further support for the involvement of brain catalase in ethanol-induced 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.

Animals↗

PubMed1999

Effects of chronic lead administration on ethanol-induced locomotor and brain catalase activity.

Several reports have demonstrated that chronic lead administration decreases brain catalase activity in animals. Other reports have shown a role of brain catalase on ethanol-induced behaviors. In the present study, we questioned whether mice treated chronically with lead, and therefore functionally devoid of brain catalase activity, exhibit some alterations in ethanol-induced behaviors. Swiss-Webster mice were exposed to drinking fluid containing either 500 ppm lead acetate or sodium acetate (control group) for 0, 15, 30, or 60 days before an acute ethanol administration. Following ethanol injection (2.5 g/kg, i.p.), animals were placed in open field chambers and locomotor activity was measured. Lead exposure had no effect on spontaneous locomotor activity. However, a reduction in ethanol-induced locomotor activity was found at all periods of lead exposure. After 60 days of treatment, the lead group demonstrated 35% less activity than the control group. Brain catalase activity was significantly reduced in the lead group following 60 days of exposure. This reduction in ethanol-induced locomotor activity and in brain catalase activity persisted after 40 days of lead withdrawal. The fact that brain catalase and ethanol-induced locomotor activity followed a similar pattern could suggest a relationship between both lead acetate effects and also a role for brain catalase in ethanol-induced behaviors.

Animals↗

PubMed1999

Daily injections of cyanamide enhance both ethanol-induced locomotion and brain catalase activity.

A role for brain catalase in the mediation of some psychopharmacological effects of ethanol has been proposed. In the present study, we investigated the effects of repeated cyanamide injections on the activity of brain catalase, as well as on the ethanol-induced locomotion of mice. Male Swiss mice were pre-treated with cyanamide (10 mg/kg; three times per day, 5 days) or saline. At different times (2, 3, 6 or 9 days) following this treatment, animals were injected with ethanol. Immediately following this ethanol challenge, animals were placed in the open field chambers and locomotor activity was assessed for 10 min. Results indicated an increase in ethanol-induced locomotion of mice pre-treated with cyanamide 2, 3 or 6 days before the ethanol challenge. Brain catalase activity showed an enhancement at the same time period and the two variables showed a significant correlation. No differences between pre-treatment groups on ethanol blood levels were observed at time of testing. In a second study, the effects of these cyanamide treatment conditions on d-amphetamine-induced locomotor activity were assessed. Results indicated no differences between pre-treatment groups in d-amphetamine-induced locomotion. Thus, these data suggest that repeated daily injections of cyanamide can simultaneously induce both brain catalase and locomotor activity, and that these effects may be strongly related. Furthermore, the present study provides further support for the notion that brain catalase activity may be a factor mediating some of the psychopharmacological effects of ethanol.

Animals↗

PubMed1999

Acute lead acetate administration potentiates ethanol-induced locomotor activity in mice: the role of brain catalase.

It has been proposed that brain catalase plays a role in the modulation of some psychopharmacological effects of ethanol. The acute administration of lead acetate has demonstrated a transient increase in several antioxidant cell mechanisms, including catalase. In the present study, we investigated the effects of acute lead acetate administration on ethanol-induced behavior, brain catalase activity, and the relation between both effects. Lead acetate (100 mg/kg) or saline was injected intraperitoncally in mice. At different intervals of time (1, 3, 5, 7, 9, or 11 days) after this treatment, ethanol (2.5 g/kg) was injected intraperitoneally and the mice were placed in open field chambers. Results indicated that the locomotor activity induced by ethanol was significantly increased. Maximum ethanol-induced locomotion increase (70% more activity than control animals) was found in animals treated with lead acetate 7 days before ethanol administration. Total brain catalase activity in lead-pretreated animals also showed a significant induction, which was maximum 7 days after lead administration. A significant correlation was found between both effects of locomotor and catalase activity. In a second study, the effect of lead administration on d-amphetamine (2.0 mg/kg) and tert-butanol-(0.5 g/kg) induced locomotor activity was investigated. Lead acetate treatment did not affect the locomotion induced by these drugs. These data suggest that brain catalase is involved in ethanol's effects. They also provide further support for the notion that acetaldehyde may be produced directly in the brain via catalase and that it may be a factor mediating some of ethanol's central effects.

Animals↗

PubMed1995

The nitric oxide synthase inhibitor NW-nitro-L-arginine methylester attenuates brain catalase activity in vitro.

Nitric oxide has been implicated in mediating the neurotoxic effects of ischemia in the brain. However, studies of the effects of nitric oxide inhibition with nitric oxide synthase inhibitors have provided controversial results. One of the reasons for the controversy may be related to the specificity of the nitric oxide synthase inhibitors, such as Nw-nitro-L-arginine methylester (L-NAME), which has recently been questioned. The present work investigated the possible interaction of L-NAME with the enzyme catalase in vitro. Catalase is an iron containing enzyme which could potentially interact with the iron-binding groups of L-NAME. Since the normal function of catalase in the brain is to remove excess hydrogen peroxide, the inhibition of this process could have potentially toxic effects. L-NAME was found to attenuate the catalase inhibiting effects of the known catalase inhibitor cyanamide in vitro, suggesting a competition between cyanamide and L-NAME for catalase. In addition, L-NAME by itself attenuated catalase activity in vitro. These results indicate that in addition to inhibiting nitric oxide synthase, L-NAME may have effects on catalase activity.

Animals↗

PubMed1993

Differences in ethanol-induced behaviors in normal and acatalasemic mice: systematic examination using a biobehavioral approach.

In studies designed to further examine the previously reported involvement of catalase in ethanol-induced effects, we attempted to confirm earlier observations by using normal (C3H-N) and acatalasemic (C3H-A) mice. These mice are identical in every respect and differ only in their catalase activity. Data suggested that the application of 3-amino-1,2,4-triazole (AT), a catalase inhibitor, to both substrains of mice resulted in a proportional decrease in motor activity, thus supporting our earlier observations. We also showed that this effect was specific to ethanol because AT did not have any effect on cocaine-induced motor activity in both substrains. Contrary to the effects of ethanol, these substrains did not differ in motor activity in response to cocaine. In an additional study, we observed that acatalasemic mice differed from the normals in their pattern of voluntary ethanol consumption. Acatalasemic mice consumed more ethanol but only when it was presented in the range of concentrations between 12 and 18%. Finally, we also obtained data suggesting that acatalasemic mice have longer duration of sleep time following ethanol administration compared to normals. Catalase activity was measured in both substrains. Results, once again, confirmed earlier data that the substrains differ in this activity and that AT further decreases brain catalase activity in both mice. Finally, when brain homogenates derived from both substrains were incubated with ethanol significant differences in the amount of generated acetaldehyde were found between the two mice strains. Together, these results provide strong support for the involvement of brain catalase in a variety of ethanol-induced behavioral effects.

Acetaldehyde↗

PubMed1993

Taurine and ethanol-induced conditioned taste aversion.

It has been reported that acute, simultaneous injections of taurine and ethanol were effective in reducing ethanol-induced locomotor activity and sleep time. The possible involvement of taurine administration in ethanol-induced conditioned taste aversion (CTA) was investigated. The results obtained in the present study following simultaneous administration of taurine (45 mg/kg) and ethanol (0.8, 1.2, and 1.6 g/kg) demonstrate a significant interaction between taurine and ethanol in their effect on ethanol-induced CTA in rats. This interaction was biphasic in nature and dependent upon the specific dose of ethanol. At the lowest ethanol dose (0.8 g/kg), which in itself resulted in a marginal CTA, taurine significantly enhanced the CTA induced by this dose. The intermediate ethanol dose of 1.2 g/kg produced a significant CTA. This CTA was blocked by administration of taurine. Finally, the CTA produced by the high dose of ethanol (1.6 g/kg) was not affected by administration of taurine. Taurine by itself does not produce a CTA. Peripheral levels of ethanol were ethanol dose dependent and the same in all animals regardless of treatment, indicating taurine had no effects on plasma ethanol levels. These data are similar to those obtained by earlier studies on the effects of taurine on ethanol-induced motor activity in mice. The present results support the findings reported by other investigators that taurine administration exerts a significant effect on ethanol-induced behaviors.

Analysis of Variance↗

PubMed1993

Cyanamide on ethanol intake: how does it really work?

Cyanamide, an aldehyde dehydrogenase inhibitor, has been shown to suppress voluntary ethanol consumption in animals. Studies were carried out to compare the effect of cyanamide on ethanol, saccharin-quinine and water intake in a restricted (10 min) access and in a free-choice nonrestricted access paradigm. An immediate and constant increase in fluid consumption was observed in the restricted access schedule paradigm independent of the fluid tested as cyanamide affected the consumption of all fluids including water. In the nonrestricted access study, cyanamide significantly increased total fluid intake. However, while saccharin-quinine-drinking animals treated with cyanamide demonstrated no change in intake preference, ethanol consumption was suppressed with a concomitant decrease in preference for ethanol. The present findings suggested that cyanamide may possess at least two, paradigm-specific, independent properties. It may enhance the consumption of fluid in general; however, it may also have a specific effect on ethanol intake when animals have continuous ethanol availability.

Alcohol Drinking↗

PubMed1992

Ethanol metabolism in rat brain homogenates by a catalase-H2O2 system.

Homogenates of perfused rat brains incubated in the presence of ethanol (50-100 mM) and glucose (10 mM) were found to oxidize ethanol to acetaldehyde. The addition of glucose oxidase, a known hydrogen peroxide generator, to the incubation medium, significantly (P less than 0.05) increased the generation of acetaldehyde. The presence in the incubation medium of metyrapone, an inhibitor of cytochrome P450, or pyrazole, an alcohol dehydrogenase inhibitor, did not affect the levels of acetaldehyde obtained. Conversely, the presence of 3-amino-1,2,4-triazole, a known catalase inhibitor, induced a concentration-dependent reduction of the amount of acetaldehyde generated after incubation, even in the presence of glucose oxidase. Homogenates of perfused brains of rats treated with 3-amino-1,2,4-triazole or cyanamide (another H2O2-dependent catalase blocker) also showed a dose-dependent reduction of the acetaldehyde obtained. These findings support the notion that a catalase-mediated oxidation of ethanol is present in rat brain homogenates. It is suggested that this local oxidation of ethanol may have important biological implications. The data of both studies increase support for the notion that acetaldehyde is produced directly in the brain and that it may be the agent mediating some of the psychopharmacological properties of ethanol and be one of the factors determining the propensity of an animal to voluntarily consume ethanol.

Acetaldehyde↗