Biomedical subjects

Z Amit

Publications and source records attributed to Z Amit.

At least 37 records · Page 2Linked to original sources

PubMed1999

Sterols of Pneumocystis carinii hominis organisms isolated from human lungs.

The opportunistic pathogen Pneumocystis carinii causes pneumonia (P. carinii pneumonia, or PCP) in immunocompromised individuals such as AIDS patients. Rat-derived P. carinii carinii organisms have distinct sterols which are not synthesized by mammals and not found in other microbes infecting mammalian lungs. The dominant sterol present in the organism is cholesterol (which is believed to be scavenged from the host), but other sterols in P. carinii carinii have an alkyl group at C-24 of the sterol side chain (C(28) and C(29) 24-alkylsterols) and a double bond at C-7 of the nucleus. Recently, pneumocysterol (C(32)), which is essentially lanosterol with a C-24 ethylidene group, was detected in lipids extracted from a formalin-fixed human P. carinii-infected lung, and its structures were elucidated by gas-liquid chromatography, mass spectrometry, and nuclear magnetic resonance spectrometry in conjunction with analyses of chemically synthesized authentic standards. The sterol composition of isolated P. carinii hominis organisms has yet to be reported. If P. carinii from animal models is to be used for identifying potential drug targets and for developing chemotherapeutic approaches to clear human infections, it is important to determine whether the 24-alkylsterols of organisms found in rats are also present in organisms in humans. In the present study, sterol analyses of P. carinii hominis organisms isolated from cryopreserved human P. carinii-infected lungs and from bronchoalveolar lavage fluid were performed. Several of the same distinct sterols (e.g., fungisterol and methylcholest-7-ene-3beta-ol) previously identified in P. carinii carinii were also present in organisms isolated from human specimens. Pneumocysterol was detected in only some of the samples.

AIDS-Related Opportunistic Infections↗

PubMed1998

Do taste factors contribute to the mediation of ethanol intake? Ethanol and saccharin-quinine intake in three rat strains.

Several recent studies have suggested that ethanol-preferring rodents may also have an affinity for sweet solutions (saccharin, sucrose) and, conversely, that saccharin preference may predict ethanol preference. The purpose of the present investigation was to determine whether intake of ethanol and saccharin-quinine (SQ) solutions would be related in three nonselected strains of rats who differ in their ethanol preference: Lewis, Wistar Kyoto, and Wistar. In the first phase of the experiment, all animals were presented with an ascending series of ethanol solutions (2 to 10%) in free choice with water, followed by a 10-day maintenance period of 10% ethanol with water. In the second phase, the same animals were presented with an ascending series of SQ solutions (saccharin: 0.4%, quinine: 0.001 to 0.04%) in free choice with water, followed by a 10-day maintenance period of 0.4% saccharin with 0.04% quinine and water. The results revealed an absence of a direct relationship between ethanol and SQ consumption. The ethanol-nonpreferring Lewis rats showed a greater preference for the SQ solutions than Wistar Kyoto rats, whereas the ethanol-preferring Wistar Kyoto strain consistently consumed significantly less SQ. Wistar rats showed relatively stable consumption levels for both solutions that fell between those of the other two strains. These results suggested that the relationship between ethanol and SQ preference in rats was not a direct one and did not support the findings in the literature of a simple overall positive relationship between sweet and ethanol preference. These data do, however, provide further evidence for taste factors in the mediation of self-selection of ethanol in rats.

Alcohol Drinking↗

PubMed1997

A descriptive analysis of the structure and temporal pattern of voluntary ethanol intake within an acquisition paradigm.

OBJECTIVE: The present experiment examined the microstructure and temporal pattern of consummatory behavior to provide insight into the behavioral processes that regulate the acquisition of voluntary oral ethanol intake. METHOD: A microcomputer-controlled data acquisition system was used to dynamically monitor food, water and ethanol intake in Long Evans rats across acquisition of ethanol drinking initiated through the presentation of a sequence of increasing concentrations of ethanol solutions in a free choice with water. RESULTS: The results showed a biphasic pattern of ethanol intake as a function of presentation of increasing concentrations of ethanol. Total ethanol intake decreased as the ethanol concentration was increased from 2% to 6%, while, inversely, ethanol intake was significantly increased as the concentration went from 6% to 10%. The initial decrease in ethanol intake, across 2% to 6% ethanol, was a function of decreases in both frequency and size of ethanol bouts. The increase in ethanol intake observed following presentation of higher ethanol presentations was solely a function of increased size of ethanol bouts. The increased size of ethanol bouts was paralleled by an increase in the rate of intake which was not evident across presentation of concentrations below 6%. The pattern of intake across the 23-hour daily sessions exhibited no differences across the dark/light cycle in ethanol or water intake as the concentrations of ethanol were increased. The results indicated, however, that food intake was characterized by increases in consumption during the first hour following the presentation of fluids and the night portion of the dark/light cycle. CONCLUSIONS: The present study revealed, for the first time, the involvement of differential, concentration dependent, behavioral processes in the mediation of the acquisition of voluntary ethanol intake.

Alcohol Drinking↗

PubMed1997

Naltrexone blocks acquisition of voluntary ethanol intake in rats.

The effects of naltrexone (NTX) on the acquisition of ethanol drinking was assessed in rats. NTX (0, 2.5, 5.0, or 10.0 mg/kg) was administered to rats presented with an ascending series of ethanol concentrations (2%, 4%, 6%, and 8% v/v) and water. The 2.5 and 10 mg/kg doses of NTX attenuated the acquisition of voluntary drinking of 8% ethanol, but the 5.0 mg/kg dose of NTX had no effect on ethanol intake. The acquisition paradigm was repeated in experiment 2 with naïve animals that received 0, 5.0, or 7.5 mg/kg of NTX. Neither dose of NTX affected ethanol intake, preference for alcohol, or water intake. Total fluid intake was suppressed in the NTX groups, but only on the second presentations of the 2% and 6% concentrations of ethanol. We suggest that the 2.5 and 10 mg/kg doses of NTX may have attenuated the acquisition of ethanol drinking by at least two different behavioral mechanisms.

Alcohol Drinking↗

PubMed1996

Influence of novel and habituated testing conditions on cocaine sensitization.

Female Swiss-Webster mice were treated daily for 10 days with cocaine (15 mg/kg i.p.) followed by 10 days with saline or ethanol (1.6 g/kg i.p.) or the reverse; following each injection in the experimental conditions locomotion was quantified in photocell cages. In animals given cocaine first, cocaine-induced locomotion was initially high and did not increase further with successive injections. In animals given prior saline or ethanol treatments, cocaine-induced locomotion was initially low but increased with successive cocaine treatments. There was no evidence of sensitization to the locomotor-stimulating effects of ethanol or of cross-sensitization between ethanol and cocaine. With respect to subsequent cocaine sensitization, the essential feature of prior saline or ethanol treatment appeared to be the handling and injection experience itself; a control group receiving prior saline injection in the home cage also showed a low level of cocaine-induced locomotion on the first day of cocaine testing but increasing locomotion with repeated cocaine testing. Thus, cocaine sensitization, rather than a progressive augmentation of motor function, may reflect a progressive reversal of the behavioral suppression caused by habituation to aspects of the testing situation or to some form of situational anxiety that precludes normal exploratory responses.

Animals↗

PubMed1996

Time-dependent exacerbation of amphetamine-induced taste aversions following exposure to footshock.

Previous studies have shown that stressors attenuate LiCI-induced conditioned taste aversions (CTA) but not morphine-induced CTA. The current studies examined the effects of footshock on the acquisition and extinction of amphetamine-induced CTA. Experiment 1 demonstrated that exposure to 30 footshocks between saccharin consumption and amphetamine injections did not alter either the acquisition or the extinction of amphetamine-CTA. Experiment 2 demonstrated that exposure to the same shock parameters 2 and 4 days before saccharin-amphetamine pairing increased the magnitude of amphetamine-CTA after one saccharin-amphetamine pairing and delayed the recovery from the CTA. Experiment 2 also demonstrated that footshock increased the initial neophobic response to novel saccharin but did not alter subsequent saccharin consumption among saline-injected animals. These results indicate that stress-induced facilitation of amphetamine CTA are time-dependent and contrast with reports that stressors attenuate LiCI CTA. They also add support to the contention that CTAs induced by self-administered drugs like amphetamine are qualitatively different from CTAs induced by toxic substances like LiCL.

Amphetamine↗

PubMed1996

Alcohol as a food: a commentary on Richter.

The present study examined the maintenance of voluntary alcohol intake in male Long-Evans rats. A microstructural analysis of consummatory behaviors (food, alcohol, water) was carried out using a computerized drinkometer system. In this sample of animals, there was no association (r = 0.07) between total food intake and total alcohol intake. There was no compensation for the extra calories ingested in the form of alcohol via a reduction in total food intake, or a reduction in food bout sizes associated with pre- or postprandial alcohol consumption. Further microstructural analyses determined that there were no significant difference between water and alcohol in terms of their distribution in relation to food (non-, pre-, or postprandial bouts). Of the total of 586 bouts of fluid intake analyzed, 45.6% were consumed postprandially, with a similar number (43.2%) consumed nonprandially. A comparison of the size of food bouts associated with different fluid bout types (pre- or postprandial) indicated that food bouts were the same size regardless of whether they were accompanied by water or alcohol. A final analysis determined that 55% of the total daily alcohol intake was consumed postprandially, and that the sizes of non-, pre-, or postprandial fluid bouts were significantly different for water vs. alcohol. Post hoc pairwise comparisons found that alcohol postprandial bouts were significantly larger than all types of water bouts. Alcohol and water bouts ranged in size from < 0.5 ml to > 5.5 ml. There was a significant difference in the distribution of bout sizes with more alcohol bouts at the high end of the distribution. Only 24% of the water bouts were > 2.5 ml compared to 48.4% of the alcohol bouts. The results of this study demonstrate that rats organize their consummatory behavior in many discrete, short bouts. There were considerable individual differences in alcohol preference, alcohol-bout frequency, duration, and size, as well as the prandial distribution of bouts. All of these variables together produce the "pattern" of alcohol intake in individual animals, and is likely to influence the level of intoxication achieved. Although rats do not dissociate their alcohol intake from normal feeding patterns, alcohol bouts occurring postprandially are significantly larger than other bouts of fluid consumption, suggesting that animals perceive the pharmacological effects of and are affected by the alcohol they consume. In animals with a preference for alcohol solutions, it is unlikely that alcohol is consumed as a food.

Alcohol Drinking↗

PubMed1996

Effects of naloxone on limited-access ethanol drinking in rats.

The hypothesis that naloxone (NAL) decreases oral ethanol intake in rats by inducing a conditioned taste aversion (CTA) to ethanol was investigated. Rats were trained to drink 8% ethanol (v/v) on a 1-hr limited-access schedule. They received 4 days of intraperitoneal injections of 10 mg/kg of NAL, 10 min before limited-access (-10MIN group), immediately after limited-access (1HR group), or 3 hr after limited-access (3HR). Ethanol intake decreased in the -10MIN and 1HR groups during the injection period and on the postinjection day. In experiment 2, rats received 4 days of NAL injections when ethanol was not available (pre-exposure), and then the paradigm was repeated. In this experiment, there was no suppression of ethanol intake for any group on the postinjection day. The decrease in ethanol intake during injections observed for the 1HR in experiment 1 and the sustained suppression postinjection was interpreted as a CTA. Pre-exposure in experiment 2 abolished the CTA. Differences in the pattern ethanol intake for the -10MIN and 3HR groups during the experiments, however, suggest that a CTA is not the sole mechanism underlying NAL's suppressant effects on ethanol intake. In conclusion, in rats both the dose of NAL and the relative timing of NAL injections and ethanol drinking effect subsequent NAL suppression of ethanol intake.

Alcohol Drinking↗

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↗

PubMed1995

Absence of mutations in superoxide dismutase and catalase genes in patients with Parkinson's disease.

BACKGROUND: Parkinson's disease (PD) is an adult-onset, neurodegenerative disorder characterized by a selective loss of the dopaminergic cells of the substantia nigra and by progressive motor decline. Studies have shown aberrant oxidative stress metabolism within the substantia nigra and other dopaminergic regions of the brain in patients with PD. OBJECTIVE: To screen the genes of three free radical detoxifying enzymes--copper/zinc superoxide dismutase, manganese superoxide dismutase, and catalase--for mutations in patients with PD. PATIENTS AND METHODS: A total of 107 unrelated patients with PD from two PD populations (familial and sporadic) were screened for mutations in the genes of copper/zinc superoxide dismutase, manganese superoxide dismutase, and catalase by single-strand conformation analysis. The diagnosis of PD was based on the clinical observations of resting tremor, rigidity, and bradykinesia. RESULTS: No mutations were identified. However, we did identify an amino acid substitution (glycine to aspartic acid) in exon 9 of the catalase gene in one patient; decreased red blood cell catalase activity was observed in this patient. CONCLUSION: Parkinson's disease is not caused by mutations in the genes of these three detoxifying enzymes. The exon 9 variant in the catalase gene in the one family with PD is most likely a silent mutation and not the genetic cause of PD in this family.

Adult↗

PubMed1995

Family history of alcoholism and the mediation of alcohol intake by catalase: further evidence for catalase as a marker of the propensity to ingest alcohol.

Earlier studies have suggested that catalase activity (CA) may represent a biological marker of alcohol intake in animals and in humans. An initial study was designed to rule out the possibility that CA is induced as a function of acute alcohol intake. Subjects (n = 80) were presented with either an alcohol (0.5 g/kg of body weight) or control solution, and asked to provide four 100-microliters blood samples at 0.0, 0.5, 2.0, and 24.0 hr. Results showed no differences in CA between individuals who had received alcohol, and controls, even when the effects of previous drinking history were covaried out. This lack of effect of acute alcohol intake on the possible induction of CA further supported the notion that CA may be a viable marker of alcohol intake, rather than the converse. In the second study, the relation between CA and alcohol intake was investigated in individuals with a family history (FH) of alcoholism (FH+), and in those without a family history of alcoholism (FH-). Subjects (n = 607) completed the Michigan Alcoholism Screening Questionnaire, the MacAndrew Scale, and the Concordia University Alcohol Screening Questionnaire; answered questions concerning their FH for alcoholism; and provided a 100-microliters blood sample. Results showed that FH+ individuals had higher mean CA compared with FH- individuals. When individuals with FH+ were compared with those with FH-, differences in the pattern of relation between CA and alcohol intake were observed. Although a significant relation between CA and alcohol intake was obtained for both FH- and FH+ individuals, this relation was significantly higher (p < 0.001) for individuals with FH+.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1993

Effects of CA antagonists on ethanol-induced excitation in habituated and nonhabituated mice: interaction with stress factors?

The effects of CA antagonists on ethanol induced locomotion in habituated (N) and nonhabituated (NH) mice was examined. H-mice were exposed to the testing apparatus for 4 days before testing. Mice were pretreated with pimozide (D2 antagonist), Schering 23390 (D1 antagonist), phenoxybenzamine (alpha 1 antagonist), or yohimbine (alpha 2 antagonist). Mice were then treated with ethanol. H mice had lower activity scores compared to NH mice. Ethanol produced an increase in activity for both groups. In NH animals, pimozide attenuated excitation in inverse relation to the ethanol dosage. In H mice, pimozide attenuated excitation only at doses that in themselves produced a decrease in activity. Schering 23390 reduced excitation only at doses that affected activity per se in both groups. Phenoxybenzamine reduced excitation dose-dependently in both groups. Yohimbine decreased excitation in both groups. Results suggest that stress emanating from a novel environment may affect not only activity per se but also the interaction between CA antagonists and ethanol.

Adrenergic Antagonists↗

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

Tolerance to effects of high doses of ethanol: 1. Lethal effects in mice.

Male Swiss Webster mice were injected with ethanol doses ranging from 6.5-10.5 g/kg (20% w/v, IP). Survival time distribution revealed three waves of deaths with peaks around 5 min, 300 min, and 33 h. There were two windows with very low density of probability of death between 30-130 min and between 22-25 h following lethal injections. This time structure of the probability density function did not significantly depend upon ethanol overdose, novelty of the experimental environment, or prior injections of saline and/or 3.5 g/kg ethanol. Injections of high doses of ethanol in BALB/c mice showed that this strain of mice was more sensitive to ethanol-induced lethality (LD50 = 6.6 g/kg) and over 99% of deaths occurred between 5-200 min following injections of the doses from 5.5-7.5 g/kg. Preexposure to ethanol increased tolerance to ethanol-induced lethality. LD50 increased from 8.1 g/kg (at 24 h following lethal injections in ethanol-naive Swiss Webster mice) to 8.5 and 9.0 g/kg in mice following four and eight injections of 3.5 g/kg ethanol, respectively. In BALB/c mice, eight prior injections of 3.5 g/kg ethanol increased LD50 also slightly but significantly to 7.15 g/kg. The results suggest that: a) Ethanol-induced lethality is not a unitary phenomenon and that deaths that occurred within distinct waves probably have different causes; b) mice strains have different susceptibility to different causes of ethanol-induced deaths; c) preexposure to 3.5 g/kg ethanol results in significant but small increase in tolerance to ethanol-induced lethality.

Animals↗

PubMed1993

Role of environmental cues as Pavlovian-conditioned stimuli in enhancement of tolerance to ethanol effects: 1. Lethal effects in mice and rats.

Twice daily for 4 days, Swiss Webster or BALB/c mice were injected with 3.5 g/kg ethanol (20% w/v, IP) immediately after moving their home cages from the colony room to the experimental room. On day 5, half the mice were moved to the same room and the other half to a novel room with different lighting, acoustic, and olfactory stimuli. All mice were injected with ethanol overdoses ranging from 4.5-10.0 g/kg. LD50 for ethanol increased following ethanol preexposure as compared to control ethanol-naive mice tested in the same experimental room. However, LD50 was lower in both Swiss Webster and BALB/c mice tested in a novel environment than in the familiar environment. Novelty increased sensitivity to the effect of low and moderate but not the highest lethal doses of ethanol. This effect of novelty occurred only in ethanol-experienced, but not ethanol-naive mice. In the following experiments, using a balanced design, Swiss Webster mice and Wistar rats were exposed to ethanol and saline alternatively in two distinct experimental rooms. On the final day, we found that there was no difference between animals tested in the room previously associated with administration of ethanol and animals tested in a saline-associated room in terms of LD50 for ethanol. These results suggest that: a) Environmental stimuli do not play a role as Pavlovian conditioning stimuli in the development of tolerance to ethanol-induced lethality; and b) novelty acts as an unconditioned stimulus that increases ethanol's lethal effects by unspecific disruption of conditioned compensatory responses to internal conditioned stimuli, such as irritation of peritoneal cavity, smell, and taste of ethanol.

Animals↗

PubMed1993

Bidirectional effects of GABAergic agonists and antagonists on maintenance of voluntary ethanol intake in rats.

The effects of THIP (GABAA agonist) and picrotoxin (GABA antagonist) on the maintenance of voluntary ethanol ingestion were examined. Thirty-three male Long-Evans rats were initially exposed to a screening procedure in which increasing concentrations of ethanol (from 2% to 9%) were presented in a free choice with water, on an alternate day schedule. Following the screening procedure, the rats were exposed to five ethanol presentations at a concentration of 9%, which constituted the baseline period, and five additional ethanol presentations during which the effects of the GABAergic manipulations were determined (test period). During the test period, the animals received IP injections of either 16 mg/kg of THIP, 2 mg/kg of picrotoxin or saline. The results suggested that the differential GABA manipulations resulted in bidirectional effects on the consumption of ethanol. More specifically, the GABAA agonist THIP increased the intake of ethanol as compared to baseline measures, while the GABA antagonist picrotoxin decreased ethanol intake. Similarly, the administration of THIP increased ethanol preference. In contrast, preference for ethanol over water was decreased following the administration of picrotoxin. It appears that the effects of these GABAergic manipulations are specific to ethanol, since total fluid intake was not influenced by the administration of either drug (i.e., THIP or picrotoxin). In light of the literature suggesting that THIP and picrotoxin are active at different sites within the GABAA chloride-ionophore receptor complex, the present findings would suggest that the GABAA receptor may play a role in regulating the voluntary intake of ethanol.

Alcohol Drinking↗

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↗