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Z Amit

Publications and source records attributed to Z Amit.

At least 73 records · Page 4Linked to original sources
PubMed1990

Effects of ethanol on locomotor depression and corticosterone release induced by restraint-stress: support for a stress-ethanol interaction.

The interaction between restraint-stress and ethanol was investigated in the rat. The effects of ethanol pretreatment (0.0, 1.0, 1.5, 2.0 g/kg, 20% v/v) on locomotor depression and corticosterone release induced by restraint-stress (15, 60 min) were measured. Restraint durations of 15, 30, 90 and 120 min were found to decrease locomotor activity while animals restrained for 60 min did not differ from home cage controls. All restraint durations induced a significant increase in plasma levels of corticosterone. Locomotor activity counts of ethanol-pretreated (1.0, 1.5, 2.0 g/kg; 20% v/v) animals restrained for 15 min were not found to be lower than those of ethanol-pretreated animals remaining in home cages. Ethanol pretreatment did not differentially affect the locomotor activity of restrained or home cage animals in the 60-min condition. Plasma corticosterone levels of ethanol-pretreated animals restrained for 15 min were identical to those of ethanol-pretreated home cage controls. However, ethanol-pretreated animals restrained for 60 min demonstrated plasma corticosterone levels higher than those obtained by ethanol pretreatment or 60-min restraint alone. Blood ethanol levels were not found to be different between ethanol-control and ethanol-stress animals. These results provide support for a stress-ethanol interaction. They also suggest a differential interaction of ethanol with different intensities of stress.

Animals↗
PubMed1990

Stress-ethanol interaction: involvement of endogenous opioid mechanisms.

Stress effects vary with different environmental situations or stress intensities. The effects of restraint stress on locomotion and or corticosterone were examined. Rats were restrained for 0, 15, 30, 60, 90 or 120 min, subsequent locomotion was measured for 10 min. Rats were also sacrificed for corticosterone determinations. Restraint stress affects both variables. Locomotion was recorded in rats pretreated with naltrexone or vehicle prior to restraint of 15 or 60 min. Naltrexone influenced the effects of stress differentially. It did not affect the results following 15 min of restraint but suppressed locomotion after 60-min restraint to a level comparable to that found after 15 min. Treatment with ethanol (1.0, 1.5, 2.0 g/kg) prior to 15 or 60 min of restraint resulted in the prevention of hypomotility induced by 15-min stress. It also interacted nonadditively with 15-min stress on corticosterone release. No such interaction occurred with 60 min stress. Also, naltrexone made it possible to block the effect of ethanol on restraint-induced hypomotility. Results describe stress as a nonunitary concept. Its effects tend to vary with its duration. The differential interaction of stress with naltrexone and ethanol depending on its duration supports the above notion. Results further suggest recruitment of opioid systems in long duration stress (60 min).

Animals↗
PubMed1989

Serotonin uptake blockers and voluntary alcohol consumption. A review of recent studies.

Previous research demonstrated that serotonin uptake blockers (e.g., zimeldine, sertraline, fluoxetine) reduce voluntary ethanol consumption in rats and humans. However, the mechanism of action of these compounds is not well understood. It has been suggested, for example, that serotonin uptake blockade interferes with the processes that mediate the reinforcement derived from ethanol ingestion. On the other hand, there is considerable experimental evidence that suggests that the effects on alcohol intake may be an expression of a more general inhibitory role that serotonin plays in consummatory behavior. This chapter presents evidence that suggests that serotonin uptake blockers may affect ethanol intake, in part via a reduction of food intake. Current issues concerning the central versus peripheral mediation of these effects, receptor specificity, as well as alternate mechanisms of action are considered.

Alcohol Drinking↗
PubMed1989

A microcomputer controlled data acquisition system for research on feeding and drinking behavior in rats.

This paper describes an inexpensive, reliable computer controlled data collection system designed for the continuous monitoring of feeding and drinking behavior in rats. This system will be useful in areas of behavioral pharmacology research requiring a detailed analysis of food and fluid intake. The configuration described herein was developed for research on the "microstructure" of alcohol drinking behavior. Variables examined include: alcohol bout size, frequency and duration, interbout intervals as well as the temporal pattern of intake and its relationship to food and water consumption. Detailed analysis of behavior using this technique will enhance our ability to interpret the nature of changes in alcohol oriented behavior produced by pharmacological manipulations, aid in the development of specific hypotheses related to the regulation of alcohol drinking behavior and provide a means of testing these hypotheses.

Animals↗
PubMed1989

Administration of a GABA antagonist selectively attenuates an ethanol-induced conditioned taste aversion.

Pretreatment with the GABA antagonist picrotoxin attenuated the development of an ethanol-induced conditioned taste aversion (CTA), while no effect of this compound was observed on the development of an amphetamine-induced CTA. These findings suggested some specificity of the effects of picrotoxin to the psychopharmacological properties of ethanol related to CTA. On the other hand, the benzodiazepine inverse agonist, Ro15-4513, purported to a specific ethanol antagonist, was shown to attenuate both an ethanol- and amphetamine-induced CTA. The results support the notion that ethanol intoxication may be mediated in part by GABAergic mechanisms. These GABA-mediated properties of ethanol may in fact underlie the development of an ethanol-induced CTA.

Amphetamine↗
PubMed1989

Effects of 3-amino-1,2,4-triazole on ethanol-induced open-field activity: evidence for brain catalase mediation of ethanol's effects.

The role of brain catalase in the mediation of ethanol's effects on motor activity was investigated. Male Long-Evans rats were pretreated with i.p. injections of the catalase inhibitor, 3-amino-1,2,4-triazole (AT) (1 g/kg) or saline (S). Four hours later, animals in each group received i.p. injections of one of two doses of ethanol (ETOH) [1.0 g/kg (E1) or 2.0 g/kg (E2)] or one of two volumes of distilled water (W1 or W2). Ten minutes after the administration of these agents, animals were placed in open-field chambers and motor activity was recorded during a 10-min testing period. Results indicated that the motor depression produced by 2.0 g/kg of ETOH was significantly attenuated in AT pretreated rats (group AT-E2). AT pretreatment, however, had no effect on motor activity for subjects injected with 1.0 g/kg ethanol or water. Total brain catalase activity in AT-pretreated animals was 15% of control animals. No differences in blood ethanol levels were observed between AT- and S-pretreated animals. An interaction between ethanol and AT at the level of the central nervous system is suggested. The results of the present study suggest that brain catalase activity may be 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.

Amitrole↗
PubMed1988

Catalase activity measured in rats naive to ethanol correlates with later voluntary ethanol consumption: possible evidence for a biological marker system of ethanol intake.

Catalase activity in blood collected from young rats naive to ethanol (65 days) was significantly and positively correlated with later voluntary consumption of ethanol. Catalase activity levels were also correlated with catalase activity in brain and blood sampled after exposure to ethanol. The results obtained in the present study extend and confirm earlier findings (Aragon et al. 1985c) that brain catalase activity and voluntary ethanol intake are unidirectionally and causally related. The results also suggest that brain catalase activity may be part of an enzymatic system controlling the production and elimination of acetaldehyde in brain. This system may be a biological marker system mediating the affinity of organisms to ingest ethanol.

Alcohol Drinking↗
PubMed1988

Housing conditions fail to affect the intravenous self-administration of amphetamine.

Rats were housed either in isolation or in groups of 4 for 6 weeks following weaning (21 days). After this housing period, some of the rats were tested for the acquisition of intravenous self-administration of amphetamine (0.004-0.25 mg/kg/infusion) and others were tested for the locomotor activating effects of amphetamine (0-1.0 mg/kg, IP). In the self-administration tests, both the isolated and grouped rats readily acquired the operant to obtain drug infusions and exhibited dose-dependent behavior. These results are in direct contrast to those we have obtained concerning the influence of the environmental manipulation on cocaine self-administration. In those tests, only isolated rats self-administered cocaine. The results of the locomotor tests indicated that whereas the isolated rats were consistently more active, the dose/response curves for the effects of amphetamine on activity were parallel for the rats reared under the different housing conditions. Thus the environment has specific effects on behavior which may be a reflection of specific neurochemical effects of the manipulation.

Amphetamine↗
PubMed1988

Stress induced analgesia plays an adaptive role in the organization of behavioral responding.

The data on ability of stressful or noxious stimuli to suppress the perception of pain was reviewed. The focus of this review has been the attempt to demonstrate that the emergent "Stress Induced Analgesia" (SIA) plays an adaptive role in the modulation of behavioral responding by organisms during periods of threat or danger to the organism. We have reviewed the experimental paradigms that normally used in these studies which point to the fact that the variables inducing SIA need not be actually aversive or even stressful. We also reviewed the data on the mechanisms of SIA and suggested that both opioid and nonopioid mechanisms are involved in the mediation of SIA and that these mechanisms are at least semiindependent and subject to differential conditioning. Finally, we have described a series of experiments carried out in our laboratory where the induction of SIA interacted with behavioral performance in an inverted U shape function, low levels of stress facilitated responding and learning while high levels disrupted responding. We argued that taken together, the effects of SIA seem to be highly adaptive in that it allowed animals to deal with a dangerous and threatening situation in a manner which increased the organism's chance of survival.

Analgesia↗
PubMed1987

Effects of naloxazone on morphine-ethanol interaction in the conditioned taste aversion paradigm.

The effects of naloxazone on the interaction between alcohol and morphine were examined in the conditioned taste aversion paradigm (CTA). Naloxazone injected 4.5 h before the pre-exposure drug significantly attenuated the pre-exposure effect of morphine on ethanol CTA as well as the effect of ethanol on morphine CTA. The results are discussed in terms of possible mechanisms of opiate-alcohol interaction.

Animals↗
PubMed1987

Cocaine self-administration in rats influenced by environmental conditions: implications for the etiology of drug abuse.

The present study investigated the possibility of environmental factors as an explanation for between-subject differences in cocaine self-administration. Weaning rats (21 days) were housed in isolated or aggregated conditions for 6 weeks and were tested for intravenous cocaine self-administration (0.1-1.0 mg/kg/infusion). Rats housed in groups failed to reliably self-administer this drug whereas isolated rats readily acquired an operant to receive infusions of cocaine. These data suggest that environmental factors play a major role in determining individual differences in the propensity to self-administer cocaine and that, as such, they should be considered more seriously by those interested in the basis and treatment of drug abuse.

Animals↗
PubMed1987

Isolation housing decreases the effectiveness of morphine in the conditioned taste aversion paradigm.

Male Long Evans rats were obtained at 21 days of age and were housed in either an aggregated (four per double cage) or isolated (one per single cage) condition for 6 weeks. They were then placed on a fluid deprivation schedule that allowed them access to fluids for 20 min daily. This schedule was maintained for the remainder of the experiment. Following habituation, sensitivity to morphine-induced conditioned taste aversion (CTA) was compared in the differentially housed rats. On the 1st day and every 5 days thereafter the rats were presented with a 0.1% solution of sodium saccharin for the 20-min drinking period, followed immediately by an injection of morphine (0, 2.5, 5.0, 10.0, or 20.0 mg/kg). On intervening days they received water as the fluid. No drugs were given on these days. There was no difference in baseline saccharin consumption as a function of housing condition. In comparison with the isolated rats, the grouped animals were more sensitive to the CTA-inducing properties of low doses of morphine. These data strengthen the already existing evidence for the influence of the early housing environment on drug sensitivity and provide additional support for the conclusion that variability in response to a number of drugs of abuse can be reduced by environmental means. Possible mechanisms for the differences between isolation and aggregation housed rats are discussed.

Animals↗
PubMed1987

Differential involvement of central cholinergic mechanisms in the aversive stimulus properties of morphine and amphetamine.

Previously, it was reported that pretreatment with the centrally-acting cholinergic antagonist atropine, but not the peripherally-acting antagonist, methyl-atropine, may serve to attenuate the positive reinforcing properties of morphine and conversely, to enhance those of amphetamine as evidenced within a drug self-administration paradigm in rats. In parallel, evidence from several sources would suggest that there may be a functional relationship between the neurochemical mechanisms mediating these drugs' positive reinforcing properties and their seemingly paradoxical capacity to act as aversive stimuli, as evidenced within a conditioned taste aversion (CTA) paradigm. Accordingly, the present study undertook to examine whether a similar differential involvement of central cholinergic mechanisms established for these drugs' positive reinforcing effects may be obtained for morphine and amphetamine-induced CTA. Using a conventional CTA paradigm, animals were pretreated with either intraperitoneal (IP) atropine or methyl-atropine (0.6 mg/kg) 40 minutes prior to consuming a novel 0.1% saccharin solution. This taste stimulus was paired with IP injection of 15 mg/kg morphine or vehicle. Results showed that atropine (but not methyl-atropine) pretreatment served to attenuate the morphine CTA. In a second experiment, atropine-pretreatment failed to attenuate, and may have slightly potentiated, a CTA induced by 1 mg/kg amphetamine. Atropine pretreatment did not affect a CTA induced by the emetic agent, lithium chloride. Pretreatment with the peripherally-acting methyl-atropine had no effect on the amphetamine CTA and served, if anything, to slightly attenuate the lithium chloride CTA.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1987

Conditioned taste aversion induced by self-administered drugs: paradox revisited.

In this paper we have reviewed the literature on Conditioned Taste Aversion (CTA) with specific attention to the "apparent paradox" in this literature. This paradox refers to the fact that drugs which are self-administered (SA) by animals and are therefore presumed to possess positive reinforcing properties are also endowed with the capacity to induce a CTA. We have argued that the CTA literature contains evidence of the existence of two qualitatively distinct types of CTA, one which is mediated by emetic agents and the other induced by SA drugs. We first provided evidence to support the notion that the traditional explanation of CTA as a function of "drug toxicity" and its resultant gastrointestinal distress does not fit the data on the nature of CTA induced by SA drugs. We proposed instead that "drug shyness" or the novelty of the drug state of these psychoactive SA drugs constitutes a better explanation of the CTA of SA drugs. We provided further evidence suggesting a functional relationship between the positive reinforcing and aversive properties of SA drugs. We have based this contention on a review of the behavioral, physiological and neurochemical data concerning the nature of CTA of SA drugs. The examination of these data reveals that the neural mechanisms underlying both the positive and aversive properties of SA drugs are the same and at the same time different from the neural mechanisms underlying the induction of CTA by emetic agents. Finally, we discussed the relevance of this interaction between the positive and aversive properties of SA drugs in the context of their abuse liability and the control they exert on drug-oriented behavior.

Animals↗
PubMed1987

Alterations in brain aldehyde dehydrogenase activity modify ethanol-induced conditioned taste aversion.

The role of peripherally and centrally acting acetaldehyde in ethanol-induced conditioned taste aversion (CTA) was investigated using various enzyme manipulations. Cyanamide, an aldehyde dehydrogenase inhibitor (ALDH) elevates blood acetaldehyde levels in the presence of ethanol. Concurrent administration with 4-methylpyrazole (4MP), an alcohol dehydrogenase inhibitor, prevents peripheral accumulation of acetaldehyde by cyanamide. Under both treatment conditions brain and liver ALDH activity is inhibited. Water-deprived rats were pretreated 4 hr prior to fluid presentation with intraperitoneal injections of saline (S+S), 4-methylpyrazole (4MP+S), cyanamide (S+C), or 4-methylpyrazole + cyanamide (4MP+C). Subsequently, animals were presented with a novel saccharin solution followed immediately by intraperitoneal injection of one of three doses of ethanol (0.4, 0.8, or 1.2 g/kg) or saline vehicle on four occasions. Results suggested that animals pretreated with cyanamide (groups S+C and 4MP+C) drank significantly less saccharin after conditioning with a subthreshold dose of ethanol (0.4 g/kg) in comparison to groups S+S and 4MP+S. Moreover, at the conditioning dose of 1.2 g/kg, cyanamide-treated animals demonstrated an attenuation of CTA compared to the other two groups. These effects cannot be attributed to elevated blood acetaldehyde levels since pretreatment with 4MP+C prevented peripheral acetaldehyde accumulation. A characteristic common to both cyanamide-treated groups was the inhibition of brain ALDH. It is therefore suggested that brain ALDH may play a role in the mediation of ethanol-induced CTAs. It is conceivable that ALDH plays this role by regulating the levels of acetaldehyde in brain.

Acetaldehyde↗
PubMed1987

Effects of serotonin uptake blockade on food, water, and ethanol consumption in rats.

Previous research has demonstrated that the serotonin uptake blocker, zimeldine, reduced voluntary ethanol consumption in rats and humans. It has been suggested that zimeldine interfered with the processes that mediate the reinforcement derived from ethanol ingestion. However, there are considerable data which suggest that serotonergic pharmacological agents may produce a general inhibition of food and fluid consumption. The present investigation was therefore designed to directly examine the effects of zimeldine on food intake. The results indicated that zimeldine had a potent anorexic action. Furthermore, the drug appeared to primarily affect food intake, with secondary decreases in the fluid most closely associated with prandial drinking. The results were discussed in terms of the effects of serotonin uptake blockade on motivational processes in general.

Alcohol Drinking↗
PubMed1987

Corticosterone response to an acute dose of ethanol in naive and ethanol experienced rats.

The corticosterone response to an acute dose of ethanol (2 g/Kg, i.p.) was measured in the same rats in three different occasions: prior to, immediately following exposure to ethanol in a free choice self-administration paradigm and after a 15 day period of abstinence following exposure. Corticosterone was measured fluorometrically from tail blood samples collected 30 minutes following the ethanol injection. Blood ethanol levels were determined by gas chromatography. Mean plasma corticosterone and ethanol levels following the acute ethanol challenge were not significantly different in the three tested periods. A significant negative correlation between plasma corticosterone levels in the naive state and subsequent levels of individual voluntary ethanol intake was obtained. No apparent relationship was observed, however, between the same levels of ethanol consumption and the corticosterone response in these animals after ethanol exposure or exposure with abstinence. These data suggest that levels of ethanol intake may be related to the initial response to acute ethanol of the adrenal-pituitary axis. If so, this acute response to ethanol may be used to predict subsequent levels of ethanol intake.

Alcohol Drinking↗