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Biomedical subjects

K A Miczek

Publications and source records attributed to K A Miczek.

At least 127 records · Page 7Linked to original sources

Sexual dimorphism in the hormonal control of aggressive behavior of rats.

Male and female rats housed together in small groups both became aggressive toward strange rats placed into their cages. However, male rats mainly attack male intruders and female rats mainly attack female intruders. The hormonal requirements for this aggression are also sexually dimorphic. Castration of the male residents causes a decrease in aggressive behavior, but ovariectomy of the female residents has little effect on their aggression. Replacement therapy to castrated males with 500 microgram/day of testosterone propionate (TP) restores all components of aggressive behavior within 2-3 weeks. Replacement therapy with 5 microgram/day of estradiol benzoate for 3 weeks had no effect on castrated males' aggressive behavior, nor did it cause the males to start attacking female intruders. Replacement therapy to ovariectomized females had a quite different effect. Treatment with EB or EB and progesterone reduced or blocked attack toward intruder females but did not alter the low level of attack toward males. Treatment with TP for 3 weeks also slightly reduced attack toward female intruders but increased the probability of attack toward male intruders. The sex-specificity of aggression and the differential influence of hormones suggests that different mechanisms may be responsible for aggression in males and in females.

Aggression↗

Analysis of amphetamine effects on agonistic and affiliative behavior in squirrel monkeys (Saimiri sciureus).

Two series of experiments were performed to differentiate the effects of d-amphetamine on social interactions from those on solitary motor behavior in adult and juvenile squirrel monkeys. In the first experiment, d-amphetamine (3x0.5 mg/kg, PO) induced pronounced stereotyped movements of the head, limbs and torso. When confronted in the colony room with an intruder monkey, the amphetamine-treated resident monkey showed reduced threat and attack behavior. In a separate test for affiliation, amphetamine nearly abolished the affiliative response toward a familiar group member. In a second series of experiments, d-amphetamine (0.3, 1.0 mg/kg, IM) decreased the affiliative behavior of juvenile monkeys towards their mothers; yet, in the presence of an unfamiliar adult male, the detrimental effect of amphetamine on affiliative behavior was prevented. Morphine (0.5, 2.0 mg/kg) increased the affiliative response toward the mother, and chlordiazepoxide (5, 10 mg/kg) was without effect in this situation. These observations suggest that amphetamine impairs a range of social behavior in adult and juvenile monkeys. The general disruption of agonistic and affiliative behaviors due to amphetamine appears to be based on mechanisms which differ from those mediating stereotyped movements. Stimulant-induced changes in social interactions in primates may be linked to disturbed affect.

Amphetamine↗

No tolerance to antiaggressive effect of d-amphetamine in mice.

Agonistic, locomotor, and stereotyped behavior were measured in male Swiss-Webster mice in their home cage, normally shared with a female, while confronting an intruder mouse. Acute administration of d-amphetamine (2, 4, 8 mg/kg, IP) to resident mice decreased the frequency of attacks toward an untreated intruder, increased the resident's locomotor activity, and induced a small amount of stereotyped behavior. Redetermination of dose-effect functions during chronic treatment (8 or 16 mg/kg/day) indicated that tolerance did not develop to the antiaggressive effect of d-amphetamine. By contrast, the chronically treated mice showed sensitization to amphetamine-induced stereotypies and a diminished sensitivity to the drug's enhancement of locomotor activity. Subsequent tests with cocaine indicated no differences between amphetamine-maintained and saline control animals, providing no evidence for cross-tolerance or cross-sensitization between cocaine's and amphetamine's effects on attack, locomotion, and stereotypies.

Aggression↗

Intruder-evoked aggression in isolated and nonisolated mice: effects of psychomotor stimulants and L-dopa.

Adult male Swiss-Webster mice were housed either singly (isolated) or with a female (nonisolated). Aggressive behavior was evoked by introducing a group-housed male mouse (intruder) into the home cage of the isolated or nonisolated mouse (resident).d-Amphetamine, methamphetamine, methylphenidate, cocaine, and L-dopa decreased attack and threat behavior by resident mice, the isolates requiring 2--4 times higher drug doses for the antiaggressive effects than the nonisolates, d-Amphetamine, methamphetamine, and methylphenidate caused intruder mice to be more frequently attacked by their non-treated resident opponents, to escape more often, to assume the defensive upright posture less, and to move about more often. L-Dopa nonspecifically de creased all elements of agonistic and nonagonistic behavior, while the amphetamines and methylphenidate suppressed attacks, increased escapes, decreased upright postures, and increased nonagonistic locomotion. By contrast, cocaine's antiaggressive effects were remarkably specific, i.e., not accompanied by changes in other behavioral elements.

Aggression↗

delta9-tetrahydrocannabinol: antiaggressive effects in mice, rats, and squirrel monkeys.

delta9-Tetrahydrocannabinol, the most active constituent of marihuana, decreased species-specific attack behavior in mice, rats, and squirrel monkeys at doses (0.25 to 2.0 milligram per kilogram of body weight) that have no effects on other elements of the behavioral repertoire. Aggressive behavior was engendered in all three species by confronting a resident animal with an intruder conspecific. The present results contrast with the widely held belief that marihuana increases aggressive behavior.

Aggression↗

Comparison of the effects of alcohol, chlordiazepoxide, and delta9-tetrahydrocannabinol on intraspecies aggression in rats.

The species-specific repertoire of attack, threat, defense, and submission was produced in pairs of male laboratory rats and measured after intraperitoneal injection of a drug or its vehicle to one of the rats. Attack behavior by dominant rats toward nondrugged opponents was increased by a low dose of alcohol (0.5 g/kg) or of chlordiazepoxide (5 mg/kg), but suppressed by delta9-tetrahydrocannabinol (THC). In experienced subordinate rats, the highest alcohol dose (1.5 g/kg) impaired the defensive upright posture whereas THC (2, 4 MG/KG) prolonged immobile crouch and submissivesupine reactions and resulted in more wounds. Naive rats administered alcohol assumed the submissivesupine posture more readily and for a longer duration, but sustained more biting attacks. Chlordiazepoxide and THC, when administered to naive rats, prolonged the immobile crouch reaction, and THC also impaired the defensive upright posture. We conclude that alcohol and chlordiazepoxide both enhance attack behavior in dominant rats, whereas THC has specific anti-aggressive effects and profoundly alters the submissive-defensive reactions.

Aggression↗

Mouse-killing and motor activity: effects of chronic delta9-tetrahydrocannabinol and pilocarpine.

Chronic administration of delta9-tetrahydrocannabinol (THC) for 5--8 weeks at 4 dose levels (2, 10, 20, 50mg/kg/day) or of pilocarpine (12.5, 25 mg/kg/day) for 3 weeks induced mouse-killing in 25--70% of previously "non-killer" rats of the Sprague-Dawley strain. The maximum percent of drug-induced mouse-killing depended on the daily dose and housing conditions, 20mg/kg/day THC and 25 mg/kg/day pilocarpine in single-housed rats being the most effective treatments. Drug-induced mouse-killing appeared to be a form of behavioral pathology, differing from the species-specific predatory response, when it first appeared. Concurrent assessment of locomotor and rearing activities showed dose-dependent depressant effects of THC and pilocarpine without evidence for tolerance. Different dose-dependencies and time courses suggest that changes in motor activities are not directly linked to the appearance of the killing behavior.

Aggression↗

Effects of scopolamine, physostigmine and chlordiazepoxide on punished and extinguished water consumption in rats.

It has been postulated that behavioral inhibition due to punishment or extinction may be mediated by brain acetylcholine, and drugs which have disinhibitory action are thought to interact with this system. This notion was tested by comparing the effects of scopolamine, physostigmine and chlordiazepoxide on punished and extinguished water consumption. Scopolamine hydrobromide (0.3, 0.5 mg/kg, i.p.), a centrally and peripherally acting antimuscarinic agent and physostigmine sulfate, (0.3 mg/kg, i.p.), a centrally and peripherally acting acetylcholinesterase inhibitor, lowered both non-punished and punishment suppressed water intake and lick rate, whereas their quaternary analogs which primarily act in the periphery, had no significant effect at comparable dose levels. Scopolamine and physostigmine suppressed punished water consumption at lower dose levels than nonpunished intake. In contrast, chlordiazepoxide (5.0, 10.0, 20.0 mg/kg, i.p.) enhanced punished as well as non-punished water intake. In a further experiment comparing punishment and extinction suppression, scopolamine and physostigmine did not affect punished or extinguished water intake; chlordiazepoxide (5.0, 10.0, 20.0 mg/kg) reliably increased punished, but not extinguished licking on the water nozzle. These results suggest (1) that scopolamine and chlordiazepoxide do not act via a common mechanism, and (2) that punishment and extinction suppression are not a pharmacological entity.

Acetylcholine↗