The time course of angry behavior in the temper tantrums of young children.
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Aggression↗
Biomedical subjects
M Potegal
Publications and source records attributed to M Potegal.
Attack priming in female Syrian golden hamsters is associated with a c-fos-coupled process within the corticomedial amygdala.
Allowing a resident hamster a single "priming" attack on a conspecific induces a transient aggressive arousal as indicated by a reduction in the latency and increase in the probability of attack on a second intruder presented within the next 30 min. We present two lines of evidence identifying the corticomedial amygdala as an important locus mediating this effect. (1) Attack priming significantly increases the number of neurons expressing immunocytochemically identified Fos protein in the corticomedial amygdala, but not elsewhere. Pursuit and biting of an inanimate object does not induce corticomedial amygdala c-fos expression of the same pattern or magnitude. The corticomedial amygdala contribution to the priming effect involves more than a non-specific arousal, since corticomedial amygdala c-fos expression does not correlate with locomotor activity, a standard indicator of such arousal. (2) Radiofrequency lesions of the corticomedial amygdala reduce aggression, the greatest reduction occurring with the more anterior lesions. Other behaviors, including a priming-like locomotor practice effect in a running wheel, are unaffected by corticomedial amygdala lesions. These findings suggest that attack priming is an aggression-specific effect resulting from a Fos-coupled change within neural circuitry of which the corticomedial amygdala is a part. From a theoretical point of view, these experiments suggest a new approach to the analysis of the mechanisms underlying aggressive behavior and the persistence of aggressive arousal. We present a sketch of a quantitative neurobehavioral model which relates attack probability to neural activation within the corticomedial amygdala. From a methodological viewpoint, these experiments extend the utility of mapping c-fos expression as a technique for localizing endogenous, behavior-specific processes within the central nervous system.
Aggression↗
Diazepam enhances conditioned defeat in hamsters (Mesocricetus auratus).
Male hamsters that have been repeatedly defeated by larger, aggressive males subsequently flee from, rather than attack, nonaggressive male intruders that are introduced into their home cages. We have referred to this generalization of flight in response to nonaggressive intruders as "conditioned defeat" (CD). In an attempt to reverse CD pharmacologically, diazepam (DZP) was administered to hamsters at two different time points relative to CD acquisition and subsequent response generalization tests, which involved the exposure of subjects to nonaggressive intruders (NAIs). In Experiment 1, subjects were given a single injection of one of 4 doses of DZP (0, 2, 6, or 20 mg/kg) immediately following CD acquisition. Twenty-four hours later, contrary to expectations, subjects that had received the 6 mg/kg dose displayed elevated flight responses in the presence of an NAI. Flight responding declined over days except in subjects that received the highest dose. In the second experiment, hamsters were administered a single injection of either 0, 2, or 6 mg/kg DZP just prior to a response generalization test occurring 24 h following CD training. Flight responses to the NAIs were again exaggerated in subjects that were given the 6 mg/kg dose, an effect that persisted several days without further drug administration. The present findings suggest the possibility that benzodiazepines can potentiate fear responses under certain stressful conditions.
Agonistic Behavior↗
Brief, high-frequency stimulation of the corticomedial amygdala induces a delayed and prolonged increase of aggressiveness in male Syrian golden hamsters.
Brief 200-Hz stimulation of the corticomedial amygdala (CMA) increases the aggressiveness of male Syrian golden hamsters for about 30 min; the effect peaks 10-15 min after stimulation. This effect is sensitive to stimulation amplitude and frequency. Stimulation at the parameters that reduce attack latency increases flank marking but does not affect copulation latency or general activity. Immunocytochemical analysis suggests that stimulation effects may be coupled to c-fos expression and that unilateral stimulation has bilateral effects. CMA stimulation effects appear to mimic part of the time course of behaviorally induced attack priming. The temporal persistence of aggression may result from long-term potentiation-like changes within CMA-related neural circuitry.
Aggression↗
Septo-hypothalamic organization of a stereotyped behavior controlled by vasopressin in golden hamsters.
In golden hamsters, microinjections of arginine vasopressin (AVP) within the anterior hypothalamus (AH) and lateral septum (LS) elicit the display of a stereotyped behavior: flank marking. As these areas are reciprocally connected, we tested whether AVP-sensitive sites constitute an organized network. Flank marking was recorded in animals with ibotenic acid lesions within the AH or LS after AVP injections within the LS or AH. While AVP injections in the AH and LS induced high flank-marking scores, certain lesions blocked the behavior. Lesions of the LS failed to affect flank marking induced by injections within the AH. In contrast, unilateral AH lesions blocked flank marking induced either by LS injections or AH injections in the contralateral side. These results suggest that the bilateral integrity of the AH is critical for the activation of flank-marking behavior by AVP. Together, these data suggest that the AH is an important relay of the neural network controlling flank-marking behavior.
Animals↗
Flight-elicited attack and priming of aggression in nonaggressive hamsters.
We report a technique for inducing attack in apparently nonaggressive hamsters that takes advantage of several behavioral effects: (a) the vigorous flight that repeatedly defeated hamsters display in the presence of conspecifics, (b) the potent, attack-eliciting properties of such flight, and (c) attack priming (i.e., aggressive arousal from exposure to an initial stimulus animal carries over to exposure to a second one). Resident hamsters that had consistently failed to attack nonfleeing intruders were found to readily attack intruders that did flee. But repeated exposure to the fleeing intruders alone did not induce long-term changes in aggressiveness. However, flight-elicited attack did successfully prime attack onto nonfleeing intruders presented immediately after the fleeing intruder was removed. Repeating such priming transfer trials induced long-term changes in the formerly nonaggressive subjects. We conclude that this is an effective procedure for inducing aggression that would be preferred when it is important to avoid exposing subjects to aversive stimuli. The changes in behavior that we observed seem to reflect heightened motivational levels.
Aggression↗
Conditioned defeat in the Syrian golden hamster (Mesocricetus auratus).
When singly housed under laboratory conditions, male Syrian golden hamsters routinely attack novel conspecific intruders introduced into their home cages. As we report here, after being repeatedly defeated by a larger, more aggressive intruder, such normal territorial aggression on the part of the resident hamsters is replaced by defensive behavior and flight. We have found that such conditioned defeat (CD) can be reliably induced by a series of 5-min trials with an aggressive intruder whether these trials are spread over 4 days or are all given on the same day. A useful behavioral criterion for the appearance of CD during acquisition is the first occurrence of anticipatory flight (AF), i.e., the first time the resident flees from the next aggressive intruder before being attacked. CD shows generalization: Animals trained to the AF criterion (AF Group) subsequently show defensive behavior toward, and even flee from, intruders which show absolutely no sign of aggressiveness. Animals in the AF Group persisted in such defense behavior for two test sessions; animals given three additional defeat trials beyond the appearance of AF (AF + 3 Group) showed a greater magnitude and persistence of defense and flight. A comparison of CD-trained animals which met a non-aggressive intruder (NAI) every day for 5 days to similarly trained animals which met the intruder only on the fifth day after acquisition suggests that CD diminishes passively as a function of time and not as the consequence of repeated encounters with a nonaggressive stimulus animal. We also found that near ideal NAIs could be prepared by treating nonaggressive hamsters with high doses of diazepam: animals so treated locomote more or less continuously around the cage virtually ignoring the subject. An unexpected observation was that subjects in the AF Group tended to closely follow these diazepam-treated, rapidly locomoting NAIs around the cage. Following may be an example of the "risk assessment" activities directed toward a potential threat. The development of a rapid and reliable technique for inducing CD in hamsters sets the stage for further physiological and pharmacological work on this interesting phenomenon.
Aggression↗
Time course of aggressive arousal in female hamsters and male rats.
This study replicates previous reports which show that allowing a female hamster to carry out an attack on a conspecific increases its aggressive arousal, i.e., transiently decreases the latency and increases the probability of an attack on a second trial. We now report that attack priming also occurs in male rats. Interpolating delays of 0, 10, 30, and 90 min between the first and second trials resulted in similar patterns of temporal changes in hamsters and rats. The differences in gender, housing condition, and other factors make the parallel in the time course of aggressive arousal in these two rodent species quite striking. The results rule out a simple model of exponential decay with a short time constant. Carrying out an attack sets in motion a complex set of internal events that affect subsequent aggressive behavior similarly in hamsters and rats.
Aggression↗
Evidence for a functional and anatomical relationship between the lateral septum and the hypothalamus in the control of flank marking behavior in Golden hamsters.
Golden hamsters with established dominant/subordinate relationships communicate their social status by rubbing pheromone-producing flank glands against objects in the environment. This behavior, called flank marking, is controlled by vasopressin-sensitive neurons localized to the anterior hypothalamus. Vasopressinergic magnocellular neurons in the nucleus circularis and medial aspect of the supraoptic nucleus are thought to be a source of neurotransmitter for the initiation of flank marking. The present study was undertaken to examine the extrahypothalamic control of flank marking. The anatomical and functional connections between the lateral septum and the vasopressin-containing nuclear groups in and around the anterior hypothalamus were examined by: (1) tracing afferent and efferent connections following microinjection of horseradish peroxidase and Phaseolus vulgaris-leucoagglutinin into the lateral septum, and (2) recording odor-induced flank marking prior to and following ibotenate lesions in the septum. The greatest number of perikarya retrogradely labeled with horseradish peroxidase were found lateral to the anterior hypothalamus and ventral to the fornix in the area of the lateral hypothalamus. The vasopressin-containing nuclear groups, e.g., paraventricular, supraoptic, suprachiasmatic nuclei, and the nucleus circularis, were devoid of labeled perikarya. Nerve terminals anterogradely labeled with Phaseolus vulgaris-leucoagglutinin were primarily localized to the anterior hypothalamus, in and around the nucleus circularis, and the medial aspect of the supraoptic nucleus. The lateral aspect of the supraoptic nucleus was devoid of nerve terminals as were the paraventricular and suprachiasmatic nuclei. The anatomical connections between the lateral septum and the hypothalamus appear to be necessary for the control of flank marking, since the microinjection of ibotenate into this limbic site significantly reduced odor-induced flank marking as compared to control microinjections of 0.9% NaCl.
Animals↗
Vasopressin in the septal area of the golden hamster controls scent marking and grooming.
Microinjection of arginine vasopressin into the lateral septum and bed nucleus of the stria terminalis of male hamsters stimulates intense flank marking and flank gland grooming, while microinjections of vasopressin in sites immediately adjacent to these areas or in the lateral ventricle are ineffective. Microinjections of oxytocin, angiotensin II and the behaviorally active C-terminal fragment of vasopressin, metabolite neuropeptide, by comparison, do not stimulate flank marking. Effective sites for vasopressin injection are clearly superimposable upon autoradiographically defined sites of high V1-receptor density. Furthermore, vasopressin-sensitive neurons in the lateral septum and bed nucleus of the stria terminalis are necessary for the expression of naturally elicited flank marking since the microinjection of a V1-receptor antagonist into these sites was able to temporarily block flank marking triggered by odors from conspecifics.
Animals↗
Aggressive behaviors in adult rats deprived of playfighting experience as juveniles.
Matched litter mates were reared in one of three conditions: in pairs or in isolation with or without one hour of daily playfighting experience from 20 to 50 days of age. The rats were then regrouped within condition so that they lived with identically reared cagemates for a month. This regrouping eliminated the transient effects of isolation such as increased fearfulness. When tested as adults, there was no effect of early rearing condition on the probability of intraspecific aggression or muricide, although isolation-reared rats were less likely to retrieve the mice. However, isolation rearing reduced the latency to initiate shock-induced defensive aggression and increased both its frequency and intensity. Isolated animals which had been given daily playfighting during development did not show the effects of early social deprivation. The mechanisms through which playfighting experience shapes later defensive behavior remain to be determined.
Aggression↗
Spontaneously hypertensive Wistar-derived male rats are more aggressive than those of their normotensive progenitor strain.
We compared a group of spontaneously hypertensive rats (SHRs) to a group of Wistar-Kyoto (WKY) rats on each of the three most commonly studied forms of aggressive behavior in rats: muricide, intraspecific aggression, and shock-induced fighting (SIF). A significantly higher proportion of SHRs were muricidal; they also fought more at the lowest shock level. A trend for a higher incidence of intraspecific offense behaviors by SHRs was not significant. SHR flinch and jump thresholds were lower than the respective WKY thresholds. Although there were no significant correlations between shock thresholds and any aspects of SIF, the possibility that strain differences in shock sensitivity may contribute to differences in SIF cannot be ruled out. Within strains, there were no correlations among the different forms of aggression. Several different inherited characteristics may be associated with the accentuation of different forms of aggression in SHRs.
Aggression↗
Vasopressin receptor blockade in the anterior hypothalamus suppresses aggression in hamsters.
Although the anterior hypothalamus has been implicated in the control of aggression in various rodent species, little is known about the neurochemical mechanisms mediating this control. It has been established that flank marking, which occurs with high frequency during agonistic encounters in hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. The present study was undertaken to determine whether intraspecific aggression in this species is similarly influenced by vasopressin in this area of the hypothalamus. Adult male hamsters, surgically implanted with guide cannulae aimed at the anterior hypothalamus, were microinjected with three different concentrations of the V1-receptor antagonist d(CH2)5Tyr(Me)AVP or a vehicle control of 0.9% NaCl. Sixty minutes after each microinjection a smaller male hamster was introduced into the home cage of the treated hamster. The resident hamsters showed a significant dose-dependent reduction in the number of biting attacks on the intruders over the 10 minute test period. The V1-receptor antagonist also caused a significant increase in the resident hamster's latencies to attack the intruder. However, the resident hamsters' total contact time with the intruder was unaffected by drug treatment suggesting that the reduction of aggression was not due to a generalized effect upon social behavior. The specificity of the drug treatment was further supported by the observation that it did not affect resident hamsters' sexual motivation or ability to mount a receptive female. These data suggest that vasopressin-sensitive neurons in the anterior hypothalamus are involved in the control of intraspecific aggression in male hamsters.
Aggression↗
Differential effects of ethyl (R,S)-nipecotate on the behaviors of highly and minimally aggressive female golden hamsters.
The GABA uptake inhibitor ethyl (R,S)-nipecotate produces a dose-dependent suppression of aggression in highly aggressive hamsters but not in minimally aggressive ones. This suppression occurs at doses below those producing peripheral cholinergic effects; at the highest dose used it persists after these effects have dissipated. Doses sufficient to suppress aggression have no significant effect on grooming, locomotor activity and other behaviors but do affect sunflower seed acceptance. The differential effects of the drug on highly and minimally aggressive animals may indicate that their differences in aggression are due to differences in endogenous GABAergic activity. These results, together with previous evidence for parallel circadian variation in GABA uptake and aggressive behavior, suggest that GABA uptake may be an important endogenous regulator of aggression.
Aggression↗
Bandage backfall: labyrinthine and non-labyrinthine components.
A cataleptic animal clings in a vertical position, unmoving, for abnormally long periods by supporting some of its weight on its hindlegs, grasping with the forepaws, flexing its forelimbs, and holding the head horizontal. When the head is snugly wrapped with a bandage, the head slowly falls backward, the neck hyperextends, the forelimbs extend and the grasp is released, resulting in the animal falling backward to the ground. It was earlier suggested that in cataleptic animals, the bandage inhibits vestibular and kinesthetic mechanisms of head support, yielding the backfall sequence [35]. However, preliminary experiments showed that labyrinthectomized rats made cataleptic by haloperidol fall backwards when placed in a vertical clinging position, even without a bandage, suggesting that in the rat the bandage-backfall reaction depends only on the vestibular system. In the present paper, this result is verified but, by additional experiments, the latter conclusion is shown to be incorrect. In labyrinthectomized rats made cataleptic by other means (lateral hypothalamic damage, or bulbocapnine), backfall from clinging did not occur unless a bandage was applied. Therefore, the bandage does indeed appear to inhibit the kinesthetic mechanisms that maintain head support in labyrinthectomized cataleptic rats. Haloperidol, particularly in high doses, greatly weakens postural support in labyrinthectomized rats (causing the animal to sag down and fall back when clinging), although the effect is not detectable in rats with labyrinths intact. However, labyrinthectomy reveals that the bandage can trigger an active dorsiflexion of the neck which in itself appears to inhibit clinging and righting. Bandage-induced dorsiflexion is present to a much lesser degree in intact animals, indicating that labyrinthine mechanisms inhibit the dorsiflexion reflex. Therefore, in the intact, cataleptic rat the bandage backfall reaction appears to be produced by the combined effects of a passive component (inhibition of kinesthetic support mechanisms), and an active component (elicitation of dorsiflexion of the neck).
Animals↗
Decline of GABA uptake in the hamster preoptic area following light offset.
The uptake of gamma-aminobutyric acid (GABA) was studied in homogenates of the accumbens-preoptic region (APR) of the hamster brain. Aggressive and non-aggressive female hamsters, maintained under a reversed 10-h dark and 14-h light cycle were sacrificed at various times after light offset. Aliquots of the APR homogenates were incubated with a series of [3H]GABA concentrations to obtain values for Vmax and Km. In both groups Vmax values declined sharply after light offset. The reduction in GABA uptake from early to later dark phase parallels the routine diminution in the aggressive activity of rodents from its peak in the early dark phase; the increase in GABAergic inhibition which presumably results from the reduced uptake may contribute to this change in aggressive activity.
Agonistic Behavior↗
Wandering and parietal signs in senile dementia of Alzheimer's type.
Among a population of nursing home patients with a diagnosis of senile dementia of Alzheimer's type (SDAT), a subgroup was identified who often became lost and wandered even in familiar surroundings. This subgroup differed from the rest of the SDAT patients on tests of parietal function but not on a generalized test of mental status. Thus, wandering in SDAT patients may be an indication of a specific parietal lobe involvement.
Aged↗
Disinhibition of muricide and irritability by intraseptal muscimol.
In two experiments we have found and replicated the observation that intraseptal muscimol profoundly facilitates muricide. It also increases irritability (response to handling). These effects are specific to aggressive behaviors in that the drug affects neither activity nor chocolate chip acceptance. The effects of the GABA synthesis inhibitor thiosemicarbazide depend upon the site of injection within the septum; in more anterior loci the drug produces the expected increase in muricide latency; in more posterior sites it produces an anomalous facilitation of muricide. The serotonergic agents quipazine and metergoline have no significant effect when injected into any of these sites. These results suggest that the septal neurons mediating the muricide-inhibitory effect of electrical stimulation [29] are subject to local, GABAergic, control. Inhibition of these neurons by muscimol produces a net disinhibition of muricide.
Aggression↗