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Biomedical subjects

D J Albert

Publications and source records attributed to D J Albert.

At least 37 records · Page 2Linked to original sources

Ovariectomy attenuates aggression by female rats cohabiting with sexually active sterile males.

Female rats were individually housed with a single castrated male with a testosterone implant that maintained sexual and aggressive behavior. At weekly intervals, the resident male was removed and an unfamiliar female intruder was introduced into the colony. Attacks, bites, on-top, and piloerection of the resident female toward the intruder were scored. Females whose level of aggression toward the intruder was substantial and stable were either ovariectomized or sham-ovariectomized. Aggression tests resumed 1 week postoperatively and continued for an additional 3 weeks. The results confirm that female cohabiting with a sterile male become aggressive. They also demonstrate that ovariectomy greatly attenuates but does not entirely abolish aggression toward an unfamiliar female intruder. The results appear to contribute to a growing body of evidence suggesting that the biological substrate and behavioral form of aggression by females housed with males (including that following parturition) is a hormone-dependent aggression which parallels testosterone-dependent social aggression of males housed with females.

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Testosterone supports hormone-dependent aggression in female rats.

Female hooded rats were ovariectomized and implanted with a single testosterone-filled Silastic tube or an empty tube. The tube size was one which allowed a release of testosterone at the high end of the mean normal serum testosterone concentration for intact females. Following a 7-day recovery period, all rats were placed on a 23-hr food-deprivation schedule and adapted to a highly palatable liquid food over a 5-day period. Each animal with a testosterone implant was then housed with an animal of similar weight but an empty implant. The pairs were subjected to a series of 3 restricted-access competition tests (1/day) followed 4 days later by a series of 3 free-access competition tests. The animals were then separated, adapted to a bland liquid food, and paired with new partners. They were then subjected to the restricted- and free-access food-competition tests but with bland food as the incentive. During the first 6 competition tests there were no significant differences between groups in aggression or in time spent licking at the food spout. During the second series of tests, females with testosterone implants were more aggressive and more successful at maintaining access to the food than were their competitors with empty implants. The difference between groups occurred during the free- as well as the restricted-access tests. The effectiveness of physiological levels of testosterone in supporting aggression is attributed to the use of a test situation that activates as well as elicits hormone-dependent aggression. These results suggest that testosterone may be the hormonal substrate for hormone-dependent aggression in female rats.

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Competitive experience activates testosterone-dependent social aggression toward unfamiliar males.

Male hooded rats (350 to 450 g) were castrated and given subcutaneous implants of testosterone-filled or empty Silastic tubes. Four weeks later, half of the animals with testosterone implants were housed with an animal with an empty implant and left for 6 weeks. The other animals were adapted to a food-deprivation schedule, housed in testosterone-implant/sham-implant pairs and given a series of food-competition tests. Following the competition tests, all animals were observed individually in their living cage for aggression toward an unfamiliar intruder. Within the competitive situation, animals with testosterone implants were more aggressive and more successful at maintaining access to food than their cagemates with sham implants. In the unfamiliar intruder test, animals with testosterone implants that had been subjected to food competition were more aggressive toward an unfamiliar intruder than were animals with testosterone implants that had not been given competitive experience. Animals with testosterone implants given competitive experience were more aggressive than their castrated cagemates, but animals with testosterone implants not given competitive experience were not more aggressive than their cagemates. These results demonstrate that testosterone-dependent social aggression fostered by a competitive situation is elicited by an unfamiliar male intruder. They also confirm other evidence that activation of social aggression does not appear to require increased testicular testosterone secretion.

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Medial accumbens lesions attenuate testosterone-dependent aggression in male rats.

Male hooded rats were castrated and implanted with testosterone-filled Silastic tubes appropriate for maintaining a normal average serum testosterone concentration. They were then given lesions of the medial accumbens nucleus or sham lesions. Twenty-four hours postoperatively each male was housed with a female. Beginning 7 days following pairing and continuing once each week for 4 weeks, each lesioned or sham-lesioned male was observed for aggression toward an unfamiliar male intruder. On the day following each test of aggression toward an unfamiliar male, each lesioned and sham-lesioned male was assessed for defensiveness toward an experimenter. Rats with medial accumbens lesions displayed significantly less aggression toward an unfamiliar male intruder during each of the weekly tests than did sham-lesioned animals. The attenuation was most pronounced in animals with lesions damaging the posterior part of the medial accumbens nucleus (also designated as anterior portion of the bed nucleus of the stria terminalis) in the region of the crossover of the anterior commissure. Although medial accumbens lesions are known to make individually housed rats hyperdefensive toward an experimenter, lesion-induced hyperdefensiveness was not observed in the pair-housed animals in the present experiment. It is argued that the medial accumbens/bed nucleus of the stria terminalis area is an important region in the anterior forebrain for the modulation of hormone-dependent aggression.

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Cohabitation with a female activates testosterone-dependent social aggression in male rats independently of changes in serum testosterone concentration.

Male hooded rats (350 to 450 g) were sham-castrated, castrated and implanted with testosterone-filled, or castrated and implanted with empty Silastic tubes. Twenty-four hours postoperatively the animals in each group were housed with a female or a male similar in size to the female. Beginning one week following surgery and continuing for three weeks thereafter, the female or male cagemate was removed once each week while a 15-min test of aggression toward an unfamiliar male intruder was conducted. During the aggression tests, lateral attacks, lunge attacks, bites, on-top, and piloerection were recorded. At the first aggression test, males housed with females were significantly more aggressive than their counterparts housed with males. In contrast, different testosterone regimes did not consistently influence the initial activation of intermale social aggression. At the second and third tests, males with testicular testosterone or a replacement were significantly more aggressive than their castrated controls on most measures but males housed with females continued to be more aggressive than the comparable group housed with males. These results suggest that normal fluctuations in serum testosterone concentration associated with sexual interaction are not necessary for the initial activation of intermale social aggression. Both repeated exposure to unfamiliar males as well as cohabitation with a female are effective stimuli for activation of testosterone-dependent social aggression.

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Defensive aggression and testosterone-dependent intermale social aggression are each elicited by food competition.

Castrated rats with medial hypothalamic lesions or sham lesions and castrated rats with testosterone implants or sham implants were placed on a 23-hr food deprivation schedule, adapted to a highly palatable liquid food, and then housed in pairs. The pairs were observed in competition for the highly palatable food over a 4-min period on each of six days. On the first three days, the food was dispensed in a way that allowed only one animal at a time to drink while during the second three days both animals could drink simultaneously. The pairs of animals were then separated, individually adapted to a bland liquid food, and paired with a different animal for a second series of competition tests. With highly palatable food as the incentive, rats made hyperdefensive by medical hypothalamic lesions were more successful at maintaining access to the food and more aggressive than their sham-lesioned competitors on tests when food access was restricted to a single animal but not on tests when both animals could drink simultaneously. With bland food as the incentive, lesioned animals were not consistently more successful in maintaining access to the food but were significantly more aggressive than their cagemates. With the highly palatable food, castrated males with testosterone implants were neither more successful in maintaining access to the food nor more aggressive than their cagemates with sham implants. However, when paired with an unfamiliar cagemate in preparation for competition tests with the bland food, most rats with testosterone implants attacked the new cagemate using a lateral attack and displaying piloerection.(ABSTRACT TRUNCATED AT 250 WORDS)

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Activation of aggression in female rats by normal males and by castrated males with testosterone implants.

Female hooded rats were continuously housed with an intact male, a castrated male with subcutaneous testosterone implants, or two other females. At weekly intervals over a 10-week period, the cagemate(s) and pups were removed and aggression by the female toward an unfamiliar female intruder was observed over a 15-min period. On the 11th week each female was subjected to this intruder test in an unfamiliar cage. On the 12th week, a final test was conducted in each female's living cage with a male rather than a female as the intruder. The aggressive behaviors recorded were attacks, bites, on-top, and piloerection. Females housed with normal males displayed a significant increase in aggression prior to parturition. Their aggressiveness persisted through the 10th test with peaks at parturition and the start of lactation. Females housed with castrated males also displayed significant increases in aggression but without the peaks associated with parturition and lactation. Their aggressiveness also persisted throughout the test period. Females housed with other females showed a small increase in aggression over weeks. All groups showed virtually no aggression in the unfamiliar cage. All females displayed some aggression toward a male intruder but the level of aggression was highest in maternal females. The results demonstrate that aggression qualitatively similar to that displayed following parturition and during lactation can be elicited in nulliparous females.

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Intermale social aggression: reinstatement in castrated rats by implants of testosterone propionate in the medial hypothalamus.

Male hooded rats were castrated, subcutaneously implanted with testosterone-filled silastic tubes, and individually housed with an intact adult female rat. An unfamiliar male intruder was introduced into each colony on a weekly basis and the aggressive behavior of the resident male was recorded. When the intermale social aggressive behavior of the resident male toward the intruder reached a high level in terms of a composite aggression score, the subcutaneous testosterone tubes were removed. Weekly tests of aggression toward unfamiliar intruders continued until the aggression of the resident male dropped to a low level for two successive weeks in terms of our composite aggression score. Bilateral implants of pellets of testosterone propionate were then made into the medial hypothalamus or adjacent tissue. A control group was implanted with cholesterol pellets into the medial hypothalamus. During four weekly tests following the implant, rats with testosterone propionate implants in the medial hypothalamus showed increases in lateral attacks, lateral attack duration, bites, and piloerection. The increase in aggression was not consistently displayed by animals with testosterone propionate implants dorsal or anterior to the medial hypothalamus or by animals with cholesterol implants in the medial hypothalamus. These results suggest that the medial hypothalamus or closely adjacent tissue contains testosterone-sensitive neural circuitry modulating intermale social aggression.

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Intermale social aggression in rats: suppression by medial hypothalamic lesions independently of enhanced defensiveness or decreased testicular testosterone.

Medial hypothalamic lesions or sham lesions were made in castrated adult male rats with subcutaneous implants of testosterone-filled silastic capsules. Seven days following surgery all animals were given a test of defensiveness (reactivity) toward an experimenter. The following day, groups composed of one lesioned male rat, one sham-lesioned male rat, and one intact female rat were placed in large cages. Beginning two weeks later, unfamiliar intruders were introduced into each colony on a weekly basis and the aggressive behavior of the residents recorded. All 12 of the sham-lesioned animals but only 2 of 12 lesioned animals displayed substantial intermale social aggression toward intruders. Analysis of individual elements of intermale social aggression indicated that the lesioned animals were deficient in attack, bite, and piloerection but not in on-top behavior. The deficit in intermale social aggression was not correlated with defensiveness toward the experimenter or body weight of the lesioned animals. It is argued that the medial hypothalamus plays a role in the modulation of intermale social aggression which is independent of its role in modulating defensiveness or testosterone production. These results also demonstrate that intermale social aggression develops even when testosterone levels are held relatively constant by replacing testicular testosterone with an artificial testosterone source.

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Competitive behavior in male rats: aggression and success enhanced by medial hypothalamic lesions as well as by testosterone implants.

Castrated male hooded rats were given electrolytic lesions of the medial hypothalamus or sham lesions. Another group of castrated rats was implanted subcutaneously with bilateral testosterone-filled Silastic capsules or empty capsules. Lesioned animals with a high defensiveness (reactivity) score toward the experimenter were each placed in a cage with a sham-lesioned animal of a similar weight. Animals with testosterone implants were likewise housed with an animal of similar weight without a testosterone implant. Following a period of adaptation to a 23-hr water deprivation schedule, each pair of rats was given daily competition tests on each of 6 days. During the tests, a single water spout was placed in the cage for a 4-min period. The spout was surrounded by a plastic ring which prevented more than one animal from drinking at any time. Access to an unencumbered water spout was present following the competition test for 1-hr each day. Rats with medial hypothalamic lesions displayed more aggression than sham-lesioned rats during the competition tests and were able to spend more time drinking. Rats with testosterone implants were more successful in maintaining access to the spout but did not consistently display more aggression than their cagemates without testosterone implants. The aggression of the lesioned rats was defensive while that of animals with testosterone implants corresponded to intermale social aggression. These results demonstrate that a competitive situation can elicit intermale social aggression mediated by testosterone and defensiveness induced by medial hypothalamic lesions.

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Competitive behavior: intact male rats but not hyperdefensive males with medial hypothalamic lesions share water with females.

Male hooded rats with medial hypothalamic lesions or sham lesions were given tests of defensiveness toward an experimenter. The 8 lesioned males with the highest defensiveness scores and 7 sham-lesioned males were each placed in a double cage with a single intact female. For each pair of rats, food was continuously present but water was available for only 1 hr/day through a single water spout. Beginning on the fifth day of water deprivation, each pair of animals was given a 4-min water competition test on 3 consecutive days. Competition for water was created by placing a plastic ring over the hole in the cage where the water spout entered the cage. The ring restricted access to the spout to a single animal and was put in place 5 min before water was given. One hr following the competition test, each pair of animals was given access to a single unencumbered spout for a 1-hr period. Rats with medial hypothalamic lesions drank significantly more and initiated more aggression than their female cagemates during the 4-min competition tests. Sham-lesioned rats neither drank significantly more nor were more aggressive than their female cagemates. These results are consistent with previous observations indicating that the aggressiveness of rats with medial hypothalamic lesions can be elicited by a competition situation.

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Defensive aggression toward an experimenter: no differences between males and females following septal, medial accumbens, or medial hypothalamic lesions in rats.

Septal, medial accumbens, medial hypothalamic, or sham lesions were each made in female and male hooded rats. Behavioral testing of defensiveness toward the experimenter was done blind at 6, 9, and 12 days postoperatively by a person who was unaware of the purpose of the experiment. There were no quantitative differences in the defensiveness displayed by male and female rats: both sexes displayed the increase in defensiveness characteristic of each lesion. It is argued that the neural systems modulating defensiveness may be similar in male and female rats and that this is related to evidence from human experiments indicating that comparable levels of defensive aggression are emitted by males and females under controlled experimental conditions.

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Intermale social aggression: suppression by medial preoptic area lesions.

The intermale social aggressive behavior of male rats cohabiting with a female rat was quantitatively scored weekly in response to the introduction of an unfamiliar intruding male. Resident male rats whose aggressiveness toward an intruder reached a criterion level were subjected to either sham lesions or bilateral lesions in the region of the medial preoptic area. The lesioned rats continued to exhibit levels of piloerection and lateral attack that were not significantly lower than those of sham-lesioned animals. However, the lesioned animals did emit significantly fewer bites and spent significantly less time in the "on-top" position than did sham-lesioned animals. The lesioned animals also displayed significantly less sexual behavior than the sham-lesioned animals but were not different in terms of defensiveness toward the experimenter. It is suggested that bilateral lesions in the region of the medial preoptic area cause a decrease in the intensity of intermale social aggression but do not prevent external stimuli from eliciting the aggression.

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Testosterone removal in rats results in a decrease in social aggression and a loss of social dominance.

Alpha male rats from mixed sex colony groups were tested for aggressiveness toward nonaggressive male intruders. Afterward, they were castrated and implanted with testosterone filled Silastic tubes, castrated and implanted with empty tubes, or sham castrated and implanted with empty tubes. There were significant declines in the aggressiveness (lateral attacks, bites, and piloerection but not on-top) of castrated rats without testosterone replacement but not in castrated rats with testosterone replacement. At a second operation, castrated animals had their testosterone capsules removed or had their empty capsules replaced with testosterone filled capsules. When tested for aggression toward nonaggressive intruders, those alpha males which had testosterone removed declined in aggressiveness while those which had it implanted returned to a level of aggressiveness close to that emitted by sham castrated control animals. Subordinate males became dominant when alpha males were castrated and not given testosterone replacement. In a final series of observations, sham castrated males were found to be more aggressive than castrated males when pitted against one another. It is argued that testosterone plays a primary role in intermale social aggression and that the decline in aggressiveness following castration is typically accompanied by a loss of social dominance.

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Spontaneous mouse killing rats: gentling and food deprivation result in killing behavior almost identical to that of rats with medial hypothalamic lesions.

Rats that were found to kill a mouse spontaneously were divided into two groups. One group was left untreated and allowed free access to food while the other was gentled for 15 min/day and given only 15 g of food/day. Nonkilling rats were induced to kill mice by lesions of the medial hypothalamus. Seven to ten days after being divided into groups or subjected to brain lesions, each rat's behavior toward a series of stimuli was observed. The stimuli were a live mouse, a second live mouse, a freshly killed mouse, and a cotton wad. Food-deprived/gentled spontaneous killers and rats induced to kill by medial hypothalamic lesions each tended to attack with higher intensities and lower latencies than control spontaneous killers. The food-deprived/gentled spontaneous killers and lesion-induced killers (but not the control spontaneous killers) also attacked a dead prey moved vertically and then held onto the prey with sufficient intensity that their feet would leave the floor of the cage before they would release their grip on the prey. It is argued that the behavior of food-deprived spontaneous killers may constitute a more valid model of spontaneous mouse killing than that of sated spontaneous killers. The close correspondence between behavior toward a prey by lesion-induced killers and food-deprived spontaneous killers suggests that the lesion-induced killers fit this model of mouse killing remarkably well.

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Medial hypothalamic and medial accumbens lesions which induce mouse killing enhance biting and attacks on inanimate objects.

The response to a series of objects by rats with lesions of the medial hypothalamus or medial accumbens was compared to that of spontaneous killing rats and sham-lesioned nonkillers. When exposed sequentially to a piece of wood, a wad of cotton, or a freshly killed mouse, there were no differences in the intensity of the initial response toward the stimulus object by spontaneous mouse killing rats and lesioned animals that were later shown to kill mice. However, lesioned animals did spend more time biting these objects and were more likely than spontaneous killers to attack the objects if they were moved about by the experimenter. When allowed to kill mice, there were no differences in the intensity of the attack by spontaneous and lesion-induced killers but again the lesioned animals bit the prey more following the kill and were more likely to attack the dead prey when it was moved by the experimenter. Sham-lesioned nonkillers spent less time biting the stimulus objects than spontaneous killers and never attacked the objects when they were moved by the experimenter. It is argued that the killing of lesioned animals is homologous to that of spontaneous killers but that the lesioned animals exhibit most components of the predatory behavior to an exaggerated degree.

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Group rearing abolishes hyperdefensiveness induced in weanling rats by lateral septal or medial accumbens lesions but not by medial hypothalamic lesions.

Lesions of the medial hypothalamus, medial accumbens, or septum were made in 21- to 25-day-old male hooded rats. Half of the animals in each group were subsequently reared in groups and the other half in isolation. When tested for defensiveness toward the experimenter at 31, 34, and 37 days postoperatively, rats with medial hypothalamic lesions were most hyperdefensive toward the experimenter if reared in isolation but were significantly more defensive than sham-lesioned animals even when reared in groups. Rats with septal lesions were significantly more defensive than sham-lesioned animals only when reared in isolation while rats with medial accumbens lesions were not different from controls whether reared individually or in groups. These results suggest that the medial hypothalamus may have a special importance in determining temperament since the hyperdefensiveness that results from interference with its functioning is resistant to experiential remediation.

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Mouse killing induced by para-chlorophenylalanine injections or septal lesions but not olfactory bulb lesions is similar to that of food-deprived spontaneous killers.

Mouse killing induced by septal lesions, olfactory bulb lesions, or parachlorophenylalanine (PCPA) injections was compared with that of sated or food-deprived spontaneous mouse-killing rats in order to evaluate whether the experimentally induced killing corresponds to killing that occurs spontaneously, which tends to be viewed as predatory. On the first mouse kill, the intensity of the initial reaction to the mouse, the site of the initial attack, and the time required to kill by all groups were similar except that bulbectomized rats required longer to kill. Following the kill, only rats with septal lesions and bulbectomized rats bit the mouse significantly more than spontaneous killers. With the second mouse kill, there was an increase in the intensity of the response to the mouse and a decrease in attack latency by all groups except the bulbectomized rats and the nondeprived spontaneous killers. When presented with a freshly killed mouse, rats with septal lesions attacked with the greatest intensity, but PCPA-injected rats and food-deprived spontaneous killers also attacked more intensely than nondeprived killers. When presented with a wad of cotton or a block of wood, there was little or no response from the animals of all groups. It is argued that the mouse killing induced by septal lesions or PCPA injections may be due to an enhanced predatory tendency similar to that occurring in food-deprived spontaneous killers. In contrast, the mouse killing by bulbectomized rats cannot be inferred to be predatory because their attacks were of low intensity and involved repeated superficial bites rather than one or two well-directed forceful bites.

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