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Biomedical subjects

D J Albert

Publications and source records attributed to D J Albert.

At least 55 records · Page 3Linked to original sources
PubMed1984

Rearing rats with mice prevents induction of mouse killing by lesions of the septum but not lesions of the medial hypothalamus or medial accumbens.

Rats which had been reared with mice and those which had not were subjected to lesions of the septum, medial accumbens, medial hypothalamus, or sham lesions. Forty-eight hours later all animals were presented with a mouse and the frequency of mouse killing recorded. In rats with lesions of the septum, the lesions induced killing only in those animals which had not been reared with mice. Rats with lesions of the medial accumbens or medial hypothalamus killed significantly more often than control animals even when they had been reared with mice. These results suggest that the septum, medial accumbens and medial hypothalamus subserve different functions in the inhibitory modulation of mouse killing behavior.

Animals↗
PubMed1984

A comparison of prey eating by spontaneous mouse killing rats and rats with lateral septal, medial accumbens, or medial hypothalamic lesions.

Rats with lesions of the medial hypothalamus and spontaneous mouse killing rats were tested for mouse and rat pup killing in their living cages 1 and 3 days postoperatively. The lesioned and spontaneous killers did not differ significantly in amount of prey eaten within 10 min following a mouse kill on either Day 1 or 3 postoperatively. Both groups ate significantly more of the prey than did sham-lesioned rats that were presented with a freshly killed mouse. When 4 hr was allowed for eating following a kill, rats with lesions of the lateral septum, medial accumbens, and medial hypothalamus each ate significantly more than spontaneous mouse killing rats. The greater prey eating by the lesioned animals is probably not the result of the prey being a highly palatable food since rats with medial hypothalamic lesions but not those with medial accumbens or septal lesions showed enhanced consumption of a sweetened lab chow over a 4 hr period. The quantitative similarity in the prey eating by spontaneous and lesion-induced mouse killers in the period immediately following the kill serves to further establish a relationship between these two kinds of killing. The greater eating that occurs in lesioned animals when a longer time is allowed for eating is consistent with other observations of excesses in the killing behavior of lesioned animals relative to spontaneous killers.

Animals↗
PubMed1984

Dissociation of prey killing and prey eating by naloxone in the rat.

Mouse killing rats matched for killing latency and prey eating were injected (IP) with 0.5, 2.0, or 5.0 mg/kg naloxone or 0.9% saline. Naloxone did not significantly inhibit prey killing or alter prey killing latency at any dose but did reduce prey eating by 50% at the two higher doses. The dissociation of prey killing and prey eating by naloxone is consistent with other evidence that these two behaviors are separate components of predation in rats.

Aggression↗
PubMed1984

Neural systems and the inhibitory modulation of agonistic behavior: a comparison of mammalian species.

The olfactory bulb, lateral septum, medial accumbens, medial hypothalamus, dorsal and median raphe, and amygdala are known from experiments in rats to participate in the inhibitory modulation of defensiveness and predation but not social aggression. The present paper surveys the influence of these structures in the inhibitory control of these same dimensions of agonistic behavior in other species. The existing evidence suggests that lesions in the lateral septum, medial accumbens, medial hypothalamus, or the dorsal and median raphe (or PCPA-induced depletion or serotonin) induce hyperreactivity to the experimenter in mice, rats, cats, dogs, and humans in every instance where they have been tested with one exception. The exception is that lesions in the medial hypothalamus of mice do not induce heightened reactivity. The same lesions do not cause this dramatic increase in reactivity to the experimenter in gerbils, hamsters, guinea pigs, or rabbits but do heighten some other species typical patterns of defensiveness such as alarm calls and avoidance of contact with conspecifics. Lesions in these same areas in monkeys have not been observed to heighten defensive behaviors. Predatory killing or killing of young conspecifics has been observed in hamsters, mice, rats, and cats in every instance where they have been examined following lesions of the olfactory bulbs, lateral septum, medial accumbens, medial hypothalamus, or the dorsal and median raphe nuclei (or PCPA-induced depletion of serotonin). Social aggression has been decreased with these same lesions in each case where they have been examined except for septal lesions in hamsters which have been reported to heighten social aggression. Across species, the consistency with which lesions of the olfactory region, lateral septum, medial accumbens, medial hypothalamus, and dorsal and median raphe nuclei alter defensiveness and predation but not social aggression supports the inference that neural systems exist which subserve the inhibitory modulation of these dimensions of behavior. Finally, the evidence that the disruption of functioning within these structures in humans results in increased agonistic responses to environmental stimuli serves to further establish the important role of this neural circuitry in the normal inhibitory modulation of agonistic behavior in humans.

Aggression↗
PubMed1984

Handling from weaning to adulthood does not prevent hyperdefensiveness induced by septal, medial accumbens, or medial hypothalamic lesions.

Weanling male hooded rats were handled or not handled for 10 min each day, 5 days/week, for 6 weeks. At the end of this time all animals received one of the following: a septal lesion, a medial accumbens lesion, a medial hypothalamic lesion, or a sham lesion. The animals were tested for defensiveness toward the experimenter on Days 3, 7, and 14 postoperatively. All behavioral testing was done blind. Each of the three lesions increased defensiveness toward the experimenter. However, with each lesion, there was no difference in the defensiveness scores of preoperatively handled and nonhandled animals at any of the postoperative test sessions while those of animals with medial hypothalamic lesions did not. These results are consistent with observations that hyperdefensiveness occurs in human subjects following tumors in each of these brain areas in spite of their familiarity with the situation in which they are observed. They contrast with observations that mouse killing induced by septal lesions is readily prevented by preoperative exposure to a mouse.

Age Factors↗
PubMed1983

Mouse killing in rats induced by lesions of the medial hypothalamus or medial accumbens: short-term preoperative exposure to a mouse does not suppress the killing.

Rats were either exposed or not exposed to a mouse in their living cage for a 48-hr period. At the end of this time a bilateral lesion was made in the medial accumbens region or in the medial hypothalamus. When tested 2 days postoperatively, the killing frequency among rats that had been exposed to mice preoperatively was not significantly lower than that of rats that were not preoperatively exposed. The ineffectiveness of preoperative experience in suppressing the mouse killing induced by medial accumbens and medial hypothalamic lesions is similar to that found previously with dorsal-median raphe lesions and olfactory bulb lesions and is in contrast to the ease with which preoperative experience prevents mouse killing induced by septal lesions and serotonergic lesions induced by 5,7-dihydroxytryptamine.

Aggression↗
PubMed1983

Non-invasive fetal monitoring using radiotelemetry.

A telemetry system for non-invasive monitoring of fetal heart rate and uterine contractions is described. Fetal heart information is obtained by means of Doppler ultrasound, and contractions information using an external tocodynamometer. The more important features of the device are described in detail; the full design is available from the authors. Typical recordings are presented, and the fetal heart rate traces are compared qualitatively with those obtained by direct ECG measurement, with the patient in bed, sitting and walking. The device is now in clinical use.

Electrocardiography↗
PubMed1982

A comparison of the effect of preoperative gentling on the mouse killing and reactivity induced by lesions of the lateral septum, the medial accumbens nucleus, and the medial hypothalamus.

Adult male rats were either gentled or not gentled 10 min each day for 5 days and then subjected to lesions of the lateral septum, the medial accumbens, the medial hypothalamus, or were given sham lesions. Mouse killing was tested in the living cage on Days 2, 7, and 14 postoperatively while reactivity to the experimenter was tested on Days 3, 8, and 15. The frequency of killing in the gentled groups was always significantly higher than that of the gentled sham-lesion controls, but the frequency of killing by the nongentled groups was seldom significantly higher than that of the nongentled sham-lesioned controls. Gentling caused a slight enhancement of killing in the lesioned animals and a slight attenuation of killing in the sham lesioned animals. Preoperative gentling attenuated reactivity to the experimenter in animals with lesions of the lateral septum but not in those with lesions of the medial accumbens nucleus or the medial hypothalamus. The observation that preoperative gentling tends to increase mouse killing confirms previous observations. The finding that preoperative gentling attenuates reactivity following septal but not medial accumbens or medial hypothalamic lesions suggests that these structures subserve different functions in the inhibitory modulation of defensive behavior.

Animals↗
PubMed1982

Medial hypothalamic lesions in the rat enhance reactivity and mouse killing but not social aggression.

In rats subjected to lesions of the medial hypothalamus, 8 of 11 animals became mouse killers and all manifested some degree of hyperreactivity to the experimenter. When introduced as intruders into a mixed sex colony group, the lesioned rats did not manifest piloerection nor did they emit flank attacks characteristic of social aggressive behavior. However, the lesioned animals did respond to the attacks of the resident male rats with significantly more counterattacks and biting than did sham-lesioned control rats. Spontaneous mouse killing rats also failed to show a level of social aggressive behavior significantly greater than that of sham-operated control rats, but the spontaneous mouse killers did kill rat pups in the colony groups. Alpha-male rats when introduced as an intruder into a colony group did exhibit piloerection and emit flank attacks characteristic of social aggressive behavior. These results demonstrate that the mouse killing and heightened reactivity associated with medial hypothalamic lesions do not represent an indiscriminant release of all forms of agonistic behavior.

Aggression↗
PubMed1982

Mouse killing in rats: a comparison of spontaneous killers and rats with lesions of the medial hypothalamus or the medial accumbens nucleus.

Mouse killing was observed and videotaped at forty-eight hr following surgery in rats with lesions of the medial hypothalamus or the medial accumbens. The initial attacks and killing bites of the lesioned rats were directed at the anterior dorsal surface, predominantly to the regions of the neck, shoulders, and thorax and did not differ from those of spontaneous mouse killing rats. The latency to attack was significantly shorter for the lesioned animals but the time required to kill following the attack tended to be longer. Lesioned animals spent significantly more time biting the prey following the kill and left significantly more bite marks on the prey than did the spontaneous killers. When the dead prey was moved about the cage following the kill, the lesioned animals showed a significantly greater tendency to attack it than did the spontaneous killers. Following the test of mouse killing, each rat was successively exposed to a freshly killed mouse, a cotton wad, and a wood block. The lesioned animals attacked the dead mouse and the cotton wad as though they were live mice whereas the spontaneous killers did not. These results suggest that while the killing is similar for lesioned and spontaneous killers, the lesioned animals show a heightened response to the killing experience. This is manifested in an exaggeration of attack behaviors toward prey and prey-like stimulus objects following an initial killing experience.

Aggression↗
PubMed1982

The inhibitory modulation of agonistic behavior in the rat brain: a review.

Neural regions which exercise an inhibitory influence on agonistic behavior are identified by the enhancement of agonistic behavior that follows their removal. The specific kinds of agonistic behaviors altered by each region are then examined. Increased reactivity to the experimenter and enhanced shock-induced fighting are produced by lesions of the region ventral to the anterior septum, the lateral septum, the medial hypothalamus, and the dorsal and median raphe nuclei. It is argued that the increased reactivity and shock-induced fighting correspond to an enhancement of defensive behavior. Mouse killing is induced by lesions of the anterior olfactory nucleus, the region ventral to the anterior septum, the lateral septum, the medial hypothalamus, the dorsal and median raphe nuclei, and the medial amygdala. Because the lesion-induced mouse killing is similar to that emitted by spontaneous mouse killers, it is argued that these regions normally exert an inhibitory control over predatory killing. The available evidence on social attack behavior has not convincingly identified regions exerting an inhibitory control over this dimension of behavior. Our conclusion is that separate brain systems exert an inhibitory control over defensive behavior, predatory killing, and social attack behavior. To a substantial extent, the regions modulating these behaviors appear to act independently of one another. The only neurotransmitter that is clearly active in these inhibitory systems is serotonin, and has only been directly implicated in the control of mouse killing by neurons originating in the dorsal and median raphe nuclei.

Aggression↗
PubMed1981

Cholinergic, dopaminergic, noradrenergic, or glutaminergic stimulation ventral to the anterior septum does not specifically suppress defensive behavior.

Three experiments investigated neurotransmitters which might function in the neural system ventral to the anterior septum modulating defensiveness in the rat. In the first experiment, a dose dependent suppression of defensive behavior to the experimenter was produced by intracranial infusion of carbachol or physostigmine but not dopamine, norepinephrine, or glutamate. The suppression of defensiveness did not occur when a carbachol-atropine sulfate mixture was infused. In a second experiment the cholinergic antagonists, atropine methyl nitrate or atropine sulfate, did not increase reactivity when infused ventral to the anterior septum although the nonspecific blocking agent lidocaine was effective. In a final experiment, the infusion of carbachol ventral to the anterior septum which had suppressed defensiveness was found to suppress eating and general activity as well, thus suggesting that the effect of carbachol on defensiveness was the result of a non-specific suppression of behavior. It is concluded that the specific modulation of defensiveness by the neural system ventral to the anterior septum is not mediated by acetylcholine, dopamine, noradrenaline, or glutamate.

Animals↗