Separate neural sites for d-amphetamine suppression of mouse killing and feeding behavior in rats

The present study was conducted to investigate several possible neural sites for d-amphetamine's effect on mouse killing and feeding behaviors. d-Amphetamine (10, 20, and 30 μg) injected into each lateral ventricle, suppressed mouse kiling, food, and water intake in a dose-dependent manner. Bilateral adminstration of d-amphetamine (20 μg) into the central amygdaloid nucleus abolished mouse killing behavior but did not affect feeding and drinking. By contrast, bilateral amphetamine injections into the substantia nigra, or into the ventral region of the caudate nucleus, did not suppress mouse killing behavior, but significantly decreased food and water intake. The lateral hypothalamus was sensitive to d-amphetamine injections, which suppressed mouse killing and food intake as well as water intake. d-Amphetamine injections into the nucleus accumbens produced inconsistent effects on mouse killing and feeding. Our observations suggest a differentiation of the neural sites that mediate feeding from those underlying mouse killing behavior.     

Factors in the waning of muricide in the rat. II. Digging behavior

If each mouse killed by a rat is removed from the rat's home cage and replaced immediately by another, the decline in the rate of killing within the one-hour sessions is accompanied by an increase in digging in the woodchip bedding material. Deprivation of the opportunity to dig by removal of the bedding material results in a statistically significant increase in kill rate. Since no other behaviors monitored showed a similar increase with this manipulation, it appears that digging may be a mechanism important in the waning of muricide. Furthermore, digging may be, in some sense, a functional equivalent of killing.     

Effects of some physiological and pharmacological manipulations on shock- facilitated mouse killing by onychomys leucogaster (Northern grasshopper mouse)

Onychomys leucogaster (northern grasshopper mice) were induced to kill mice with response-contingent shock, and the effects of several physiological, pharmacological, and endocrinological variables were assessed. Lesions of the septum facilitated mouse killing, while lesions of the amygdala abolished spontaneous mouse killing and delayed shock-facilitated killing. Chlorpromazine (2.5–5 mg/kg) and chlordiazepoxide (5–10 mg/kg) facilitated mouse killing on postdrug trials but did not affect killing when the animals were drugged. Adrenalectomy, castration, and castration adrenalectomy did not alter the frequency of kill nor were sex-related differences in killing noted. These results were compared to those found by others studying the effects of lesions and drugs on mouse killing by rats.     

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.     

Pharmacological antagonism of mouse-killing behavior in the olfactory bulb lesion-induced killer rat

Representative agents from all of the major classes of drugs that have been reported to be selective antagonists of spontaneous mouse-killing behavior (i.e., antidepres-sants, antihistamines, anticholinergics, and stimulants) were tested for their ability to antagonize the mouse-killing response in rats that became killers following removal of the olfactory bulbs (O.B. lesion-induced killer rat) and in spontaneous killers. All of the drugs tested selectively antagonized the killing behavior of both spontaneous and lesion-induced mouse-killing rats. Several drugs (i.e., imipramine, amitriptyline, d-amphetamine, and chlorpheniramine) were found to be significantly less potent antagonists of mouse killing in the 0.6. lesioned rat as compared to spontaneous killers. Since all of the drugs that exhibited significant differences in activity between the two models have been shown to possess the ability to elevate norepinephrine levels at receptor sites in the brain, alterations in noradrenergic systems may account for the differences in sensitivity that were observed in this study. The possibility that there may be a common neural substrate for mouse killing in the two models is discussed.     

Mouse killing by rats: Suppression by electrical stimulation ventral to the anterior septum

Killing of mice was suppressed in 18 out of 24 rats by electrical stimulation of the region ventral to the anterior septum lying between the vertical arm of the diagonal band of Broca and the rostral limb of the anterior commissure. The mean effective minimum stimulation intensity was 8.2 uA (60 HZ, RMS). Stimulation of the cingulate cortex did not suppress mouse killing (mean stimulus intensity: 38.7 uA). Electrical recordings revealed after discharge in response to the stimulation in only one animal. At the stimulation intensity which suppressed mouse killing, there was no significant suppression of eating in 6 of 9 animals tested. These results are consistent with other evidence implicating the region ventral to the anterior septum in the modulation of mouse killing in the rat.     

Enhanced social docility in male hooded rats by dermal cautery of the vibrissal pads

Ablation of the vibrissal pads in rats causes subsequent deposition of scar tissue with little or no regrowth of the vibrissae. Cauterized and intact mature male Long Evans rats were tested for shockelicited fighting, mouse killing, and colony intrusion forms of laboratory-induced aggression. The results revealed that only conspecific social fighting is blocked by ablation of the major vibrissal follicles. Although no significant group differences were noted in tests for mouse killing, shock-elicited paired fighting and territorial defense against a strange intruder were minimal in cauterized groups. The results emphasize the importance of specific sensory experience in reference to distinct forms of aggressive responding and support a new experimental technique for further investigation of sensory interactions with sources of aggressive behavior.     

Interspecific aggression and reactivity in rats: Effects of selective raphe lesions and additional olfactory bulb ablation

Large depletion of brain 5 HT has been shown to induce mouse-killing behavior in the rat. Selective lesions of the raphe nuclei have been investigated in order to determine whether the various components of the 5 HT system exert some specific control over this aggressive behavior. Electrolytic lesions of the dorsal or the median raphe nucleus do not induce mouse killing, whereas combined lesions of these nuclei elicit this behavior in about 40% of naive rats. Consequently, it appears that serotonergic neurons originating in the dorsal and median raphe nuclei work synergistically in mediating inhibitory control over mouse-killing behavior. Loco-motor activity is increased in novel environments by each of the selective lesions and to a larger extent by combined raphe lesions; 24 hours activity in resting conditions is unchanged during the light period, and increased during the dark period of the daily cycle by the various lesions. As it has been shown previously that hyper-activity in response to novelty following raphe lesions is not directly related to the 5 HT decrease in the brain, it appears that interspecific aggression and motor responsiveness must not be dependent on the same neural substrate within the raphe nuclei. The raphe lesions do not facilitate the elicitation of mouse killing by further olfactory bulb ablations, in contrast to earlier results where bulbectomy facilitated the induction of this behavior by raphe lesions.     

Short- and long-term decrements in toxicosis-induced odor-aversion learning: the role of duration of exposure to an odor

Six experiments employed an odor-aversion paradigm to investigate the role of the duration of exposure to an odor in determining that odor's subsequent associability with illness. Rats were exposed to an odor at times T1 and T2, and the second of these exposures was followed by toxicosis. When the initial odor exposure was brief, the odor aversion was attenuated with a moderate T1-T2 interval of 3 hr (Experiment 1) but not with long intervals of 28 hr and 76 hr (Experiment 2). In contrast, when the initial odor exposure was long, the odor aversion was attenuated at a long T1-T2 interval (Experiment 3). With a T1-T2 interval of 24 hr, a brief initial exposure did not attenuate odor aversions when the context either remained the same or was changed from T1 to T2, whereas a long initial exposure attenuated such aversions when the context remained the same but not when the context was changed (Experiment 4). With a T1-T2 interval of 3 hr, a brief initial exposure attenuated odor aversions when the context remained the same or was changed from T1 to T2, whereas a long initial exposure attenuated such aversions when the context remained the same but not when the context was changed (Experiment 5). A brief exposure at T1, either with or without a subsequent context "extinction," attenuated odor aversions when the T1-T2 interval was 3 hr but not when this interval was 24 hr; a long initial exposure at T1, without a subsequent context "extinction," attenuated odor aversions when the T1-T2 interval was 4 hr and 24 hr but with a subsequent context "extinction" did not attenuate such aversions at either 4-hr or 24-hr T1-T2 intervals (Experiment 6). The results demonstrate that the duration of exposure to an odor determined whether that odor presentation caused short- or long-term decrements in odor conditionability and are discussed in terms of the relation between self- and retrieval-generated processes.     

Some aspects of predatory behavior

Predatory behavior is conceived of as a loose chain of responses including searching for relevant stimuli, hunting or chasing potential prey, capturing or attacking prey, and killing and feeding on prey. These aspects, which may occur independently, are described and discussed separately with an emphasis on mammalian species of carnivores. Particular attention is paid to opportunism in prey selection, specific searching images with their possible antecedents, the role of hunger in prey attack, and the phenomenon of surplus killing. Finally a discussion of mouse killing by rats attempts to show similarities between this and other more traditional examples of predation.     

Learned helplessness in the rat: time course, immunization, and reversibility.

Rats, like dogs, fail to escape following exposure to inescapable shock. This failure to escape does not dissipate in time; rats fail to escape 5 min, 1 hr., 4 hr., 24 hr., and 1 wk. after receiving inescapable shock. Rats that first learned to jump up to escape were not retarded later at bar pressing to escape following inescapable shock. Failure to escape can be broken up by forcibly exposing the rat to an escape contingency. Therefore, the effects of inescapable shock in the rat parallel learned helplessness effects in the dog.     

A comparative,cross‐national analysis of partner‐killing by women in cohabiting and marital relationships in Australia and the United States

Using a national‐level United States database, T. K. Shackelford [Partner‐killing by women in cohabiting relationships and marital relationships. Homicide Studies 5: 253‐266, 2001] calculated rates of partner‐killing by women by relationship type (cohabiting or marital), by partner ages, and by the age difference between partners. Men in cohabiting relationships were 10 times more likely to be killed by their partners than were married men. Within marriages, the risk of being killed by a partner decreased with a man's age. Within cohabiting relationships, in contrast, middle‐aged men were at greatest risk of being killed by their partners. The risk that a man will be killed by his partner generally increased with greater age difference between partners. We sought to replicate the findings of Shackelford [2001] using national‐level data held as part of the National Homicide Monitoring Program (NHMP) at the Australian Institute of Criminology in Australia. The NHMP holds data on over 3,500 homicides that occurred in Australia between 1989 and 2000. Despite the higher rate of partner‐killing in the United States, and despite other cultural differences between the two countries (for example, the prominent gun culture in the United States), we replicated the key patterns with the Australian data. Aggr. Behav. 30:206–216, 2004. © 2004 Wiley‐Liss, Inc.     

Trace decay and the priming of short-term memory in long-delay taste aversion learning: Disruptive effects of novel exteroceptive stimulation

A variation of Kalat and Rozin's two-presentation paradigm was used to test the hypothesis that the first, as opposed to the second, presentation of a flavor conditioned stimulus (CS) constitutes the functional CS in two-presentation experiments involving moderate interflavor intervals (IFIs), and results in flavor aversions that are a function of the primary, as opposed to the secondary, conditioned stimulus-unconditioned stimulus (CS-US) interval. Contrary to the hypothesis, it was shown in Experiment 1 that holding the primary CS-US interval constant at 4 hr for each of three groups, while decreasing the secondary CS-US interval (i.e., the interval between the second flavor presentation and the illness) from 3.75 hr to 2.5 hr to .5 hr, resulted in the flavor aversion increasing as the secondary CS-US interval decreased. However, the aversion acquired by the group with a 0.5 hr secondary CS-US interval was also found to be significantly weaker than that acquired by a single-presentation 0.5 hr control group. In Experiment 2 it was demonstrated that animals exposed to novel exteroceptive stimulation (NES) immediately prior to a second flavor presentation that preceded the US by 0.5 hr acquired an aversion as strong as that acquired by a 0.5-hr control group. In Experiment 3 it was demonstrated that, in the absence of a second flavor presentation, animals exposed to novel exteroceptive stimulation 0.5 hr prior to the US acquired a weaker flavor aversion than did animals not exposed to novel exteroceptive stimulation during the 4-hr flavor CS-illness US interval. The contrasting effects of novel exteroceptive stimulation observed in Experiments 2 and 3 were replicated in Experiment 4. The results suggest, consistent with the trace-decay hypothesis and Wagner's (1976) general model of stimulus processing, that exposure to novel exteroceptive stimulation disrupts continued processing of the short-term memory (STM) trace of the initial presentation of a flavor CS, and hence minimizes stimulus preexposure effects attributable to the priming of STM.     

Aggression as a reinforcer: operant behavior in the mouse-killing rat

Two experiments examined mouse killing as a reinforcer of key pressing by rats that killed mice. In Experiment I, mouse-killing rats performed the key-pressing response when each press was reinforced with presentation of a mouse. Offered a choice between a key that yielded presentation of mice and one that did not, the rats preferred the key that yielded mice. When the contingency was reversed, the rats preferred the other key and continued to kill mice. In Experiment II, mouse-killing rats that did not kill rat pups performed a key-pressing response reinforced with presentation of mice on a variable-interval schedule. In tests for responding reinforced on that schedule with presentation of normal mice, anesthetized mice, dead mice, or rat pups, these rats that killed mice but not rat pups exhibited a decline in response rate when rat pups were the reinforcer. Altering the condition of the mice did not significantly affect performance.     

Killing and the Time-relative Interest Account

Jeff McMahan appeals to what he calls the “Time-relative Interest Account of the Wrongness of Killing” to explain the wrongness of killing individuals who are conscious but not autonomous. On this account, the wrongness of such killing depends on the victim’s interest in his or her future, and this interest, in turn, depends on two things: the goods that would have accrued to the victim in the future; and the strength of the prudential relations obtaining between the victim at the time of the killing and at the times these goods would have accrued to him or her. More precisely, when assessing this interest, future goods should be discounted to reflect reductions in the strength of such relations. Against McMahan’s account I argue that it relies on an implausible “actualist” view of the moral importance of interests according to which satisfactions of future interests only have moral significance if they are satisfactions of actual interests (interests that will in fact exist). More precisely, I aim to show that the Time-relative Interest Account (1) does not have the implications for the morality of killing that McMahan takes it to have, and (2) implies, implausibly, that certain interest satisfactions which seem to be morally significant are morally insignificant because they are not satisfactions of actual interests.     

Undernutrition by rearing in large litters delays the development of reflexive, locomotor, and memory processes in mice

In three experiments, the effects of early postnatal undernutrition on the ontogeny of several behavioral capacities of varying complexity were investigated in the mouse. Following birth, mouse pups in all experiments were reared in either "normally nourished" or "undernourished" conditions by maintaining litter sizes at 6 or 16, respectively. Experiments 1 and 2 examined the development of adultlike patterns of swimming behaviors and spontaneous locomotor activity, respectively, as a function of litter size. The maturation of both behavior patterns was delayed by about 2 days in the 16-litter mice. In Experiment 3, normally nourished and undernourished mice received 25 trials in a shock-escape T-maze at 9, 11, and 13 days of age, followed by similar retention tests 24 hr later. Although litter size had little effect upon correct turns at each age during training, mice reared in litters of six exhibited significant retention of prior training by 12 days of age, whereas comparable retention was not noted for the large litter mice until 14 days of age. Overall, these results suggest that nutritional deficits, imposed by rearing in large litters during the postnatal period of rapid central nervous system maturation, retard the development of behavioral capacities involving both unlearned and learned responses.     

Rapid, Labile, and Protein Synthesis– Independent Short-Term Memory in Conditioned Taste Aversion

Short-term memory is a rapid, labile, and protein-synthesis-independent phase of memory. The existence of short-term memory in conditioned taste aversion (CTA) learning has not been demonstrated formally. To determine the earliest time at which a CTA is expressed, we measured intraoral intake of sucrose at 15 min, 1 hr, 6 hr, or 48 h after contingent pairing of an intraoral infusion of 5% sucrose (6.6 ml over 6 min) and toxic lithium chloride injection (76 mg/kg). Rats were implanted with intraoral catheters to allow presentation of taste solutions at arbitrary times. Intraoral intake was measured under conditions of long-delay, single-trial learning typical of CTA. Rats decreased intraoral intake of sucrose at 15 min after contingent pairing of sucrose and LiCl, but not after noncontingent LiCl or sucrose. Thus CTA learning can be expressed rapidly. To determine if short-term CTA memory is labile and decays in the absence of long-term memory, we measured intraoral intake of sucrose after pairing sucrose with low doses of LiCl. Rats received an intraoral infusion of 5% sucrose (6 ml/6 min); 30 min later LiCl was injected at three different doses (19, 38, or 76 mg/kg). A second intraoral infusion of sucrose was administered 15 min, 1 hr, 3 hr, 4.5 hr, 6 hr, or 48 hr later. The formation of long-term CTA memory was dependent on the dose of LiCl paired with sucrose during acquisition. Low doses of LiCl induced a CTA that decayed within 6 hr after pairing. Central administration of the protein synthesis inhibitor cycloheximide prior to LiCl injection blocked long-term CTA expression at 6 and 48 hr, but not short-term CTA expression at 1 hr. Thus, short-term memory for CTA learning exists that is acquired rapidly and independent of protein synthesis, but labile in the absence of long-term memory formation.     

Healing from Moral Injury: A Qualitative Evaluation of the Impact of Killing Treatment for Combat Veterans

This paper evaluates the Impact of Killing (IOK) treatment—a psychological intervention designed to address moral injury and trauma associated with killing in war. Using qualitative data from interviews with 28 combat veterans, we examine IOK’s impact, how it differs from other trauma-focused treatments, and how it can be improved to better meet veterans’ needs. We found that many veterans processed their killing experiences for the first time in IOK, even though all had previously completed evidence-based treatments for posttraumatic stress disorder. Several described killing in war as the most distressing and transformative trauma of their lives, and all affirmed the value of an intervention focused directly and explicitly on moral injury and killing. IOK helped veterans to acknowledge their grief, shame, and distress; gently but critically examine their thoughts and beliefs about killing in war; and make strides toward acceptance, reconciliation, and forgiveness.     

A moral justification for killing in self-defence

In the first part of this paper I will argue that for a case to be one of killing in self-defence at least the following three important conditions need to be met: (i) the defender's death must seem to him/her to be imminent; (ii) there must be a choice forced upon the defender between being killed or killing his/her attacker; (iii) the responsibility for (i) and (ii) must be the attacker's. I go on to point out that a lethal use of force which meets conditions (i)—(iii) is thought by most people to be morally permissible. However we believe also that everyone has the right to life and this cannot be taken away under any circumstances. But if this is so, how can we justify one person intentionally killing another? Or to put the point differently: what, in our moral assessment of such cases, are we to claim an attacker has done that is so morally wrong we are prepared to argue that if one of them has to be killed, it is the attacker? I hope to answer this question in the second part of my paper by developing a strand of ethical thought, associated with Kant.     

Judging the Goring Ox: Retribution Directed Toward Animals

Prior research on the psychology of retribution is complicated by the difficulty of separating retributive and general deterrence motives when studying human offenders (Study 1). We isolate retribution by investigating judgments about punishing animals, which allows us to remove general deterrence from consideration. Studies 2 and 3 document a “victim identity” effect, such that the greater the perceived loss from a violent animal attack, the greater the belief that the culprit deserves to be killed. Study 3 documents a “targeted punishment” effect, such that the responsive killing of the actual “guilty” culprit is seen as more deserved than the killing of an almost identical yet “innocent” animal from the same species. Studies 4 and 5 extend both effects to participants' acceptance of inflicting pain and suffering on the offending animal at the time of its death, and show that both effects are mediated by measures of retributive sentiment, and not by consequentialist concerns.