Predatory behavior in laboratory mice: strain and sex comparisons.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This report presents studies which relate limbic epileptic excitability to behavioral measures of defensive suppression of predatory attack in cats. Correlated with heightened defensiveness to environmental stimuli among non-killer cats is a heightened amygdaloid epileptic excitability, as well as a heightened conduction of amygdaloid epileptic activity to thalamic and hypothalamic substrates of predatory response in the amygdala to the complex visual stimuli presented by rat prey. These neurosensory responses correlate well with measures of epileptic excitability. Brain and behavior measures appear related since enhancement of excitability in the amygdala and of projection of epileptic activity by repeated electrical stimulation of predatory attacks. Furthermore, the ventral hippocampus seems capable of antagonizing the behaviorally suppressive effects of heightened amygdaloid excitability perhaps at points of convergence of amygdaloid and hippocampal output.
Previous studies have shown that, at certain dose levels, ethanol can exert a powerful, facilitatory effect on aggressive behavior in both animals and humans. In the cat, however, it was discovered that ethanol differentially alters two forms of aggression that are common to this species. Defensive rage behavior is significantly enhanced, whereas predatory attack behavior is suppressed by ethanol administration. One possible mechanism governing alcohol's potentiation of defensive rage behavior is that it acts on the descending pathway from the medial hypothalamus to the midbrain periaqueductal gray (PAG)-an essential pathway for the expression of defensive rage behavior that uses excitatory amino acids as a neurotransmitter. This hypothesis is supported by the finding that the excitatory effects of alcohol on defensive rage behavior are blocked by administration of the N-methyl-D-aspartate antagonist alpha-2-amino-7-phosphoheptanoic acid (AP-7) when microinjected into the periaqueductal gray, a primary neuronal target of descending fibers from the medial hypothalamus that mediate the expression of defensive rage behavior. Thus, the present study establishes for the first time a specific component of the neural circuit for defensive rage behavior over which the potentiating effects of ethanol are mediated.
The exposure in humans to ethanol or barbiturates during prenatal or neonatal development is common. There are indications that the magnitude of the resulting symptoms may be genetically determined. In the present article, an animal model was established for the study of the genetic determination of the neurosensitivity to ethanol and barbiturates administered during prenatal and/or neonatal development. Inbred C57BL/10 (C57) and DBA/1 (DBA) mice were employed in the ethanol studies and these strains and the outbred HS/Ibg (HS) were used in the barbiturate studies. Early ethanol administration induced a long lasting increase in the susceptibility to audiogenic seizures in both strains but to a greater degree in C57. Neuropharmacological studies implicated the serotonergic but not the noradrenergic system as mediating the early ethanol induced changes in audiogenic seizures. Open field activity was decreased but only in C57. Male agonistic behavior and predatory behavior were greatly reduced by early ethanol administration but mainly in DBA. Long term induction of the activity of the hepatic enzymes, alcohol dehydrogenase and microsomal ethanol oxidizing system, occurred in both strains after early exposure to ethanol. After early exposure to phenobarbital HS mice had long lasting increases in the susceptibility to audiogenic seizures and in the hippocampus related behaviors, spontaneous alternations and eight arm maze performance. The hepatic microsomal drug oxidizing system was induced in adult HS mice with early phenobarbital (PhB) exposure. Early PhB exposure also caused long term decreased sensitivity to ethanol narcosis and an accelerated acquisition to barbiturate tolerance, possibly mediated via a change in the sensitivity of the post synaptic dopamine receptors. Changes in the PhB treated offspring also included a reduction in the levels thyroid hormone. Early exposure to PhB resulted in a long term deficit in the area of brain layers, number of neurons, dendritic spines and the ultrastructure. Strain comparison suggested that DBA was less neurosensitive to early PhB administration than both HS and C57. It was concluded that genotype-environment interaction exists in the effect of drugs on the developing CNS.
The topographic distribution of retinal ganglion cells and their cell body size have been studied in five Falconiform species, including predatory (chilean eagle Buteo fuscenses australis, and sparrow hawk Falco sparverius) and carrion-eating (chimango caracara Milvago chimango; condor Vultur gryphus, and black vulture Coragyps atratus) birds. All these species had a well defined nasal fovea and a horizontal streak. Instead of a temporal fovea as in eagles and hawks, an afoveate temporal area is present in chimango, condor, and vulture. The highest ganglion cell density was found in the nasal fovea of Falco and Buteo with 65,000 and 62,000 cells/mm2, respectively. A negative correlation between ganglion cell density and cell body size was found in all the species studied. The specializations of the temporal retina showed a rather homogenous population of medium sized neurons, while the nasal foveas showed a homogeneous population of smaller ganglion cells. Finally, the peripheral retina showed a heterogeneous population of large, medium, and small ganglion cells. Predatory behavior appears to be closely related to foveal specializations, and is best exemplified in the eagle and hawk and to a lesser extent in the chimango.
The medial amygdala is known to powerfully suppress predatory attack behavior elicited by electrical stimulation of the lateral hypothalamus of the cat. In the preceding paper, it was shown that the initial limb of a pathway subserving suppression of predatory attack from the medial amygdala to the lateral hypothalamus projects to the ventromedial hypothalamus and its functions are mediated by substance P. The present study tested the hypothesis that the second limb of the pathway subserving medial amygdaloid suppression of predatory attack behavior projects from the medial to lateral hypothalamus and its functions are mediated by GABA. Cannula electrodes were implanted into the lateral hypothalamus for elicitation of predatory attack behavior as well as for the microinfusion of GABA compounds. Monopolar stimulating electrodes were implanted into sites within the medial amygdala from which subseizure levels of stimulation could suppress predatory attack behavior. Initially, the effects of dual stimulation of the medial amygdala and lateral hypothalamus upon response latencies for predatory attack were compared with single stimulation of the lateral hypothalamus alone. Dual stimulation was shown to significantly suppress predatory attack elicited from the lateral hypothalamus. Then, the GABAA receptor antagonist, bicuculline, was microinjected into sites within the lateral hypothalamus from which predatory attack was elicited in doses of 0.015, 0.075 and 0.15 nmol and paired trials of single and dual stimulation were again repeated in a manner identical to that applied prior to drug administration. Drug infusion produced a blockade of medial amygdaloid suppression of predatory attack in a time- and dose-dependent manner. Conversely, microinfusions of the GABAA receptor agonist, muscimol (10, 25 and 50 pmol), into the same lateral hypothalamic 'attack' site in the absence of medial amygdaloid stimulation suppressed predatory attack, thus simulating the effects of medial amygdaloid stimulation. Furthermore, pretreatment with bicuculline microinjected into the lateral hypothalamus blocked the suppressive effects of substance P, that was infused into the ventromedial hypothalamus, upon predatory attack. Receptor autoradiography demonstrated the presence of high affinity binding for GABAA receptors in the lateral hypothalamus. A combination of immunocytochemical and retrograde axonal tract tracing procedures, in which Fluoro-Gold was microinjected into the lateral hypothalamic attack sites, revealed the presence of populations of neurons labeled for both Fluoro-Gold and GABA in the ventromedial hypothalamus. These findings provide new evidence for the existence of a pathway from the medial to lateral hypothalamus whose functions are mediated by GABA. Thus, the overall findings provide support for the view that the pathway from the medial amygdala to the lateral hypothalamus underlying suppression of predatory attack behavior involves a two-neuronal arc: the first neuron projects from the medial amygdala to the medial hypothalamus and its functions are mediated by substance P: the second neuron involves a GABAergic pathway originating in the ventromedial hypothalamus and which projects to the lateral hypothalamus.
The medial amygdala is known to powerfully suppress predatory attack behavior in the cat, but the mechanisms underlying such modulation remain unknown. The present study tested the hypothesis that medial amygdaloid suppression of predatory attack is mediated, in part, by a pathway from the medial amygdala to the medial hypothalamus which utilizes substance P as a neurotransmitter. Stimulating electrodes were implanted into the medial amygdala and cannula electrodes were implanted into both the medial and lateral hypothalamus. Predatory attack behavior was elicited by electrical stimulation of the lateral hypothalamus. In the first phase of the study, paired trials compared attack latencies of single stimulation of the lateral hypothalamus with those following dual stimulation of the lateral hypothalamus and medial amygdala. Attack latencies were significantly elevated following dual stimulation of the medial amygdala and lateral hypothalamus. In the second phase of the study, dose and time dependent decreases in response suppression were noted following the infusion of the substance P (NK1) receptor antagonist, CP96.345 (in doses of 0.05, 0.5 and 2.5 nmol) into the medial hypothalamus. In third phase of the study, the effects of microinjections of the substance P receptor agonist, [Sar9.Met(O2)11]-substance P (in doses of 0.5, 1.0 and 2.0 nmol), directly into the medial hypothalamus upon lateral hypothalamically elicited predatory attack behavior were determined. Microinfusion of this drug elevated attack response latencies in a dose- and time-dependent manner. In addition, pretreatment with CP96,345 into the medial hypothalamus blocked the suppressive effects of subsequent delivery of [Sar9,Met(O2)11]-substance P into the same medial hypothalamic site. Other parts of the study demonstrated the presence of: (1) high densities of substance P receptors in the ventromedial hypothalamus, and (2) neurons that are positively labeled for substance P that project from the medial amygdala to the ventromedial hypothalamus as demonstrated by retrograde labeling with Fluoro-Gold. These findings provide support for the hypothesis that medial amygdaloid suppression of lateral hypothalamically elicited predatory attack behavior includes a substance P pathway from the medial amygdala to the medial hypothalamus. The findings further suggest that stimulation of the medial amygdala activates substance P receptors in the medial hypothalamus, thus triggering an inhibitory mechanism from the medial to the lateral hypothalamus, resulting in suppression of predatory attack behavior.
Aggressive behavior can be classified into three major categories: defense, social attack and predatory behavior. The predatory behavior of rats, which prompts them to prey on mice (muricidal behavior) may be induced by injection of high doses (11 mg/kg) of Delta9-tetrahydrocannabinol (THC) or by acute magnesium deficiency. We have studied the effect of a single injection of low doses of THC (2, 4 or 8 mg/kg) in rats with a severe (50 ppm magnesium diet) or moderate (150 ppm) magnesium deficiency. The combination of moderate magnesium deficiency with low doses of THC induced muricidal behavior in all the rats and an increase in aggressiveness at the doses of 4 or 8 mg/kg of THC. Hyperaggressiveness increased with magnesium deficiency severity. Serotonin is probably involved in aggressiveness induced by both moderate magnesium deficiency and low doses of THC, but implication of other neurotransmitters and magnesium deficiency-induced alterations of CB1-and/or CB2-receptor expression are not excluded.
Praying mantids are thought to be so strictly predacious that, historically, carnivorousness has been used as a defining characteristics of the taxon Mantodea, and no data exist on other ingestive behaviors. We observed food- and water-deprived male and female Tenodera aridifolia sinensis (Sauss.) and Sphodromantis lineola (Burr.) in various situations and found that their ingestive behaviors are more variable than generally recognized. Both species regularly drink water in response to deprivation, the amount imbibed being correlated with the total (but not daily) percent of initial body weight lost. When presented with stimuli consisting of plastic beads of different reflective quality (shiny clear, opaque frosted, or matte black), lighted by a single direct light source, the shiny stimuli consistently elicited the most drinking-like behavior by the mantids. The preference was consistent, whether stimuli were presented together or singly. This suggests that visual cues can be used to identify water and are alone capable of maintaining drinking-like behavior. When S. lineola were presented with various stimuli, including diced apple and diced banana, in a five-way or a three-way choice test, mantids that chose a stimulus within the allotted time consistently ate the diced banana. When presented one of two stimuli differing only in odor (30 x 20 x 15 mm cloth bags filled with either plastic beads or banana), S. lineola did not attempt to eat the former, but 50% attempted to eat the bag of banana. Eating bouts were always preceded by antennae drumming in the direction of, or over the stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)
The present study was carried out in five cats which did not attack the rats spontaneously. Predatory attack on an anaesthetized rat was elicited by electrical stimulation of extreme lateral regions of hypothalamus. These sites were stimulated at a current strength from 300-700 microa to evoke a predatory attack on an anaesthetized rat. The attack was accompanied by minimal affective display such as alertness, pupillary dilatation, and culminated in beck biting at higher current strength. A scoring system allowed the construction of stimulus response curves, which remained fairly constant when repeated over a period of 3-4 weeks. Microinfusions of norepineprine and clonidine in 4.0 and 5.0 microg dose respectively in locus ceruleus and adjoining tegmental fields facilitated the predatory attack and there was a significant reduction in the threshold current strength for the elicitation of affective and somatomotor components. Microinfusions of yohimbine, an alpha-2 blocker, in 5 microg dose completely blocked the predatory attach response as indicated by an increase in the threshold current strength for the affective components. The somatomotor components were completely inhibited and could not be elicited even when the current strength was increased to 1000 microA. The predatory attack behavior remained completely inhibited for almost two hours following microinfusion of yohimbine. During this period, the animal was extremely drowsy and reacted very slowly even to a painful stimulus such as pinching of tail. Microinfusions of propranalol (beta-blocker), practalol (beta-1 blocker), prazosin (alpha-1 antagonist), propylene glycol as well as saline in similar volumes (0.5 microl) as control failed to produce any blocking effect, thus indicating the involvement of alpha-2 adrenoceptive mechanisms in the modulation of predatory attack in this region of midbrain. The facilitatory effects of norepinephrine and clonidine were significant at P<0.01 and P<0.05 respectively with Wilcoxon's signed rank test. The inhibitory effects of yohimbine were significant at P<0.05. The present study indicates the involvement of alpha-2 adrenoceptive mechanisms in the facilitation of hypothalamically elicited predatory attack.
The predatory behavior of rattlesnakes includes many distinctive preparatory phases leading to an extremely rapid strike, during which venom is injected. The rodent prey is then rapidly released, removing the snake's head from retaliation by the prey. The quick action of the venom makes possible the recovery of the dispatched prey during the ensuing poststrike period. The strike is usually completed in less than 0.5 s, placing a premium on an accurate strike that produces no significant errors in fang placement that could result in poor envenomation and subsequent loss of the prey. To clarify the basis for effective strike performance, we examined the basic kinematics of the rapid strike using high-speed film analysis. We scored numerous strike variables. Four major results were obtained. (1) Neurosensory control of the strike is based primarily upon sensory inputs via the eyes and facial pits to launch the strike, and upon tactile stimuli after contact. Correction for errors in targeting occurs not by a change in strike trajectory, but by fang repositioning after the jaws have made contact with the prey. (2) The rattlesnake strike is based upon great versatility and variation in recruitment of body segments and body postures. (3) Forces generated during acceleration of the head are transferred to posterior body sections to decelerate the head before contact with the prey, thereby reducing impact forces upon the snake's jaws. (4) Body acceleration is based on two patterns of body displacement, one in which acute sections of the body open like a gate, the other in which body segments flow around postural curves similar to movements seen during locomotion. There is one major implication of these results: recruitment of body segments, launch postures and kinematic features of the strike may be quite varied from strike to strike, but the overall predatory success of each strike by a rattlesnake is very consistent.
We compared the tendency for 4th-instar larvae to prey on newly hatched larvae, and the vulnerability of those 1st instars to such predation for Aedes triseriatus (Say), Ae. aegypti (L.), and Ae. albopictus (Skuse), all container-breeding mosquitoes. The latter 2 species were introduced to North America and are now sympatric with Ae. triseriatus, a native species in eastern North America. The experiment also enabled the assessment of species-specific influences of food supplements and spatial heterogeneity on predatory behavior. Ae. triseriatus was substantially more predatory and less susceptible to attack than the other 2 species. These differences were amplified in food-deprived and spatially simple conditions, indicating that Ae. triseriatus predatory behavior may have important retarding effects on the colonization of occupied treehole habitats by Ae. albopictus. Ae. aegypti and Ae. albopictus were similar in imposing little (Ae. aegypti) or almost no (Ae. albopictus) predation on 1st instars and in being susceptible to predation by Ae. triseriatus. The general lack of species-specific differences between Ae. aegypti and Ae. albopictus indicates that interspecific predation is not a likely explanation for the rapid displacement of Ae. aegypti by Ae. albopictus in domestic containers in the southeastern United States.
The search for useful model systems to study sensory processing in vertebrate nervous systems has resulted in many neuroethological studies investigating the roles played by a single sensory modality in a given behavior. However, animals behaving in a complex, three-dimensional environment receive a large amount of information from external and internal receptor arrays. Clearly, the integration of sensory afference arising from different modalities into a coherent 'gestalt' of the world is essential to the behaviors of most animals. Over the past several years researchers in my laboratory have examined the roles played by the visual and lateral line sensory systems in organizing the feeding behavior of two species of predatory teleost fishes, the largemouth bass, Micropterus salmoides and the muskellunge, Esox masquinongy. The free-field feeding behaviors of these fishes was studied quantitatively in intact animals and compared to animals in which the lateral line and visual systems had been selectively suppressed. The data show that both bass and muskie employ similar approach and strike behaviors. Vision is crucial to the initial detection of, and orientation to, prey. Lateral line and vision together determine the optimum distance and angular deviation for the initiation of a rapid strike toward the prey. Blinded animals are able to strike accurately at prey at very close ranges and small angular deviations, indicating that this modality presents sufficient information to direct the behavior during the final phases of the strike. The results demonstrate that there is a hierarchy of senses involved in feeding behavior, with different modalities playing critical roles in succeeding phases.