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During competitive interactions, such as fighting and predation, animals perform various actions, some of which are easy to characterize and label, some of which are reliably repeated. Such 'behavior patterns' are often the measures of choice when comparing across species and experimental contexts. However, as Bob Blanchard and others have pointed out, such measurements can be misleading as in competitive interactions in which the animals compete for some advantage, often the biting or otherwise contacting a particular target on the opponent's body. In this context, the animals' behavior is better analyzed in terms of the tactics of attack and defense deployed by the combatants to gain or avoid contact with those targets. Several examples are shown to reveal that this is an important distinction as simply scoring predefined behavior patterns can obscure the dynamic context in which the actions are performed. This can lead to confounding species and experimental differences and the mislabeling of combat actions as communicatory signals., (Copyright © 2015. Published by Elsevier Inc.)

We monitored the number of intravascular platelet-leukocyte aggregates (PLAs) and thrombotic occlusions (TOs) by intravascular microscopy in the mesentery of rats receiving antiphospholipid (aPL) immunoglobulin G (IgG) purified from the sera of patients with antiphospholipid syndrome. aPL IgG had no procoagulant effect, but it caused rapid endothelial deposition of fibrinogen, followed by PLA and TO in rats receiving an intraperitoneal injection of bacterial lipopolysaccharide 3 hours before IgG infusion. Anti-beta2-glycoprotein I-depleted aPL IgG failed to induce PLAs and TOs. C3 and C9 colocalized with aPL IgG on the mesenteric vessels. The number of PLAs and TOs was markedly reduced in C6-deficient rats and in animals treated with anti-C5 miniantibody, suggesting the contribution of the terminal complement (C) complex to the aPL antibody-mediated intravascular thrombosis. In conclusion, our data indicate that antibodies to beta2-glycoprotein I trigger coagulation subsequent to a priming proinflammatory factor and that the terminal C complex is the main mediator of the coagulation process.

The infrequent occurrence of septic shock in patients with inherited deficiencies of the terminal complement components experiencing meningococcal disease led us to suspect that the terminal complement complex is involved in vascular leakage. To this end, the permeabilizing effect of the cytolytically inactive soluble terminal complement complex (SC5b-9) was tested in a Transwell system measuring the amount of fluorescein-labeled BSA (FITC-BSA) leaked through a monolayer of endothelial cells. The complex caused increased permeability to FITC-BSA after 15 min as opposed to the prompt response to bradykinin (BK). The effect of SC5b-9 was partially reduced by HOE-140 or CV-3988, two selective antagonists of BK B2 and platelet-activating factor receptors, respectively, and was completely neutralized by the mixture of the two antagonists. Also, DX-88, a specific inhibitor of kallikrein, partially inhibited the activity of SC5b-9. The permeabilizing factor(s) released after 30 min of incubation of endothelial cells with SC5b-9 caused a prompt leakage of albumin like BK. Intravital microscopy confirmed both the extravasation of circulating FITC-BSA across mesenteric microvessels 15 min after topical application of SC5b-9 and the complete neutralization by the mixture of HOE-140 and CV-3988. SC5b-9 induced opening of interendothelial junctions in mesenteric endothelium documented by transmission electron microscopy.

Borrelia burgdorferi, the etiological agent of Lyme disease, comprises three genospecies, Borrelia garinii, afzelii, and burgdorferi sensu strictu, that exhibit different pathogenicity and differ in the susceptibility to C-mediated killing. We examined C-sensitive and C-resistant strains of B. burgdorferi for deposition of C3 and late C components by fluorescence microscope and flow cytometry. Despite comparable deposition of C3 on the two strains, the resistant strain exhibited reduced staining for C6 and C7, barely detectable C9, and undetectable poly C9. Based on these findings, we searched for a protein that inhibits assembly of C membrane attack complex and documented an anti-human CD59-reactive molecule on the surface of C-resistant spirochetes by flow cytometry and electron microscopy. A molecule of 80 kDa recognized by polyclonal and monoclonal anti-CD59 Abs was identified in the membrane extract of C-resistant strains by SDS-PAGE and Western blot analysis. The molecule was released from the bacterial wall using deoxycholate and trypsin, suggesting its insertion into the bacterial membrane. The CD59-like molecule acts as C inhibitor on Borrelia because incubation with F(ab')(2) anti-CD59 renders the serum-resistant strain exquisitely susceptible to C-mediated killing and guinea pig erythrocytes bearing C5b-8, unlike the RBC coated with C5b-7, are protected from reactive lysis by the bacterial extract. Western blot analysis revealed preferential binding of the C inhibitory molecule to C9 and weak interaction with C8 beta.

Play fighting in rats is most frequent in the juvenile phase (30-40 days) and then wanes following puberty. During the juvenile phase, the most commonly used defensive tactic to block access to the nape (i.e., the play target) is to rotate around the longitudinal axis to supine. From this position of lying on its back, the defender uses its limbs to hold off the attacking pup. With the onset of puberty males, but not females, switch to more adultlike patterns of defense. The adultlike pattern involves partially rotating around the longitudinal axis of the body, but retaining ground contact with the hindpaws. In this position, the defender is able to rear to a defensive upright posture, or can slam into the partner with its hip. In this study, the manner of onset of play fighting and its components was investigated by daily videotaped observations of six litters of Long Evans hooded rats, starting at 15 or 16 days and ending at 30 days postnatally. The predominant form of social interaction in the midteens was allogrooming, but by 20 days, playful attacks to the nape were the most common form of contact. Allogrooming was most often directed to the head, not the nape. With respect to playful defense, the more adultlike tactics matured first, with all tactics present in the repertoire by 20 days. The fully juvenile pattern of defense did not mature until 25-30 days with both males and females exhibiting the same developmental pattern. These data lead to several conclusions. First, play fighting is a separate category of behavior from the outset, and does not emerge from allogrooming. Second, the adultlike defense patterns do not emerge gradually from the juvenile ones at puberty, but rather, all are present in the repertoire from infancy; and third, both males and females have the same pattern of onset of play fighting. These conclusions are discussed with respect to the possible functions of juvenile play fighting.

In rats (Rattus norvegicus), juvenile males engage in more play fighting (a male-typical behavior) than do juvenile females, and this difference is based on perinatal influences of androgens. We show that there are qualitative and quantitative differences between the sexes in the type of defensive responses and their manner of execution. In defensive responses rats try to avoid having their napes contacted by the partner's snout. The sex differences arise from females' greater response distance; that is, females responded to an approach when the partner's snout was further from the nape. This permits females to use different defensive responses and to use them more successfully. This greater response distance is defeminized by the neonatal administration of testosterone propionate. Our findings suggest that play fighting in rats has both male- and female-typical features and that these are, at least in part, influenced perinatally by androgens.

Although the red nucleus consists of cells of origin for the rubro-spinal and rubro-olivary tracts, fibers of passage, including those of the superior cerebellar peduncle, which project from the cerebellum to the ventrolateral thalamus, pass through it. This study examined the relative effect of cell vs. fiber damage in the red nucleus on a number of behaviors thought to involve the red nucleus, including a skilled movement of reaching for food with a forelimb, postural righting on a surface and in the air, and learning a place response in a swimming pool test. Rats received unilateral or bilateral red nucleus lesions, using either the relatively cell-specific neurotoxins, ibotenic and quinolinic acid, or non-specific electrolytic anodal lesions. Both neurotoxic lesions effectively eliminated all red nucleus cell bodies, and in some animals they produced small cavities in the red nucleus and/or loss of cells in adjacent structures. Electrolytic lesions destroyed both cells and fibers, leaving a large cavity. The severity of the behavioral deficits were not related to the loss of red nucleus cells and there was a close relation between fiber damage and behavioral impairments on all of the tasks. The results suggest that for a number of behaviors, which have been thought to involve the red nucleus, impairments are more closely associated with fiber damage or damage to structures outside the red nucleus than they are to damage to cells of the red nucleus.

The development of righting was studied in the young of Dasyurus hallucatus, a small marsupial from northern Australia. Young were tested from birth to weaning. Righting began at 40 days, when tactile input on the snout triggered rotation to prone. Over the next 15-20 days, asymmetrical tactile input on the body triggered righting movements by the hindlegs (and later by the forelegs). Vestibular righting reflexes developed after these tactile righting reflexes. Furthermore, asymmetrical vestibular righting (i.e., when the young are held laterally in the air) developed before symmetrical vestibular righting (i.e., when held downward by the pelvis or placed supine in water). Vestibular righting triggered by falling supine in the air did not develop until about 80 days. This study further demonstrates that righting behavior does not consist of a single, integrated motor pattern, but a suite of motor patterns having independent control mechanisms and patterns of development.

Play is a distinctive behavior of young mammals, especially mammals with a well-developed forebrain. For this reason it is thought that there may be a relation between forebrain evolution and highly elaborated play behavior. This study investigated the contribution of the cortex to play behavior by comparing play in control and neonatally decorticated rats (Rattus norvegicus). Play fighting in rats involves the combination of attack by one rat and defense by the recipient, with pinning arising when specific patterns of defense are used. Whether paired with another decorticate or with an intact pairmate, decorticates attacked pairmates as frequently as did intacts, and they were just as likely to defend against playful attacks as were intacts. Where decorticates differed from intacts was on a measure of pinning, in which one rat stands over a supine partner, decorticate rats displayed a reduction of 50% relative to control rats during the juvenile stage in which play is most pronounced (days 25 to 40). Juvenile decorticate rats adopted types of defensive responses which were less likely to result in the pinning configuration. Thus, a reduced pinning frequency reflects an altered pattern of defense, not a reduced level of play fighting. Rather, the decorticate patterns of defense were typical of those defensive responses displayed by adult rats. That is, decorticate juveniles exhibit a precociously mature pattern of playful defense. As intact controls mature, they come to resemble the decorticates in their defensive responses, and hence the difference in pinning frequency between decorticate and intact pairs diminishes. This suggests that the cortex may inhibit the escalation of defense in juveniles and thus promote prolonged ventral-ventral contact during play fighting. The results further suggest that the cortex is involved in the development of adult behavioral skills by facilitating juvenile play.

Vision plays two roles in air-righting, it can trigger air-righting in the absence of the labyrinths, and it can modulate the onset and speed of air-righting depending upon the height of the fall. While the visual cortex is known to be necessary for visual triggering, the neural systems necessary for visual modulation are unclear. In this study, the role of the visual cortex and the superior colliculus in visual modulation by rats was analysed. Rats can visually modulate vestibularly-triggered righting, but not trigger righting visually in the absence of the labyrinths. Adult rats with complete neonatal decortication, and adult rats with more specific ablation of the visual cortex were able to visually modulate air-righting. Ablation of the superior colliculi as well as the visual cortex, or ablation of the superior colliculi alone, resulted in loss of the ability to visually modulate air-righting. It is concluded that the superior colliculus is necessary for visual modulation in rats. It is hypothesized that in cats also, the superior colliculus, not the visual cortex, is necessary for visual modulation.

The vestibular head righting reflex can be demonstrated by holding an adult rat vertically downward, so that the snout points downward. In this situation, the animal dorsiflexes its head and neck, bringing the head towards its normal orientation in space. Bilateral labyrinthectomy not only blocks this response, but releases an actively maintained ventroflexion of the head and neck. Bilateral electrolytic lesions of the lateral hypothalamus (LH) exaggerate such ventroflexion in labyrinthectomized rats. By themselves, LH lesions had no such effect. Therefore, it is argued that there are vestibular and supraspinal inhibitory mechanisms which, in the intact adult animal, keep this ventroflexion response in check. In addition, when the rats were held with their heads down, and with gentle paw contact with the ground, they did not ventroflex. However, they ventroflexed immediately upon releasing this paw contact. These observations suggest that there are tactile mechanisms which can also inhibit this exaggerated ventroflexion released by labyrinthectomy.

The current explanation of air righting in animals is that when falling supine in the air, labyrinthine stimulation triggers head rotation. The head rotation involves neck rotation which, via the cervical righting reflex, triggers rotation of the body. (In cats and monkeys, when the labyrinths are absent, visual stimulation when falling supine can also trigger this righting sequence.) In the present paper, a descriptive analysis of air righting in the rat shows that the shoulders rotate, carrying the unmoving head and neck passively along. Thus, for this species, labyrinthine input appears to trigger shoulder rotation directly, independently of the cervical righting reflex. This suggests that at least two physiological mechanisms exist for labyrinthine control of head rotation during air righting, one via the neck and the other via the shoulder girdle.

Reaching for food by rats, with the limb contralateral to limb area motor cortex damage, was analyzed using end-point scores, videoanalysis, and Eshkol-Wachmann Movement Notation (EWMN). End point results from groups of rats with small, medium, and large lesions showed reaching success and amount of food grasped per reach decreased with increases in lesion size. Videoanalysis and EWMN showed that the impairments were attributable to: (1) an inability to pronate the paw over the food by abduction of the upper arm, and (2) an inability to supinate the paw at the wrist to orient the food to the mouth. There were no obvious impairments in locating food using olfaction, in positioning the body in order to initiate a reach, or in clasping the digits to grasp food. There were only mild impairments in lifting, aiming, and advancing the limb. In rats with medium and large lesions, loss of pronation and supination were compensated for by a variety of whole body movements. These findings are discussed in reference to neural and behavioral mechanisms underlying recovery of function and the contribution of the motor cortex to skilled movements in the rat and other species.

During postweaning development, rats exhibit several well documented trends in their play fighting: (1) It peaks between 30-40 days and then declines with the approach of sexual maturity; (2) males initiate more play fights than females; and (3) the overall complexity of play fights, as expressed by such measures as duration of bouts, also decreases with increasing age. Such trends could arise from changes in attack or defense, or some combination of both. In this article it is shown that (a) the decline in play fighting with the onset of sexual maturity in rats results from a decline in attack, not in defense; (b) the differences in play fighting by male and female rats are due to sex-specific rates of both attack and defense; and (c) the developmental decrease in the complexity of play fighting arises from a decrease in the frequency of counterattacks (i.e., after an animal defends itself, it is less likely to launch an attack). In this way, age and sex differences in play fighting can be traced to differences in its subcomponents.

Contact righting, that is, turning from a recumbent position to prone, is abolished for a few days after large electrolytic lesions of the lateral hypothalamus. With recovery, contact righting reappears, but does so in a distinct manner. At first the body is righted by backleg movements, in the absence of any active axial rotation. Later, righting switches from back to front, so that righting begins in the shoulders and then proceeds to the pelvis. Such righting is achieved by axial rotation, that is, the limbs are carried by the torso, rather than vice versa. Labyrinthectomy, when combined with lateral hypothalamic (LH) damage, slows this recovery (now taking as long as 3 weeks), and reveals many intermediate stages of contact-righting. The absence of axial rotation in the early stages of recovery from combined LH damage and labyrinthectomy is compared to the 'axial apraxia' seen in some parkinsonian patients.

Three experiments were conducted to investigate the phenomenon of atropine-induced stereotypic trapping in rats reported by Schallert, De Ryck, and Teitelbaum (1980). The first two showed that such trapping was disrupted by previous experience with the specific trapping task or the test context alone. The third showed that, in response to the test context, specific behaviors were altered in rats experienced with the context. Inexperienced atropine-treated animals moved slowly and showed a strong thigmotaxis to surfaces with the body and particularly the snout. The hindquarters did not cooperate well with the movements of the forequarters. In contrast, atropine-treated animals familiar with the context moved with medium-speed, coordinated movements, were independent of surface contact with body and snout, and the hindquarters cooperated fully with forequarter movements. These reactions of drugged animals were exaggerated forms of those of undrugged animals to the unfamiliar and familiar context, respectively. Thus, atropine enhances the reactions of the rat to both a novel and a familiar environment. The enhanced reactions to a novel environment appear as stereotyped behaviors that trap the animal in particular configurations of surfaces. The enhanced reactions to a familiar environment abolish the stereotypic trapping normally produced by atropine. This pattern of results indicates that it is not atropine per se that leads to trapping. Rather, stereotypic trapping develops as a consequence of an interaction between the adaptive responses of the rat to a novel environment and atropine.

Previously it was found that during the loss of postural support induced by combined administration of haloperidol and morphine, rats became markedly hypothermic. The present work was a more detailed study of this hypothermia. Morphine alone (20 mg/kg) produced a slight hyperthermia (1 degrees C) in female rats and no effect in males. Haloperidol alone (5 mg/kg) elicited a hypothermia of about 3 degrees C in females and no effect in males. The combination of both elicited a greater decrease of temperature (about 5 degrees C) in female rats and, unexpectedly, a decrease of 3 degrees C in males. According to these data, increased endorphinic activity with a concomitant decrease in dopamine in some unidentified regions of the central nervous system causes hypothermia.

In the Syrian golden hamster Mesocricetus auratus, play-fighting precedes serious fighting during postweaning development, and so may be thought to be a developmental precursor to adult aggression. However, based on both the targets attacked--that is, the cheek pouches during play-fighting and the rump or flanks during serious fighting, and the behavior patterns employed to attack and defend these targets--these two forms of fighting are shown to remain distinct from each other throughout development, even during the ages where they overlap. The decline of play in post-sexually-mature animals is shown to result from an increasing intolerance to contact between animals, and hence greater difficulty in the maintenance of a "playful mood." Therefore, these data show that play-fighting does not grade into serious fighting, and thus does not serve as a developmental precursor to adult aggression.

Unlike cats, which can initiate righting in the air either with vestibular or visual input alone, the rat is dependent solely upon the labyrinths to trigger this response. We show, however, that the rat can modulate the onset and speed of its rotation according to the height above the ground from which it is dropped. In the absence of vision, rates initiate rotation with a latency of about 50 ms, irrespective of the height from which they are dropped. With vision, rats can modulate their latency to begin rotation, from about 102 ms at 50 cm, to about 39 ms at 7.5 cm. Similarly, as height of release decreases, the speed of rotation (i.e. degrees/ms) increases. Thus, in rats, even though vision cannot trigger air-righting, it does adaptively modulate this behavior as an allied reflex, increasing the likelihood that the animals will land on their feet.

In earlier work, we showed that in rats, proprioceptive-tactile information is sufficient for contact-righting on the ground (from lying on one side to prone). Thus, axial rotation, starting with the shoulders and followed by the pelvis, occurs normally in labyrinthectomized animals with eyes occluded. After damage to the lateral hypothalamus, even with labyrinths intact, contact-righting is at first abolished (1-2 days postoperatively), and when it reappears, involves pushing by the hindlegs. Rostrocaudal contact-righting, involving axial rotation, takes 3-4 days to recover. If labyrinthectomy is combined with lateral hypothalamic damage, the deficit is exaggerated and recovery is greatly slowed down, now requiring 2-3 weeks. The present paper shows that during this prolonged period of recovery several transitional forms of righting are present, each produced by a different combination of limb and body axis movements. At first, axial rotation is absent, and righting is achieved only by pushing with the limbs. This is followed by a transitional form in which, even though axial rotation cannot be triggered directly by contact with the ground, it can be triggered indirectly as an allied reflex when the paw places on the ground. Eventually the body axis actively initiates the rotation to proneness (at first, in the pelvis, later in recovery, in the shoulders), with the limbs being carried. Recovery of axial rotation overlaps with the recovery of cephalic dominance, yielding complex intermediate forms of righting.

Paradoxically, animals exhibiting haloperidol-induced cataleptic immobility can be induced to leap vigorously, by pushing them forward from behind. It is shown here that such jumping can also be produced by placing them on a board and tilting it tail-end upward until about 50 degrees above horizontal. In both situations, jumps only occurred when the animal's hindlegs began to slip forward, as they lost their postural stability. As alternatives to jumping from the slope, rats turned to face upwards (negative geotaxis), or adopted a spread-eagled posture during head-first downward sliding, with the body and head flattened against the substrate. All 3 responses to the sloping board were present in some undrugged rats. Such rats, and those given low doses of haloperidol (0.5, 1.0 mg/kg), were more likely to turn upwards than to jump or slide. At high doses (7.5, 10.0 mg/kg), they were more likely to slide downward than to turn or jump. Jumping was most likely to occur at an intermediate dose (5 mg/kg), approximately 60 min after injection. We suggest that in the absence of haloperidol, and at low doses, locomotion is dominant over reflexes defending static equilibrium, and hence rats are more likely to turn upwards (which involves stepping). In contrast, at higher doses, locomotion is more fully suppressed, reducing the likelihood of turning. At very high doses of haloperidol and later in the action of the drug, muscle tonus appears to be weakened, reducing the likelihood of jumping. This possibility was supported by the finding that combined injection of the optimal dose of haloperidol and 2 mg/kg diazepam reduced the ability to cling vertically (suggesting weakness of muscle tone). In such rats, jumping from the sloping board was decreased, and active downward sliding was increased. Thus, different factors influence the occurrence of jumping at different doses of haloperidol. However, these are all active defensive responses to postural instability, and hence are similar to the other reflexes used by haloperidol-treated rats to defend against displacement from static stable equilibrium, such as standing immobile, bracing, clinging, and righting. Jumping in response to loss of stability on the sloping board also occasionally occurred in undrugged rats. Unlike jumps by haloperidol-treated rats, those by undrugged animals only occurred when they could be directed to a safe landing place. Thus, if the board faced the edge of the table, so that the jump would carry the animal into space over the edge, undrugged rats either did not jump or jumped off the side of the board onto the table.(ABSTRACT TRUNCATED AT 400 WORDS)

During postnatal development, young laboratory rats, Rattus norvegicus, exhibit a variety of locomotor-rotational movements, that is, runs and jerk-jumps, in both playful and nonplayful contexts. The frequency of movement types differed between contexts. Some contexts, such as exploration and sleeping, contained spontaneously (i.e., possible eliciting stimuli were not observed) occurring jerk-jumps which varied with increasing age. In some contexts, such as social play, in which locomotor-rotational movements were elicited by observed stimuli, the frequency of jerk-jumps remained similar throughout ontogeny. During social play some locomotor-rotational movements were found to have immediate functions, such as achieving advantage over the partner during play-fighting, and as a means of terminating sensory input from the partner at the end of social contact.

In this article, we show that feline predation involves a continuous gradient of activation between defense and attack and that predatory "play" results from an interaction of the two. Benzodiazepines (oxazepam, diazepam) escalated attack toward killing, so that cats that had avoided mice prior to the drug now played with them, cats that had originally played now killed, and cats that killed mice now did so with less preliminary contact. In such shifts, no sharp demarcation between play and predation was evident. Lateral hypothalamic lesions disrupted the escalation of attack. During recovery, attack was escalated once again along the gradient toward killing, but in the absence of both defense and play. A similar result was obtained in intact killers and nonkillers by the application of mild tail pinch. These results suggest that play with prey is a misnomer for predatory behavior that fails to escalate along the gradient between defense and attack. Movement notation analysis revealed that playful movements are adaptive in that they protect the cat from injury.

Although cataleptic rats do not spontaneously orient, scan, or walk, they will cling, stand, right themselves in the air, and resist being displaced from a stable position (Schallert, Whishaw, De Ryck, & Teitelbaum, 1978). Morphine produces a state of immobility in which all reflexes used for stable static support (e.g., standing, righting, clinging, and bracing) appear to be inhibited (De Ryck, Schallert, & Teitelbaum, 1980). Addition of morphine to haloperidol abolished or reduced those reflexes used to defend against slow postural displacements (e.g., bracing) but left intact those used to protect against fast postural displacements (e.g., righting in the air). However, although intact, these responses to fast postural displacements were completely abolished by labyrinthectomy, showing that they were controlled only by vestibular inputs. During recovery from morphine's effects, the responses to slow postural displacements reemerged, revealing fractional subcomponents. Furthermore, the reorganization of the subcomponents proceeded along specific body gradients; for example, bracing and standing reemerged caudorostrally, while at the same time, righting and clinging reemerged rostrocaudally.