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S M Pellis

Publications and source records attributed to S M Pellis.

At least 55 records · Page 3Linked to original sources

The role of the cortex in play fighting by rats: developmental and evolutionary implications.

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.

Aggression↗

Visual modulation of vestibularly-triggered air-righting in rats involves the superior colliculus.

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.

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Labyrinthine and other supraspinal inhibitory controls over head-and-body ventroflexion.

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.

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Air righting without the cervical righting reflex in adult rats.

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.

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The impairments in reaching and the movements of compensation in rats with motor cortex lesions: an endpoint, videorecording, and movement notation analysis.

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.

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The structure of skilled forelimb reaching in the rat: a proximally driven movement with a single distal rotatory component.

The movements of rats trained to reach through an aperture for food pellets, located on a shelf, were videorecorded and filmed from lateral and ventral perspectives for analysis using Eshkol-Wachman Movement Notation (EWMN). Reaching was subdivided into phases of locating the food and advancing the limb to grasp the food, bringing the food to the mouth, and returning to the starting position. Further analysis of the movements comprising these acts revealed a number of novel findings. (1) Most of the first phase of the movement is produced proximally, with the limb lifted, aimed, and advanced from the shoulder. (2) After the limb is lifted from the substrate to initiate reaching, it is carried to a parasagittal position so that the long axis of the forearm is aligned along the midline of the body. This aspect of the movement 'aims' the limb toward the target. (3) The digits are opened as the limb is advanced from the aiming position toward the food. As the paw approaches the food, pronation of the palm is accomplished by abduction of the upper arm. (4) As the limb is retracted, the digits are closed to grasp the food. As retraction ends, the paw is supinated by a rotatory movement at the wrist. This is the only distal rotatory movement. (5) The position taken by the second forelimb, as it is adducted to aid in holding the food pellet for eating, resembles the 'aiming' posture. The results are discussed in reference to the kinematics, neural control, and the evolutionary origins of reaching in the rat and other animals. Additionally, the results provide a framework for analysis of changes in movements produced by physiological manipulations.

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Labyrinthine and visual involvement in the dorsal immobility response of adult rats.

The dorsal immobility response (DIR) is typically seen in the infants of many altricial mammalian species. Lifting the animal into the air by the nape of the neck is the primary releasing stimulus. Functionally, this response appears to facilitate carrying of the infants by the adults. When grasped by the nape and lifted into the air, adult rats will also exhibit the DIR. In this paper, the role of the labyrinths in the DIR of adult male rats was examined. Vestibular stimulation produced by vertical circular acceleration increased the duration of the DIR, while labyrinthectomy greatly diminished the DIR. In rats with intact labyrinths, visual occlusion greatly potentiated the DIR, whereas, in labyrinthectomized rats, visual occlusion had little effect. These data indicate that the vestibular system plays a major role in mediating the DIR of adult rats. The retention of the DIR into adulthood and the possible increased role of the labyrinths in the control of the adult DIR, are discussed with respect to the possible role of the DIR as an anti-predator mechanism.

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Differential rates of attack, defense, and counterattack during the developmental decrease in play fighting by male and female rats.

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.

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An open-field activity analysis of labyrinthectomized rats.

A detailed behavioral analysis was performed on rats that received bilateral labyrinthectomies. They were placed in a walled activity monitor (39 x 39 cm) that allowed the animal to move freely within the enclosure. Their behavioral activities were automatically recorded. These activities were placed into twelve different categories. The results show a lower rate of habituation for the labyrinthectomized animal as well as an overall increase in activity over all dimensions as compared to the control. This increase in behavior may be exploratory and a necessary feature in the formation of spatial maps.

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Seemingly paradoxical jumping in cataleptic haloperidol-treated rats is triggered by postural instability.

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)

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Recovery from axial apraxia in the lateral hypothalamic labyrinthectomized rat reveals three elements of contact-righting: cephalocaudal dominance, axial rotation, and distal limb action.

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.

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Visual modulation of vestibularly-triggered air-righting in the rat.

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.

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Play-fighting in the Syrian golden hamster Mesocricetus auratus Waterhouse, and its relationship to serious fighting during postweaning development.

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.

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Escalation of feline predation along a gradient from avoidance through "play" to killing.

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.

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'Axial apraxia' in labyrinthectomized lateral hypothalamic-damaged rats.

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.

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Sex differences in the effects of haloperidol, morphine, and their combination on colonic temperature in rats.

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.

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Pharmacological subtraction of the sensory controls over grasping in rats.

Catecholamine-depletion-induced catalepsy isolates and leaves intact an aggregate of allied reflexes (e.g., righting, standing still, bracing, and clinging) which involve all the body and limb segments in defending stable static equilibrium. Because other movement subsystems (locomotion, orienting, scanning, directed use of mouth or forepaws) are depressed, such animals cling in a vertical position for an abnormally long period of time. As a consequence, grasping reflexes may be studied independently of other responses. Haloperidol, a dopamine antagonist, abolishes visually elicited reaching and grasping, but leaves intact tactile and proprioceptive control of grasping. The grasping of haloperidol-treated rats can be further simplified by the pharmacological removal of the remaining sensory controls. The addition of morphine to haloperidol abolishes tactile grasping, while the addition of diazepam to haloperidol abolishes both tactile and proprioceptive (traction-elicited) grasping. Although visual, tactile, and proprioceptive grasping are abolished by haloperidol-plus-diazepam, some vestibular input to clinging remains: such rats, in response to being held vertically upright in the air, flex their digits with sufficient strength to allow them to cling vertically. The strength of forepaw digit flexion is severely diminished by labyrinthectomy, but the digits of the hindpaws appear to be unaffected. This residual non-labyrinthine digit gripping appears to be induced by proprioceptive inputs from the head, neck and torso in response to the vertical body position. Wrapping an elastic bandage snugly around the head and neck of a labyrinthectomized rat given haloperidol-plus-diazepam further diminishes the strength of forepaw digit flexion, and to a lesser degree hindpaw digit flexion.(ABSTRACT TRUNCATED AT 250 WORDS)

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Abnormal gait sequence in locomotion after atropine treatment of catecholamine-deficient akinetic rats.

Excessive, abnormal locomotion occurs after a high dose (25-50 mg/kg) of atropine sulfate to rats already akinetic due to catecholamine deficiency from intraventricular administration of 6-hydroxydopamine. This abnormal locomotion involves an abnormal gait sequence [right (R) hindleg (H), left (L) foreleg (F), LH, RF] instead of the normal gait sequence (RH, RF, LH, LF). In such animals atropine progressively (i) decreases hindleg step size, (ii) decreases arching of the trunk, and (iii) increases foreleg step size. These factors combine to change the ratio of front/hind body support. If the body stretches too far and the hindleg step is too small, a given hindleg step supports insufficient weight to remove weight from the ipsilateral foreleg; consequently, the opposite foreleg must execute the next step, producing the abnormal gait sequence. Thus, atropine affects gait sequence indirectly; it acts on at least three variables that affect how body weight is distributed and shifted during locomotion. To maintain stability during such locomotion, gait sequence is appropriately altered.

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