PubMed Health⌕ Search

Biomedical subjects

P Teitelbaum

Publications and source records attributed to P Teitelbaum.

At least 55 records · Page 3Linked to original sources
PubMed1985

The morphogenesis of stereotyped behavior induced by the dopamine receptor agonist apomorphine in the laboratory rat.

The seemingly unrelated stereotyped locomotor "acts" reported in the literature to be produced by apomorphine in rats are shown to be composites, whose form and sequence are determined by the particular values of a few component variables which form a common denominator in each of the behaviors. Three variables, continuous snout contact, forward progression and turning, account for much of the behavior. In the course of the drug's action these emerge in succession and vary in amount, the latter two successively reaching a peak and subsiding. The interaction between forward progression and turning yields in sequence, forward walking, circling, revolving, tight pivoting and finally side-to-side movements of the forequarters around the relatively stationary hindquarters. Later behaviors in this list are gradually incorporated into the sequence as earlier ones are eliminated. The course of change in forward progression and turning is also reflected in changes in the sequence and in the direction of stepping of each of the four legs. The order in which the behavior unfolds under the drug is opposite to that manifested in ontogeny and in recovery from lateral hypothalamic damage, suggesting that at the particular high dose used, apomorphine is acting not only to activate the behavior but also to shut it down.

Animals↗
PubMed1985

Previous experience disrupts atropine-induced stereotyped "trapping" in rats.

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.

Animals↗
PubMed1984

Morphine catalepsy as an adaptive reflex state in rats.

These experiments demonstrate that morphine-induced catalepsy consists of two complementary, but opposite, behavioral extremes (rigid immobility and sudden locomotor bursts), each of which can be controlled by distinct classes of external stimuli. When stimuli that involve pain and/or nonnociceptive skin pressure are tonic (continuous), morphine-induced electroencephalographic (EEG) deactivation and behavioral immobility are potentiated, even to the extent that a stimulation-bound reversible coma results. In contrast, phasic (discrete) stimulation produces behavioral and/or EEG activation. EEG and behavioral rebound effects are observed following stressful (intense, prolonged) stimuli. On the basis of the observed stimulus controls, sensorimotor characteristics, and EEG reactions, it is suggested that similarities may exist between morphine-induced catalepsy and defensive reactions of immobility and escape in drug-free animals (i.e., the adaptive death- feigning reflex).

Adaptation, Physiological↗
PubMed1984

Reversal of akinesia and release of festination by morphine or GABA applied focally to the nucleus reticularis tegmenti pontis.

Focal application of 5 micrograms of morphine sulfate to the nucleus reticularis tegmenti pontis (NRTP) in rats reversed the akinesia induced by 5 mg/kg systemic haloperidol or 40 mg/kg systemic morphine and released festinating forward locomotion. gamma-Aminobutyric acid (200 micrograms) applied to this nucleus also reversed such akinesia. Intraventricular naloxone (10 micrograms) or picrotoxin (0.1 microgram), respectively, blocked the effects of such focally applied drugs. Thus, morphine and gamma-aminobutyric acid appear to act physiologically on the cells of the NRTP. The results suggest that systemic morphine, in addition to producing immobility, simultaneously facilitates a readiness for locomotion by inactivating a final common inhibitory system in the region of the NRTP.

Animals↗
PubMed1983

The pontine reticular formation is part of the output pathway for amphetamine- and apomorphine-induced lateral head movements: evidence from experimental lesions in the rat.

Electrolytic lesions in the caudal part of the medial pontine reticular formation (PRF) in the rat abolished apomorphine- or amphetamine-induced stereotypic lateral head movements and turning to the damaged side. Rats with unilateral PRF lesions turned and circled only to the intact side, and rats with bilateral lesions did not turn at all. PRF lesions were also effective in abolishing or reducing amphetamine-induced circling in rats with unilateral nigrostriatal bundle damage. Thus, head movements induced by dopamine agonists are added to the class of head movements mediated by the PRF. It is proposed that the decussations of the motor pathways for drug-induced turning are located between the midbrain and caudal pons.

Animals↗
PubMed1983

Morphine versus haloperidol catalepsy in the rat: an electromyographic analysis of postural support mechanisms.

Electromyographic recordings from antagonistic flexor and extensor muscles in the forelegs (biceps and triceps) and hind legs (tibialis and gastrocnemius-soleus) of freely moving rats demonstrated that haloperidol (5 and 10 mg/kg, i.p.) and morphine (20 and 40 mg/kg, i.p.) produced contrasting patterns of rigidity. Haloperidol catalepsy was characterized by increases in frequency, intensity, and duration of simultaneous tonic cocontractions in antagonistic flexor and extensor muscles of the limbs. Such synergistic rigidity suggested the release of an adaptive mechanism involved in static support and the maintenance of stable static equilibrium (the positive supporting reaction of Schoen and Magnus), at the expense of locomotor mechanisms. In contrast, morphine produced antagonistic/reciprocal rigidity, which was insensitive to challenges to static equilibrium, and was compatible with locomotion. Contrary to the haloperidol-induced limb postures, which were enhanced supporting reactions, those induced by morphine were "frozen" phases of the step cycle. Haloperidol-induced synergistic rigidity and morphine-induced antagonistic/reciprocal rigidity are discussed as manifestations of contrasting movement subsystems underlying these functionally opposite immobility states. In addition, we present hypotheses concerning supraspinal and spinal mechanisms underlying cataleptic rigidity states, and their relevance as models of parkinsonian rigidity and akinesia.

Animals↗
PubMed1983

The inhibition of movement by morphine or haloperidol depends on an intact nucleus reticularis tegmenti pontis.

Electrolytic damage of the nucleus reticularis tegmenti pontis (NRTP) in rats produces a form of accelerating forward locomotion, indicating that this region is part of a system that inhibits locomotion and movement. In animals with such damage, 5 mg/kg haloperidol does not block forward locomotion although it produces complete akinesia in normal rats [2]. Our present results demonstrate that doses of morphine sulfate that render normal rats completely akinetic (40, 50, or 60 mg/kg) also fail to block forward locomotion. Furthermore, 200 micrograms gamma-aminobutyric acid applied intracranially in the region of the NRTP can reverse the akinesia produced by systemically administered haloperidol or morphine. We suggest that there are two types of akinesia--direct and indirect--and that morphine and haloperidol may produce akinesia indirectly via an inhibitory system which includes the NRTP.

Animals↗
PubMed1982

Snout contact fixation, climbing and gnawing during apomorphine stereotypy in rats from two substrains.

Apomorphine, at doses greater than or equal to 10 mg/kg (intraperitoneally), produced two patterns of stereotypy. In rats from one supplier it induced predominantly gnawing while in those from another predominantly climbing, suggesting that the response to the drug is influenced by genetic and/or experimental factors. At lower doses, apomorphine induced climbing in both groups (ED50 = 1.4 mg/kg in each group) but oral behavior in only one of them (ED50 = 1.3 mg/kg in one, and 8 mg/kg in the second group). Thus, at a given dose of apomorphine, different patterns of stereotypy may result from an interaction between two phenomena: the relative setting of the thresholds to mouth and to climb, and an inverse relation between oral activity and climbing. Analysis of climbing suggests that this response is comprised of two (previously unidentified) fundamental effects of apomorphine: snout contact fixation and bodywise forward progression.

Animals↗
PubMed1982

Subcortical waking and sleep during lateral hypothalamic "somnolence" in rats.

Following extensive bilateral lateral hypothalamic damage, rats appear "somnolent." Cortical EEG shows persistent high voltage delta, reinforcing the impression of sleep. Preoperatively and postoperatively, we simultaneously measured cortical and subcortical (hippocampal and pontine) EEG, muscular events (neck muscle EMG and eye movement EOG), and behavior, which, as aggregates, differentially define quiet sleep, active sleep, and waking. Postoperatively, though cortical activity was persistently slow, subcortical EEG, muscular events, and behavior, as aggregates, revealed quiet sleep, active sleep, and waking, organized subcortically, intact and alternating, but disconnected from the persistent slow cortical activity. For example, preoperatively, active sleep included cortical low voltage fast activity, hippocampal theta, episodic pontine spike bursts, flat EMG, nd rapid eye movements, without any organized behavior. Postoperatively, the same aggregate of subcortical and muscular events indicated the presence of active sleep. Similarly so, for subcortically organized quiet sleep and spontaneous waking. Such waking, termed "drowsy-wakefulness," is a low-arousal form, perhaps related to drowsiness in other species, and to human hypersomnia.

Animals↗
PubMed1982

Methysergide releases locomotion without support in lateral hypothalamic akinesia.

Rats made profoundly akinetic by large bilateral electrolytic partial transections of the lateral hypothalamus were released from their akinesia by methysergide maleate (45 mg/kg, IP). When tested as soon as 24 hr postoperatively, lateral hypothalamic rats treated with methysergide displayed vigorous forward locomotion without postural support for as long as an hour and a half. By postoperative day 5, the locomotion elicited by methysergide was integrated with postural support to produce a more normal form of walking. Although atropine sulfate (50 mg/kg, IP) releases excessive walking in akinetic rats treated with 6-hydroxydopamine [53] it did not release locomotion lateral hypothalamic rats. Similarly, apomorphine, clonidine and phentolamine did not do so. Assuming that methysergide in the dose used exerts its effects primarily via the blockade of serotonin systems, we suggest that, in addition to an inhibitory cholinergic system, an independent inhibitory serotonergic system may also exaggerate the akinesia seen following treatments that diminish the action of brain catecholamine systems. Furthermore, the type of locomotion released by methysergide is a fractional form not previously isolated.

Animals↗
PubMed1981

"Warm-up" along dimensions of movement in the ontogeny of exploration in rats and other infant mammals.

When some infant mammals are placed outside their nest, a sequence of exploratory behavior occurs, displaying a regular buildup and spread of activity. This "warm-up" involves repetition of movement along specific dimensions and an orderly transition from one dimension to the next, with cephalocaudal recruitment of body and limb segments. A similar principle of organization applies to neurological recovery from lateral hypothalamic akinesia.

Animals↗
PubMed1981

Galloping induced by pontine tegmentum damage in rats: a form of "Parkinsonian festination" not blocked by haloperidol.

Localized lesions or local applications of gamma-aminobutyric acid (GABA) in the nucleus reticularis tegmenti pontis (NRTP) of rats cause rapidly accelerating forward locomotion. Such "festination" can coexist with blockade of the dopamine system. We suggest that (i) the akinesia produced by dopamine deficiency results at least in part from release of excessive inhibition of locomotion by a neural system whose final common inhibitory path includes the region of the NRTP and (ii) when it occurs in addition to nigrostriatal damage, destruction in the region of the NRTP might be the cause of a form of festination seen in some patients suffering from Parkinsonism.

Animals↗
PubMed1980

Morphine versus haloperidol catalepsy in the rat: a behavioral analysis of postural support mechanisms.

Our experiments demonstrate that morphine and haloperidol produce two distinct and contrasting behavioral states, which can be thought of as exaggerated, isolated, and simplified forms of organized adaptive behavioral states functioning as components of normal motivated behavior. Haloperidol catalepsy constitutes an organized state in which tonic reactions subserving the maintenance of stable static equilibrium prevail, at the expense of phasic locomotor reactions. In contrast, morphine produces an immobility state characterized by inhibition of the postural support subsystem, and compatible with or preparatory to locomotor rather than static postural reactions. haloperidol-treated rats (1, 2.5, 5, 10 mg/kg i.p.) display exaggeraged bracing reactions to passive displacement as well as to stimuli which do not actively challenge stable equilibrium. In contrast, rats treated with morphine sulfate (10, 20, 40, 80 mg/kg i.p.) show a dose-dependent suppression of bracing and an exaggerated tendency to run in response to stimuli which produce bracing in haloperidol-treated rats. Further evidence that haloperidol-treated rats are organized to stand still in stable equilibrium includes their typical posture during akinesia (i.e. broad-based support), bradykinesia, tonic grasping and enhanced postural components of contact- and air-righting. Under morphine, however, the postural support subsystem is dispensed with, as evidenced by the posture of akinesia (i.e. a frozen phase of the locomotor step cycle associated with loss of limb support), absence of tonic grasping, and nature of the deficits in contact- and air-righting. Furthermore, the opiate-induced immobility state is accompanied by an increased readiness to locomote. Morphine produces an alternation between two extreme behavioral states: complete immobility (inhibition of the postural support subsystem) versus locomotor paroxysms (varying degrees of 'explosive motor behavior'). We suggest that the postures or actions adopted by morphine-treated rats involve movement subsystems concerned with the adaptive behavioral state known as the 'immobility reflex' ('tonic immobility', 'animal hypnosis').

Animals↗
PubMed1980

Atropine stereotypy as a behavioral trap: a movement subsystem and electroencephalographic analysis.

An analysis was made of the movement subsystems involved in the stereotyped behaviors and electroencephalographic (EEG) activity that appear in rats given the anticholinergic drug atropine sulfate (50-75 mg/kg). One form of stereotypy occurred when the drugged faced the closed end of an alleyway. Instead of scanning briefly and then turning around to face the open end, as undrugged rats do, they typically "trapped", i.e., they continued to engage in rapid, repetitive scanning by the snout up and down or side to side along the surfaces of the closed end for long periods of time. Atropine appears to produce an exaggerated snout thigmotaxis. Accordingly, the behavioral pattern can be manipulated simply by changing the configuration of the environment, which alters sensory input to the snout. Therefore, such stereotyped behavior is not a motor automatism but rather a circular chain of reflexive reactions to surfaces which trap the animal. During rapid shifts in direction of movement in undrugged rats, there were often extremely brief periods of hippocampal theta that could be blocked by atropine. The presence of theta during such shifts might be important for normal behavioral sequencing. This could partially account for the fact that atropine-treated rats failed to change from their initial reactions in the alleyway to more adaptive behaviors. When a low roof was placed over the alleway, head scanning was greatly limited, and immobility in a lying posture rapidly became the more frequent behavior. This immobility was accompanied by a sleeplike (synchronized) neocortical EEG pattern rather than the activated (desynchronized) neocortical pattern that occurs during repetitive thigmotactic scanning. It is hypothesized that scanning stereotypy and activated EEG are maintained through movement-concurrent positive feedback.

Animals↗
PubMed1980

Recovery of forelimb placing after lateral hypothalamic lesions in the cat: parallels and contrasts with development.

Recovery of forelimb placing after lateral hypothalamic lesions in the cat is similar in several respects to the development of placing in kittens. In both recovery and development, the sequence in which sensory systems acquire control over placing is the same: vestibular--proprioceptive--tactile--visual. In addition, within each sensory modality, placing is initially sluggish, exaggerated in amplitude, and susceptible to rapid habituation. Unlike development, however, the recovery of visually guided placing does not require visuomotor experience.

Age Factors↗