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At least 19 recordsLinked to original sources
PubMed1978

[Studies on righting reflexes in newborn cats falling in the air (author's transl)].

The classical righting reflexes have been well illustrated in the familiar example of a falling adult cat, which always lands deftly on all four feet. It, however, has never been clear when newborn animals come to turn themselves in the air after birth. In the present studies the newborn cats were dropped in the air with legs pointed upward from a height of about 30 approximately 40 cm, and the observations were continued for the period of 36 days. The results were as follows: 1. The newborn cats fell plump on their back when they were dropped with legs pointed upward in the air. 2. No righting reflexes were observed in the cats of 27 days and downward. 3. The eyelids (rima palpebrarum) of the cats came to be open on the 8th approximately 14th after birth. 4. The cats which were suggested to obtain full eyesight judged from the observations of their behaviours had no visual righting reflexes when dropped with legs pointed upward. 5. The walking pattern of the cats changed in association with their growth. For the period of 20 days after birth the type of locomotion was creeping, for the period of 21st approximately 26th plantigradation, and after the 26th approximately 27th digitigradation. 6. It has been concluded that the righting reflexes as compound reflexes are never observed in the experimental cats for about one month after birth even though the cats have obtained each postural reflex, i.e. tonic neck or labyrinthine reflex which constitutes righting reflexes.

Animals↗
PubMed1997

Pretreatment with the protein kinase C activator phorbol 12,13-dibutyrate attenuates the ethanol-induced loss of the righting reflex in mice: modification by diabetes.

The effects of the protein kinase C (PKC) activator phorbol 12,13-dibutyrate (PDBu) on the ethanol-induced loss of the righting reflex were studied in diabetic and non-diabetic mice. The ethanol-induced loss of the righting reflex was significantly less in diabetic mice than in non-diabetic mice. Intracerebroventricular (i.c.v.) pretreatment with PDBu dose- and time-dependently reduced the ethanol-induced loss of the righting reflex in non-diabetic mice. The reduction of the ethanol-induced loss of the righting reflex caused by PDBu was reversed by concomitant i.c.v. pretreatment with calphostin C, a selective PKC inhibitor. On the other hand, PDBu had no effect on the ethanol-induced loss of the righting reflex in diabetic mice. I.c.v. pretreatment with calphostin C (10 pmol) increased the ethanol-induced loss of the righting reflex in diabetic mice but not in non-diabetic mice. These results suggest that the activation of PKC reduces the ethanol-induced loss of the righting reflex in mice. Furthermore, it is possible that this attenuation of the ethanol-induced loss of the righting reflex in diabetic mice may be due in part to increased PKC activity.

Animals↗
PubMed1995

The effects of long-term, low-dose diazepam treatment on the guinea pig righting reflex and medial vestibular nucleus neuronal activity.

Guinea pigs received a 2 mg/kg IP injection of diazepam, or an equivalent volume of vehicle, daily for 28-60 days. To determine whether tolerance developed to the ataxic effects of diazepam on the righting reflex, daily righting reflex latency (RRL) measurements were made before and 20, 30, and 40 min following the diazepam or vehicle injection for 28 days. Analyses of the RRLs for individual animals indicated that a significant decrease in RRL over time (indicating tolerance) occurred in only one out of nine animals receiving diazepam and in none of the vehicle animals. Medial vestibular nucleus (MVN) neurons in brain stem slices from animals receiving chronic diazepam treatment had a significantly higher average firing rate than those from vehicle controls. These results suggest that: a) long-term treatment with single 2 mg/kg daily IP injections of diazepam does not result in tolerance to diazepam's ataxic effects on the righting reflex in the majority of animals; b) this form of diazepam treatment may, nonetheless, induce a hyperactivity of brain stem MVN neurons that may be consistent with the occurrence of a withdrawal syndrome.

Animals↗
PubMed1999

Modification of the effect of diazepam on the propofol-induced loss of the righting reflex in mice by diabetes.

The effect of diabetes on the effect of diazepam on the propofol-induced loss of the righting reflex was investigated. There was no significant difference in the duration of the propofol-induced loss of the righting reflex between non-diabetic and diabetic mice. Diazepam increased the duration of the propofol-induced loss of the righting reflex in both diabetic and non-diabetic mice. The diazepam-induced enhancement of the effect of propofol was significantly lower in diabetic mice than that in non-diabetic mice. These effects were antagonized by the pretreatment with flumazenil. Pretreatment with FG7142, a benzodiazepine receptor inverse agonist, attenuated the duration of the propofol-induced loss of the righting reflex in non-diabetic mice, but not in diabetic mice. These results suggest that the attenuation of the diazepam-induced enhancement of the duration of the propofol-induced loss of the righting reflex in diabetic mice may be due to the dysfunction of benzodiazepine receptors.

Anesthetics, Intravenous↗
PubMed2003

Effect of the neuronal nitric oxide synthase inhibitor 7-nitroindazole on the righting reflex ED50 and minimum alveolar concentration during sevoflurane anaesthesia in rats.

BACKGROUND AND OBJECTIVE: The aim was to determine the effect of acute and chronic administration of 7-nitroindazole, a selective neuronal nitric oxide synthase inhibitor, on the righting reflex ED50 and the minimum alveolar concentration during sevoflurane anaesthesia in rats. METHODS: 7-Nitroindazole was acutely (0, 50 and 100 mg kg(-1)) and chronically (0 and 150 mg kg(-1) day(-1), 4 days) administered to rats. After the preparation, the minimum alveolar concentration and the righting reflex ED50 were measured. The concentration of cGMP in the brain, cerebellum and spinal cord was also measured. RESULTS: Acute administration reduced the minimum alveolar concentration (50 mg kg(-1), 58.8% (95% CI: 50.3-67.3%) of the baseline value, P < 0.01; 100 mg kg(-1), 55.8 (46.9-64.7), P < 0.01) and the righting reflex ED50 (50 mg kg(-1), 27.2 (17.2-37.2), P < 0.01; 100 mg kg(-1), 14.3 (6.6-22.0), P < 0.01). Chronic administration did not reduce the minimum alveolar concentration; however, it reduced the righting reflex ED50 (65.3 (52.9-77.7), P < 0.01). Overall, the reduction in minimum alveolar concentration in the acute and chronic protocol did not correlate with that of the righting reflex ED50. 7-Nitroindazole (100 mg kg(-1), acute) reduced the cGMP concentration within the cerebellum by 55.4%; however, it did not decrease concentrations in the brain or spinal cord. CONCLUSIONS: Different mechanisms are responsible for the observed alterations to the minimum alveolar concentration and the righting reflex ED50 following treatment with 7-nitroindazole. The nitric oxide-cGMP pathway might play a less important role in the determination of minimum alveolar concentration than the righting reflex ED50.

Anesthetics, Inhalation↗
PubMed1996

Possible involvement of mu 2-opioid receptor-mediated mechanisms in morphine-induced enhancement of the pentobarbital-induced loss of the righting reflex in the mouse.

The effects of pretreatment with selective mu-, delta- and kappa-opioid receptor antagonists on the enhancement of the pentobarbital-induced loss of the righting reflex by morphine were examined in mice. Mice injected with pentobarbital (50 mg/kg, i.p.) showed an increased duration for the loss of the righting reflex after administration of morphine. This enhancement of the pentobarbital-induced loss of the righting reflex produced by morphine (10 mg/kg, s.c.) was significantly antagonized by pretreatment with beta-funaltrexamine, a selective mu-opioid receptor antagonist, but not by pretreatment with naloxonazine, a selective mu 1-opioid receptor antagonist. Furthermore, neither naltrindole, a selective delta-opioid receptor antagonist, nor nor-binaltorphimine, a selective kappa-opioid receptor antagonist, had a significant effect on the enhancement of the pentobarbital-induced loss of the righting reflex by morphine. These results suggest that mu 2-, rather than mu 1-, delta- and kappa-, opioid receptor-mediated mechanisms are involved in the morphine-induced enhancement of the pentobarbital-induced loss of the righting reflex.

Animals↗
PubMed1992

The development of righting reflexes in the pouch young of the marsupial Dasyurus hallucatus.

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.

Aging↗
PubMed1982

Cocaine potentiates ketamine-induced loss of the righting reflex and sleeping time in mice. Role of catecholamines.

Cocaine in graded doses potentiated ketamine-induced loss of the righting reflex and sleeping time. Potentiation of drug-induced sleep with cocaine was not a generalized phenomenon inasmuch as it had no effect on sleep induced by pentobarbital or hexobarbital and decreased sleep induced by phenobarbital. Pentylenetetrazole reduced ketamine sleep but d-amphetamine had a potentiative action. dl-alpha-Methyl-p-tyrosine methyl ester itself increased both the number losing the righting reflex and the sleeping time induced by ketamine. However, the effect cocaine on sleeping time was blocked 3 h after the dl-alpha-methyl-p-tyrosine methyl ester was given. The alpha and beta adrenergic blocking drugs, phenoxybenzamine and propranolol, increased the number of animals losing the righting reflex with ketamine, and phenoxybenzamine lengthened the sleeping time. Alpha and beta adrenergic agonists, l-phenylephrine and isoproterenol, increased the number of animals going to sleep with ketamine but did not significantly alter how long they would sleep. The agonists had no effect on the cocaine interaction with ketamine, whereas the antagonists blocked the effect of cocaine. Both stimulation and blockade of dopamine receptors led to increased loss of the righting reflex and sleeping time with ketamine but only receptor blockade antagonized the effect of cocaine on ketamine-induced sleep. Thus, both the noradrenergic and dopaminergic systems appear to be involved in the ability of cocaine to potentiate ketamine-induced sleep.

Animals↗
PubMedDate not supplied

Angiotensin II antagonists block ethanol effects on the aerial righting reflex.

The purpose of the present study was to determine the effects of an angiotensin II (AII) AT1 antagonist, losartan 10, 15, and 20 mg/kg IP, and the AII AT2 antagonist, PD 123319, 20 mg/kg IP on ethanol (EtOH) intoxication as measured by the aerial righting reflex in male rats. EtOH (25%), 2.0 g/kg, was administered by stomach tube under mild metaphane anesthesia and the aerial righting reflex was determined at 30-min intervals for 3.5 h. The AII antagonists were administered IP 2 h before the EtOH. There were six groups of 10 rats each: EtOH alone, 10, 15, or 20 mg/kg losartan plus ethanol, 20 mg/kg losartan plus 20 mg/kg PD 123319 plus EtOH, and 20 mg/kg losartan alone. Data were analyzed by a two-way ANOVA with repeated measures on one factor, time. Results show a clear intoxicating effect of ethanol on the aerial righting reflex that was blocked significantly by losartan in a dose-dependent way. Losartan alone had no observable effect. The administration of both antagonists, losartan and PD 123319 injected IP in two different sites, completely blocked the EtOH effect on the aerial righting reflex. The involvement of AII in the mediation of EtOH intoxication effects on the aerial righting reflex supports results of our previous studies on the effects of EtOH on open field behavior, AII impairment of the retention of an inhibitory shock avoidance response, and AII inhibition of hippocampal granule cell long-term potentiation, all of which can be blocked by losartan.

Angiotensin II↗
PubMed1991

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.

Animals↗
PubMed2005

Head-body righting reflex from the supine position and preparatory eye movements.

CONCLUSION: Saccular and utricular maculae can provide information on the supine static position, considering that both have pronounced curved structures with hair cells having a variety of polarization vectors that enable them to sense an inverted position and thus direct the righting reflex. OBJECTIVE: The vestibular system is essential for the structuring of motor behaviour, senses linear and angular acceleration and has a strong influence on posture and balance at rest, during locomotion and in head body righting reflexes. MATERIAL AND METHODS: Using guinea pigs in the supine position with a symmetrical head and trunk position, the ocular position was analysed to ascertain whether any ocular movement that occurred would adopt a spatial deviation indicative of the subsequent head and body righting. The characteristics of the righting reflex (direction, latency, duration and velocity) were analysed in guinea pigs from position signals obtained from search coils implanted in the eye, head and pelvis. The animals were kept in a supine position for a few seconds or even minutes with the eyes in a stable primary position and the head and body symmetrical and immobile. RESULTS: The righting reflex took place either immediately or after a slow deviation of the eyes. In both cases the righting sequence (eyes, head, body) was stereotyped and consistent. The direction of head and body righting was along the longitudinal axis of the animal and was either clockwise or anticlockwise and the direction of righting was related to the direction of the eye deviation. The ocular deviation and the direction of deviation that initiated and determined the direction of the righting reflex could be explained by possible otolithic activation.

Animals↗
PubMed1992

Simple device for quantifying drug effects on the righting reflex.

A simple, inexpensive device is described that allows quantification of the effects of drugs on the righting reflex. This device consists of a modified set of kitchen scales connected to a digital timer. Two moveable Hall effect switches are positioned around the pointer, which registers the weight of the animal on the scales; when the animal is placed on the scales in the supine position, the initiation of a righting reflex causes the pointer to cross one of the switches, stopping the digital timer and providing a measure of righting reflex latency (RRL). We describe an efficient protocol for using this device that provides quantification of drug effects on the RRL, which can then be subjected to analysis using parametric statistics such as analysis of variance.

Animals↗
PubMed1993

The tolerometer: a fast, automated method for the measurement of righting reflex latency in chronic drug studies.

We describe a fast, automated system for the measurement of righting reflex latencies in drug studies. This system, which we call a 'tolerometer', is especially useful for studies of drug tolerance which require a simple measurement of motor behaviour on a daily basis, for long periods of time. The tolerometer consists of a semi-cylindrical platform positioned on a 2 kg load cell, connected to a strain gauge amplifier (Radio Spares Ltd). The output from the amplifier is connected to a MacLab data acquisition system (Analog Digital Instruments), controlled by a Macintosh Classic computer. The MacLab Chart program is used to display, on the Macintosh screen, the load changes which occur during a righting reflex; sampling frequencies up to 40 kHz can be used, but we find 20-100 Hz adequate. Using measurement cursors provided by the Chart program, the latency from the point at which an animal is placed on the tolerometer platform in the supine position, until the completion of a righting reflex, can be measured accurately and easily.

Amplifiers, Electronic↗
PubMed2003

Neuroactive steroid 3 alpha-hydroxy-5 alpha-pregnan-20-one modulates ethanol-induced loss of righting reflex in rats.

Systemic ethanol administration elevates plasma and brain levels of GABAergic neuroactive steroids, including 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP) that contribute to specific behavioral actions of ethanol. The present study determined the effect of adrenalectomy and 5alpha-reductase type-1/type-2 enzyme inhibition, known to reduce neuroactive steroids, on ethanol-induced increases in cerebral cortical levels of 3alpha,5alpha-THP and hypnotic effects in male rats. Systemic ethanol administration to male rats increases plasma levels of progesterone and corticosterone similar to acute stress, indicating release of these steroids from adrenal glands. Adrenalectomy markedly reduced the elevation of cerebral cortical 3alpha,5alpha-THP and plasma progesterone levels and reduced the duration of ethanol-induced loss of righting reflex. Prior systemic administration of 5alpha-dihydroprogesterone (10 or 15 mg/kg, i.p.), an immediate precursor of 3alpha,5alpha-THP, to adrenalectomized rats not only restored the ethanol-induced increases in cerebral cortical 3alpha,5alpha-THP levels but also reversed the effect of adrenalectomy on ethanol-induced loss of righting reflex. Prior administration of the 5alpha-reductase inhibitor finasteride (2 x 25, 2 x 75 or 2 x 150 mg/kg, s.c.) and the 5alpha-reductase type-1 inhibitor SKF-105,111 (50 mg/kg, i.p.) did not reduce ethanol-induced increases in the cerebral cortical levels of 3alpha,5alpha-THP at hypnotic doses of ethanol. Furthermore, these drugs did not alter the duration of loss of righting reflex. However, significant correlations between cerebral cortical 3alpha,5alpha-THP levels and the duration of loss of righting reflex were obtained regardless of finasteride administration. These results demonstrate the contributory role of neuroactive steroids in the ethanol-induced loss of righting reflex and the source of ethanol-induced elevation of GABAergic neuroactive steroids. Ethanol-induced increases in neurosteroids could be pertinent to the etiology of sleep-related disorders associated with alcoholism.

Adrenalectomy↗