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Results for “Reflex, Righting”

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At least 73 records · Page 4Linked to original sources

PubMed2002

Heteromeric nicotinic inhibition by isoflurane does not mediate MAC or loss of righting reflex.

BACKGROUND: Neuronal nicotinic acetylcholine receptors (nAChRs) have been implicated in the mechanism of action of isoflurane as they are inhibited at subanesthetic concentrations. Despite clear evidence for nicotinic inhibition at relevant isoflurane concentrations, it is unclear what behavioral result ensues, if any. METHODS: The authors have modeled two behaviors common to all general anesthetics, immobility and hypnosis, as minimum alveolar concentration that prevents movement in response to a supramaximal stimulus (MAC) and loss of righting reflex (LORR). They have tested the ability of nicotinic pharmacologic modulators and congenital absence of most heteromeric nAChRs to affect concentration of isoflurane required for these behaviors. RESULTS: Neither mecamylamine, 5 mg/kg, nor chlorisondamine, 10 mg/kg, affected isoflurane MAC. Nicotine caused a small decrease in MAC. None of the above agents had any effect on the concentration of isoflurane required for LORR. Mice genetically engineered to lack the beta 2 nicotinic gene product were not different in MAC or LORR from controls. CONCLUSIONS: Nicotinic antagonists do not cause MAC or LORR. Inhibition of nicotinic acetylcholine receptors by isoflurane is not likely related to its ability to provide immobility and hypnosis in a surgical setting. This is perhaps not surprising as the inhibition of nAChRs in vitro is complete at an isoflurane concentration equal to one half of MAC. Nicotinic inhibition may, however, be involved in anesthetic behaviors such as amnesia and analgesia, which occur at lower anesthetic concentrations.

Anesthetics, Inhalation↗

PubMed2001

Blockade of AMPA receptors and volatile anesthetics: reduced anesthetic requirements in GluR2 null mutant mice for loss of the righting reflex and antinociception but not minimum alveolar concentration.

BACKGROUND: The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) subtype of glutamate receptor mediates fast excitatory neurotransmission in the central nervous system. Many general anesthetics inhibit AMPA receptors in vitro; however, it is not certain if this inhibition contributes to the behavioral properties of these drugs. AMPA receptors lacking the GluR2 subunit are resistant to blockade by barbiturates in vitro. Paradoxically, GluR2 null mutant (-/-) mice are more sensitive to barbiturate-induced loss of the righting reflex (LORR) compared with wild-type (+/+) littermates. To determine if interactions between anesthetics and AMPA receptors account for the increased sensitivity of (-/-) mice, the effects of volatile anesthetics that do not directly inhibit AMPA receptors were examined. METHODS: Isoflurane, halothane, desflurane, or sevoflurane were administered to (-/-) and (+/+) littermate controls. Anesthetic requirements for LORR, movement to tail clamp (minimum alveolar concentration [MAC]), and hind-paw withdrawal latency (HPWL) were determined. Electrophysiologic methods examined the inhibition of AMPA receptors by isoflurane and halothane. RESULTS: Anesthetic requirements for LORR and HPWL were decreased, whereas MAC values were unchanged in (-/-) mice. Isoflurane and halothane caused minimal inhibition of AMPA receptors at clinically relevant concentrations. CONCLUSIONS: Direct blockade of AMPA receptors did not account for the increased sensitivity to volatile anesthetics in GluR2 null mutant mice for HPWL or LORR. Thus, the deficiency of GluR2-containing AMPA receptors increases the sensitivity of neuronal circuitry mediating these end points, but not MAC. GluR2-containing receptors do not contribute appreciably to MAC in this mouse model. These results illustrate the difficulties in attributing behavioral responses to drug-receptor interactions in genetically engineered animals.

Analgesia↗

PubMed1984

The development of air-righting reflex in postnatal growing rabbits.

The investigations were carried out in 6 growing rabbits from the 5th day of life up to the 17th day in intervals of 3 days, as well as in 6 adult animals. The movements of the animals were filmed during free fall by means of a high speed camera (1000 pictures/s) in the frontal or the lateral view. The age-dependent development of head and shoulder rotation is described; the latency of this sensorimotor reaction decreases, and the head rotation velocity increases. The air-righting reflex is interpreted as a programmed command act. The postnatal changes in the timing of this reflex allow conclusions regarding the functional development of the spinal cord along the craniocaudal axis.

Aging↗

PubMedDate not supplied

Temperature in mice after ethanol: effect of probing and regain of righting reflex.

The handling involved in rectally probing a mouse in order to measure body temperature is a stress which results in an increase in body temperature. However, after an injection of ethanol the fall in body temperature caused by ethanol is exacerbated by probing. In mice, decreases in temperature following probing are ethanol-dose dependent and can be generated on both the falling and rising phases of the ethanol induced change in temperature. The effect of probing can be observed when the mice are under the hypnotic influence of ethanol, and regain of righting reflex itself is followed by a fall in temperature. The resumption of motor activity in undisturbed mice following an hypnotic dose of ethanol also is accompanied by a fall in temperature. Therefore, the drop in temperature observed in any of these procedures which involve moving the mice may be attributable to the disruption of heat conservation rather than a stress interaction.

Animals↗

PubMed1985

Kinetics of drug action in disease states. IX. Effect of experimental fever on phenobarbital concentrations at onset of loss of righting reflex in rats.

The purpose of this investigation was to determine the effect of fever on the concentration-pharmacologic activity relationship of phenobarbital (PB). Fever was produced in adult female Lewis rats by either bacterial endotoxin or brewer's yeast. Endotoxin elevated body temperature by 0.9 +/- 0.6 degrees C in one study and by 1.0 +/- 0.4 degrees C in another. Brewer's yeast caused a more pronounced and protracted elevation of temperature averaging 1.8 +/- 0.3 degrees C at the time of the pharmacodynamic measurements. PB was administered by slow i.v. infusion until the rats lost their righting reflex. The concentrations of PB at that time in serum, cerebrospinal fluid and brain were appreciably lower in the hyperpyrexic than in control (saline-treated) animals, irrespective of the method used to produce fever. Thus, fever is associated with an increased sensitivity of the central nervous system to the depressant effect of PB. This observation may be of particular relevance to the use of PB for the treatment and prevention of febrile convulsions.

Animals↗

PubMed1987

Interactions of clonidine with phencyclidine and ketamine: studies of radial maze performance and righting reflex in rats.

Rats were trained to obtain food pellets in an 8-arm radial maze until a criterion of 89% efficiency, i.e., all arms entered within 9 arm entries, was reached in 5 consecutive sessions. Decreases in efficiency caused by phencyclidine (PCP; 4 to 9 mg/kg, IP, 15 min before testing) or ketamine (25 mg/kg, IP, 5 min) were attenuated when subjects were pretreated with clonidine (0.05 mg/kg, IP, 30 min). However, significant improvements in performance in the maze were not observed when clonidine (0.05 to 0.4 mg/kg, IP) was administered 15 min after PCP (9 mg/kg, IP, 45 min). Subsequent studies of righting reflex demonstrated an increased frequency and duration of anesthesia when clonidine (0.05 mg/kg, IP) was administered 15 minutes before PCP (12.5 to 50 mg/, IP) or ketamine (50 to 100 mg/kg, IP). When clonidine (0.05 mg/kg, IP) was administered 15 minutes before [3H]PCP (40 microCi/kg, IP), brain levels of tritium were reduced by 42 to 55%. The present findings do not support the suggestion that clonidine may be useful in the treatment of PCP intoxication. The data does indicate that pretreatment of surgical patients with clonidine may reduce the dose of ketamine required for anesthesia.

Anesthesia↗

PubMed1999

Dissociated vertical divergence: a righting reflex gone wrong.

Dissociated vertical divergence (DVD) is an ocular motor disorder characterized by a slow, upward drift of 1 eye when the other eye is fixating a target. I propose that DVD is a dorsal light reflex in which asymmetrical visual input to the 2 eyes evokes a vertical divergence movement of the eyes. This primitive visuo-vestibular reflex functions as a righting response to restore vertical orientation in lower lateral-eyed animals by equalizing binocular visual input. The dorsal light reflex is suppressed in humans but can manifest as DVD when early-onset strabismus precludes normal binocular development.

Animals↗

PubMed1983

CL 218872 antagonism of diazepam induced loss of righting reflex: evidence for partial agonistic activity at the benzodiazepine receptor.

A recent hypothesis suggests that the "selective anxiolytic" activity of the triazolopyridazine, CL 218872, is a reflection of this compounds high affinity for a benzodiazepine (BZD) receptor subtype. Subsequent to this proposal, the observation was made that CL 218872 does not effectively discriminate BZD receptor subtypes in vitro at physiological temperatures (37 degrees C). Based upon this observation, a selective effect in vivo related to the high affinity of CL 218872 for a BZD receptor subtype appears unlikely. The present study provides evidence for an alternative hypothesis to explain the unique pharmacological properties of CL 218872. The ability of CL 218872 to antagonize diazepam induced loss of righting reflex and enhance the anticonvulsant effect of diazepam in mice suggests that this triazolopyridazine may act as a partial agonist at the BZD receptor. Compared to the pharmacologically active BZDs, the unique actions of CL 218872 may be related to the lower intrinsic activity of this compound.

Animals↗

PubMed2002

[Effects of fentanyl on acetylcholine release from hippocampus and righting reflex in rat: an in vivo brain microdialysis study].

Fentanyl, a synthetic mu-opioid agonist, is one of the most popular opioids in clinical anesthesia. It is well-known that memory is affected by opioids and opioid antagonists in animals. Cholinergic neurones releasing acetylcholine (ACh) particularly in the hippocampus have been shown to be related to memory. This study, therefore, was conducted to examine the effects of fentanyl on hippocampal ACh release in rats. The experiments were performed on male SD rats under freely moving condition by in vivo brain microdialysis technique. After taking initial three samples, test drugs were administered. The ACh release was determined by HPLC-ECD method. Effect on behavior was determined as loss of righting reflex (LRR). Fentanyl 50, 100 and 200 micrograms.kg-1 i.p. significantly decreased the ACh release from the rat hippocampus. Naloxone, a mu-antagonist, 100 micrograms.kg-1 i.p. antagonized the inhibitory effect of fentanyl 100 micrograms.kg-1 i.p. on the ACh release in the hippocampus. Only fentanyl 200 micrograms.kg-1 i.p. produced LRR. The effects of fentanyl, the dose of which is so little that it does not produce LRR, on the rat hippocampal ACh release may be controlled by the inhibitory actions of mu-opioid receptors.

Acetylcholine↗

PubMed2005

Effects of first- and second-generation histamine-H1-receptor antagonists on the pentobarbital-induced loss of the righting reflex in streptozotocin-induced diabetic mice.

The second-generation histamine-H(1)-receptor antagonists, such as epinastine and cetirizine, are used as non-sedating antihistamines for treating allergic symptoms due to their poor ability to penetrate blood-brain barrier. Because it has been reported that the blood-brain barrier system is disturbed in diabetes, it is possible that second-generation histamine-H(1)-receptor antagonists may easily penetrate the blood-brain barrier and cause potent sedation in diabetics. In the present study, we investigated the effects of first-generation (diphenhydramine) and second-generation (epinastine and cetirizine) histamine-H(1)-receptor antagonists on the duration of pentobarbital-induced loss of the righting reflex (LORR) in non-diabetic and diabetic mice. Systemic treatment with diphenhydramine (3 - 30 mg/kg, s.c.), and intracerebroventricular treatment with epinastine (0.03 - 0.3 microg/mouse) and cetirizine (0.03 - 0.3 microg/mouse) dose-dependently and significantly increased the duration of pentobarbital-induced LORR in both non-diabetic and diabetic mice. Although systemic treatment with epinastine (3 - 30 mg/kg, s.c.) and cetirizine (3 - 30 mg/kg, s.c.) did not affect the duration of pentobarbital-induced LORR in non-diabetic mice, these treatments significantly prolonged it in diabetic mice. Our results suggest that the systemic administration of second-generation histamine-H(1)-receptor antagonists may produce a central nervous system depressant effect in diabetes.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1998

A distributed control model for the air-righting reflex of a cat.

A multisegment, multijoint model of a falling animal is presented to examine the effectiveness of a two-stage control scheme in a zero-momentum self-righting maneuver. The model contains a much larger number of degrees of freedom than is required to execute a self-righting maneuver and is thus capable of providing multiple solutions for the same task. The decentralized control scheme is designed to achieve gross turning in minimum time and to maintain a steady orientation relative to gravity after the turn has been achieved. The scheme is able to determine the sequence of steps necessary to execute the motor task and also incorporates learning features. Results from various simulations are presented and their implications discussed.

Animals↗

PubMed1998