SEARCH · PubMed Health

Results for “Reflex, Righting”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources

PubMed1984

Kinetics of drug action in disease states. I. Effect of infusion rate on phenobarbital concentrations in serum, brain and cerebrospinal fluid of normal rats at onset of loss of righting reflex.

The purpose of this investigation was to develop a method to determine the effect of various diseases on the concentration-pharmacologic activity relationship of phenobarbital (PB) in a manner that excludes or accounts for pharmacokinetic variables affecting drug disposition. Adult female rats (congruent to 180 g) received an i.v. infusion of PB at one of five different rates (0.412-4.12 mg/min) until the animals lost their righting reflex (after 8.0 +/- 0.4 to 62 +/- 10 min of infusion). The total dose, the serum concentration (both total and unbound drug) and the brain concentration of PB at onset of loss of righting reflex (LRR) increased with increasing infusion rate. The PB concentration in cerebrospinal fluid at onset of LRR (mean +/- S.D.: 108 +/- 19 micrograms/ml, n = 29) was not affected by the infusion rate. Concomitant infusion of PB and its p-hydroxy metabolite had no apparent effect on the concentrations of PB at onset of LRR even though the serum concentration of p-hydroxy PB was higher than upon infusion of PB only. The results of this investigation indicate that cerebrospinal fluid, unlike some regions of the brain, equilibrates very rapidly with the biophase of the receptors for PB-induced LRR. Determination of PB concentrations in the cerebrospinal fluid at the onset (rather than offset) of action facilitates assessment of the effect of diseases on the PB concentration-pharmacologic activity relationship by avoiding development of acute tolerance and excluding or minimizing effects due to disease-associated pharmacokinetic variables such as altered plasma protein binding and body distribution of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Genetically determined differences in the antagonistic effect of pressure on ethanol-induced loss of righting reflex in mice.

Hyperbaric exposure antagonizes ethanol's behavioral effects in a wide variety of species. Recent studies indicating that there are genetically determined differences in the effects of body temperature manipulation on ethanol sensitivity suggested that genotype might also influence the effects of hyperbaric exposure on ethanol intoxication. To investigate this possibility, ethanol injected long sleep (LS)/Ibg (2.7 g/kg), short sleep (SS)/Ibg (4.8 g/kg), 129/J (2.9 g/kg), and C57BL/6J (3.6 g/kg) mice were exposed to one atmosphere absolute (ATA) air or to one or 12 ATA helium-oxygen (heliox) at ambient temperatures selected to offset ethanol and helium-induced hypothermia. Hyperbaric exposure significantly reduced loss of righting reflex (LORR) duration in LS, 129, and C57 mice, but not in SS mice. A second experiment found that hyperbaric exposure significantly reduced LORR duration and increased the blood ethanol concentration (BEC) at return of righting reflex (RORR) in LS mice, but did not significantly affect either measure in SS mice. These results indicate that exposure to 12 ATA heliox antagonizes ethanol-induced LORR in LS, 129 and C57 mice, but not in SS mice. Taken with previous results, the present findings suggest that the antagonism in LS, 129, and C57 mice reflects a pressure-induced decrease in brain sensitivity to ethanol and that the lack of antagonism in SS mice cannot be explained by pressure-induced or genotypic differences in ethanol pharmacokinetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Kinetics of drug action in disease states. XIII. Effect of dialyzable component(s) of uremic blood on phenobarbital concentrations in rats at onset of loss of righting reflex.

The purpose of this investigation was to determine if the previously demonstrated increased sensitivity of the central nervous system of uremic rats to the hypnotic activity of phenobarbital is caused, wholly or in part, by the accumulation of one or more endogenous substances. Blood was obtained from normal donor rats and from rats made uremic by administration of uranyl nitrate 5 days earlier. The serum was dialyzed against water, using a cellophane membrane with a molecular exclusion limit of 12,000 to 14,000 daltons, and the dialysate was lyophilized. A concentrate of the dialysate was administered by i.v. infusion to normal rats who also received a slow i.v. infusion of phenobarbital until they lost their righting reflex. Samples of cerebrospinal fluid, blood (for serum) and the brain were obtained at that time and were assayed for phenobarbital. Compared to the two control groups, i.e., rats infused with serum dialysate from normal animals or with normal saline solution, rats infused with serum dialysate from uremic rats lost their righting reflex at significantly lower phenobarbital concentrations in serum, brain and cerebrospinal fluid. This shows that the serum of uremic rats contains appreciable concentrations of one or more dialysable components capable of potentiating or contributing to the hypnotic activity of phenobarbital.

Age Factors↗

PubMed1994

Quantification of the depressive effects of diazepam on the guinea pig righting reflex.

The effects of 5 mg/kg/day diazepam (IP for 21-39 days) on righting reflex latency (RRL) and neuronal activity in the medial vestibular nucleus (MVN) were investigated in guinea pigs. Diazepam treatment increased the RRL relative to vehicle-injected controls (p < 0.05, ANOVA); although the average RRL in the diazepam-treated animals did decrease over time, this decrease was not statistically significant and therefore evidence of tolerance was not obtained. MVN slices were removed from diazepam-treated animals and recordings were made from MVN neurons in vitro. The average resting activities for MVN neurons in slices from diazepam-treated animals and uninjected animals from a previous study were not significantly different.

Animals↗

PubMed1983

Analysis of righting reflex in cats with unilateral and bilateral labyrinthectomy.

High-speed cinematographic analysis of cats' righting reflex was done in conjunction with surgical ablation of vestibular end organs (unilateral and bilateral). The body rotating direction after labyrinthectomy (regardless of first side or second side) was found to be contralateral almost exclusively. Post-operatively, the righting time for each body segment showed some delay but subsequently improved after the trial repetition along the time course. At that late post-bilateral labyrinthectomy stage, cats could indeed right without any vestibular input, and even with additionally and randomly eliminated visual cue by blindfold.

Animals↗

PubMedDate not supplied

A new method for evaluating air-righting reflex ontogeny in rats using prenatal exposure to phenytoin to demonstrate delayed development.

The air-righting reflex has been used for many years to assess reflex integrity in rodent developmental neurotoxicity investigations. However, little refinement of the technique has occurred. We describe two methodological improvements: (a) an improvement in the method of positioning rats for air-righting, and (b) a stop-action photographic method to capture the rat's mid-air performance. We also compare results obtained using a visual scoring method to the newly developed photographically based scoring method. Prenatal phenytoin exposure has been shown to induce marked delays in air-righting development (14), therefore, phenytoin was used as a positive control treatment. Pregnant rats were administered 200 mg/kg phenytoin in propylene glycol or propylene glycol alone by gavage once/day on E7-18. Offspring were tested in the same apparatus twice and scored for air-righting success either by direct observation or photographed and the photographs scored subsequently. Rats were administered 6 trials per day (3 trials with each method) on days 16-24 of postnatal development. Detailed analyses of the two methods included subdividing phenytoin animals into those exhibiting the neurological abnormality of circling later in life and those that did not. Both methods revealed that phenytoin animals were delayed in air-righting development compared to controls and both methods revealed that phenytoin-circlers were more impaired than phenytoin-noncirclers. Advantages of the photographic method were that it provided a more precise method of scoring and a permanent record of the animal's response. One disadvantage was that it did not distinguish groups quite as well as the visual method.

Age Factors↗

PubMed2001

Influence of brain catalase on ethanol-induced loss of righting reflex in mice.

The effect of lead acetate and 3-amino-1, 2, 4-triazole (AT) on ethanol-induced loss of righting reflex (LORR) and brain catalase activity was studied in an attempt to confirm earlier observations on the involvement of catalase in ethanol-induced effects. Lead acetate (0 or 100 mg/kg) or AT (0 or 500 mg/kg) was injected (acutely) into mice 7 days or 5 h before testing. Other mice were exposed to drinking fluid containing 500 ppm lead acetate for 60 days. On the test day, mice received an intraperitoneal injection of ethanol (4.0 or 4.5 g/kg) and the duration of LORR was recorded. Acute lead-treated animals demonstrated a reduction in the duration of the LORR. However, both chronic administration of lead acetate and AT treatment increased the duration of ethanol-produced LORR. Furthermore, brain catalase activity in acute lead pretreated animals showed a significant induction, whereas it was reduced in chronic lead and AT treated mice. These results suggest that brain catalase activity, and by implication centrally formed acetaldehyde, may modulate ethanol-induced LORR.

Animals↗

PubMed1995

Use of repeated measures in an analysis of ethanol-induced loss of righting reflex in inbred long-sleep and short-sleep mice.

We present a repeated-measures analysis of ethanol-induced loss of righting reflex (LRR) in Inbred Long-Sleep (ILS) and Inbred Short-Sleep (ISS) strains of mice and their F1 and F2 cross progeny. Mice were administered a 4.1 g/kg intraperitoneal dose of ethanol at two times, 7-10 days apart. Repeatability is nonsignificant in ILS, ISS, and F1 mice, but is highly significant (0.47, p < 0.01) in the F2 mice. Mean LRR does not differ between trials 1 and 2, with the exception of the ISS strain in which the interaction of sex with LRR sensitization is significant. This two-trial method leads to increased accuracy of genotype assessment for pharmacological or behavioral traits where trial 1 does not influence the outcome of trial 2. The repeated-measures design facilitates novel analyses of the duration of LRR, and results suggest that most environmental variance for LRR is due to nonreplicable influences.

Alcoholic Intoxication↗

PubMed1984

Antagonism of xylazine plus chloral hydrate loss of the righting reflex in mice. A simple in vivo procedure for the evaluation of selective alpha 2-adrenoceptor antagonists.

Xylazine causes a dose-related loss of the righting reflex (LRR) in mice when combined with a subanesthetic dose of chloral hydrate. Compounds that preferentially block alpha 2-adrenoceptors antagonize this xylazine plus chloral hydrate LRR at low doses and in a dose-related manner. This action of these compounds appears related to their alpha 2-adrenoceptor blocking properties insofar as their activity in this test correlates reasonably well with their activity in other in vivo and in vitro procedures thought to reflect alpha 2-antagonism. Also, compounds without any appreciable alpha blocking properties or without selectivity for blocking alpha 2-adrenoceptors are not active in this procedure. At higher doses, the alpha 2-blockers antagonize the reversal of the LRR caused by low doses. This action may be indicative of the in vivo alpha 1 blocking properties of these compounds, which may in turn be related to their sedating properties. In any event, antagonism of xylazine plus chloral hydrate LRR in mice appears to be a simple, rapid, and quantitative procedure for the in vivo evaluation and comparison of selective alpha 2-adrenoceptor antagonists.

Adrenergic alpha-Antagonists↗

PubMed2000

Potentiation of ethanol-induced loss of the righting reflex by ascorbic acid in mice: interaction with dopamine antagonists.

The present investigation was carried out to determine the effect of ascorbic acid on ethanol-induced loss of the righting reflex (LORR) and the interactions between ascorbic acid and dopamine receptor antagonists in affecting this action of ethanol in mice. To test the effect of each drug on ethanol-induced LORR, ascorbic acid (31.25, 62.5, 125, 250, 500, 1000 mg/kg intraperitoneally [IP]) and dopamine receptor antagonists (haloperidol 0.5, 1.0 mg/kg; L-sulpiride 20, 40, 80 mg/kg; clozapine 0.625, 1.25, 2.5 mg/kg; SCH 23390 0.5, 1.0, 2.0 mg/kg subcutaneously [SC]) were administered, respectively, 30 min before ethanol (4.0 g/kg IP) administration. Ascorbic acid, at the dose of 1000 mg/kg, significantly potentiated ethanol-induced LORR in mice. Dopamine D(2) antagonists haloperidol (0.5, 1.0 mg/kg SC), and L-sulpiride (80 mg/kg SC) also significantly prolonged the duration of LORR induced by ethanol. Clozapine and SCH 23390, at the doses used, did not affect ethanol-induced LORR. In the interaction study, the synergistic effect of ascorbic acid (1000 mg/kg IP) on ethanol-induced LORR was significantly enhanced by dopamine D(2) antagonists haloperidol, L-sulpiride, and clozapine, and the highest dose of dopamine D(1) antagonist SCH 23390. These results suggest that ascorbic acid may potentiate ethanol-induced LORR partially via a mechanism mainly linked to blockade of dopamine D(2) receptors.

Animals↗

PubMed1992

Effects of the subcutaneous administration of enkephalins on tail-flick response and righting reflex of developing rats.

The s.c. administration of [Met5]-enkephalin to 10-day-old rats pretreated with the mixture of 3 peptidase inhibitors, amastatin, captopril and phosphoramidon, produced the inhibition of tail-flick response and loss of righting reflex. When infant rats were pretreated with the mixture of any combination of two peptidase inhibitors, however, the change in both the response and the reflex were not produced at all by enkephalin injection, indicating that 3 kinds of enzymes, amastatin-sensitive aminopeptidase(s), captopril-sensitive peptidyl dipeptidase A and phosphoramidon-sensitive endopeptidase 24.11, played an important role in the inactivation of enkephalin after its systemic administration. Additionally, the fact that the two enkephalin-induced effects were more effectively antagonized by naloxone, a relatively selective mu-opioid antagonist, than by naltrindole, a specific delta-antagonist, or by nor-binaltorphimine, a specific kappa-antagonist, showed that these two effects were produced by the interaction of enkephalin with mu receptors. Moreover the involvement of mu receptors in the production of these two effects was shown by the fact that the s.c. administration of [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin, a selective mu agonist, also produced these two effects which were more effectively antagonized by naloxone than by naltrindole or nor-binaltorphimine. Since the magnitude of the two effects induced by enkephalins in 15-day-old rats was significantly lower than that in 10-day-old rats, and the two enkephalin-induced effects were not produced at all in 20-day-old rats, a maturation-induced decrease in the permeability of the blood-brain barrier against opioid peptides was indicated.

Aging↗

PubMed1981

Differential effects of TRH, amphetamine, naloxone, and fenmetozole on ethanol actions: attenuation of the effects of punishment and impairment of aerial righting reflex.

The effects of four putative ethanol antagonists [thyrotropin releasing hormone (TRH), naloxone, d-amphetamine, and fenmetozole] on two distinct behavioral actions of ethanol were compared. TRH (20-40 mg/kg) reduced ethanol-induced impairment of the aerial righting reflex (ARR) but enhanced the ethanol-induced increase in punished drinking (anticonflict effect). Naloxone antagonized both actions of ethanol but only at high doses (20-60 mg/kg). Amphetamine (1-4 mg/kg) abolished the ethanol effect on punished drinking but did not alter its impairment of the ARR (1-8 mg/kg). Conversely, fenmetozole antagonized the ethanol impairment of the ARR (15-30 mg/kg) but not ethanol's anticonflict action. The inconsistent pattern of "antagonist" interactions of these drugs with the behavioral actions of ethanol suggests that ethanol alters several neurochemical systems to produce its behavioral effects.

Amphetamine↗

PubMed1985

Effect of pregnancy on ethanol concentrations at onset of loss of righting reflex in rats.

To determine if the pharmacodynamics of ethanol are altered in advanced pregnancy, 20-days pregnant Lewis rats and nonpregnant rats of the same age received an i.v. infusion of ethanol, 96 mg/min/kg, until they lost their righting reflex. The concentrations of ethanol at that time in adult and fetal serum, and in the cerebrospinal fluid (CSF) and brain of the adult animals were determined. Ethanol concentrations in the pregnant rats were only slightly (less than 10%) but statistically significantly lower than in nonpregnant controls. Brain/serum, CSF/serum, and CSF/brain concentration ratios of ethanol were essentially identical in pregnant and nonpregnant rats, indicating no apparent effect of pregnancy on the distribution kinetics of ethanol. The serum concentrations of ethanol in mothers and their fetuses were similar and significantly correlated. The results of this investigation show that the central nervous system depressant effect of ethanol is not appreciably altered by pregnancy.

Animals↗

PubMed1994

Effects of furazolidone on duration of righting reflex loss induced with hexobarbital and zoxazolamine in the rat.

Effects of furazolidone (FZ) on the sleeping time induced with hexobarbital (HEX) and paralysis time induced by zoxazolamine (ZOX) were investigated by measuring the length of time required to recover from righting reflex loss in rats after oral administration of FZ at doses of 50, 100, 200 and 400 mg/kg/day for 4 successive days. Administration of 50 mg/kg to rats of both sexes induced no effect on the HEX sleeping time, but of 100 mg/kg FZ or more induced prolongation of sleeping time dose-dependently. In female rats, HEX sleeping time of the control group was twice that of the male rats, but HEX sleeping time after receiving FZ above 200 mg/kg was approximately the same as in the male rats. ZOX paralysis time exhibited no sex differences in the control rats, and it was significantly prolonged by FZ at a dose of 100 mg/kg or more. No significant differences in blood levels of HEX and ZOX at the time of recovery were found between the control and FZ treated rats, suggesting that FZ produced prolongation of the drug effects was due to the maintenance of the blood levels rather than the change in the sensitivities of rats at the receptor sites. Body weight gains were inhibited in the rats treated with FZ at doses over 100 mg/kg. Cytochrome P-450 content in hepatic microsomes in the rats which received 100 mg/kg FZ were slightly increased. It is suggested that successive oral administration of FZ to rats at high doses impaired drug clearance and this resulted in the prolongation of HEX sleeping and ZOX paralysis times.

Administration, Oral↗

PubMed2005

Effect of sleep deprivation on righting reflex in the rat is partially reversed by administration of adenosine A1 and A2 receptor antagonists.

BACKGROUND: Similarities between naturally occurring sleep and general anesthesia suggest that the two states may interact physiologically. The authors have previously demonstrated that sleep deprivation potentiates anesthetic-induced loss of righting reflex (LORR) in rats. One possible mediator for this effect is adenosine, which accumulates in the brains of sleep-deprived animals and reduces anesthetic requirements. The authors tested in rats the hypothesis that potentiating effects of sleep deprivation on LORR can be altered by adenosine A1 and A2a receptor antagonists. METHODS: Five experiments were conducted. In each, rats underwent four trials, consisting of a 24-h period of either sleep deprivation or ad libitum activity followed by administration of a fixed dose of an adenosine antagonist or vehicle. Rats were then given isoflurane, and the time to LORR and recovery were measured. Each experiment tested a specific dose of an A1 receptor antagonist (8-cyclopentyltheophylline given via microinjection into the basal forebrain), an A2a receptor antagonist (ZM241385 via intraperitoneal administration), or both. In each experiment, all rats received all combinations of activity and drug/vehicle, separated by 5-7 days. RESULTS: In rested rats, neither antagonist altered the time to LORR. In sleep-deprived rats, both ZM241385 and 8-cyclopentyltheophylline prolonged the time to LORR and shortened recovery in a dose-dependent manner. Prolongation also occurred when subtherapeutic doses of both agents were coadministered. CONCLUSION: Both antagonists partially reversed the effect of sleep deprivation on anesthetic action. This result implies that deprivation-induced changes in adenosine receptor activity can alter LORR. Neither antagonist completely reversed this effect, suggesting possible non-adenosine-mediated effects of sleep deprivation.

Adenosine A1 Receptor Antagonists↗

PubMed1982

The influence of electrostimulation on hexobarbital induced loss of righting reflex in rats.

Electrostimulation (ES) of slow (SF, 10 Hz) or fast (FF, 500 Hz) frequency decreases the sleeping time of rats anaesthetized by administration of acute doses of hexobarbital. When ES is applied via the ears, both SF and FF are equally efficient in reducing the loss of righting reflex (LRR), whereas if ES is applied peripherally via the paws, only FF decreases the acute narcosis time. Applied cranially, either continuous stimulation or administration of intermittent current (5 minutes on and off) were equally effective in reducing narcosis. A decreased period of 30 minutes' continuous stimulation will reduce sleeping time only if administered immediately after LRR. When restrained animals received ES for periods of up to 3 hours prior to administration of the barbiturate, the sleeping time of the stimulated and sham treated animals were not significantly different.

Animals↗

PubMed2003

Effects of stress and etifoxine on pentobarbital-induced loss of righting reflex in Balb/cByJ and C57BL/6J mice.

We hypothesized that functional changes in the GABAergic system induced by stress would differ between two inbred mouse strains BALB/cByJ and C57BL/6J. We compared the effects of restraint stress and of the anxiolytic drug etifoxine (EFX) on the duration of pentobarbital-induced loss of righting reflex (hypnotic effect) in the two strains. Naive BALB/cByJ mice were less sensitive than naive C57BL/6J mice to the hypnotic effect of pentobarbital. C57BL/6J mice exhibited a shortening in the duration of pentobarbital-induced hypnosis following stress whereas stress had no effect in BALB/cByJ mice. EFX reversed the shortening of pentobarbital-induced hypnosis elicited by stress in C57BL/6J and shortened the duration of pentobarbital-induced hypnosis after stress in BALB/cByJ mice. Alterations in the GABAergic function in BALB/cByJ mice could be corrected by EFX, an enhancer of GABAergic transmission.

Animals↗

PubMed1985

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

To investigate the effect of diabetes on the sensitivity of the central nervous system to the hypnotic action of a barbiturate, studies were conducted on adult female Lewis rats made diabetic by injection of either streptozotocin or alloxan. The animals then received a slow i.v. infusion of phenobarbital (PB) until the onset of a defined pharmacologic effect [loss of righting reflex (LRR)] and the PB concentrations at that time in serum (total and unbound drug), brain and cerebrospinal fluid (CSF) were determined. In the experiments on rats with streptozotocin-induced diabetes, animals not treated with insulin had significantly lower serum concentrations of total PB at onset of LRR than did animals treated with insulin and nondiabetic control rats. Otherwise, there were no significant differences in PB concentrations between untreated diabetic and control animals. Additional experiments on untreated diabetic rats showed that, as in normal rats, the PB concentrations in CSF (but not in serum and brain) at onset of LRR were independent of PB infusion rate over a 10-fold range, indicating that PB equilibrates very rapidly between CSF and receptor sites. Experiments in rats with alloxan-induced diabetes showed no significant differences between untreated diabetic, insulin-treated diabetic, alloxan-nonresponding and nondiabetic control rats with respect to PB concentrations at onset of LRR in serum (total and unbound drug), brain and CSF and in serum protein binding. These results show that the central nervous system response to the hypnotic effect of PB is not significantly affected in two different experimental models of diabetes.

Animals↗