Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Rotarod Performance Test”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 271 records · Page 15Linked to original sources
PubMed1992

Species differences in diisopropylfluorophosphate-induced decreases in the number of brain nicotinic receptors.

DBA and C3H mice were injected chronically with 2.0 mg/kg diisopropylfluorophosphate (DFP) every other day for 2 or 4 weeks. Although acetylcholinesterase (AChE) activity and muscarinic receptor numbers ([3H] quinuclidinyl benzilate (QNB) binding) were decreased in DFP-treated DBA and C3H mice, the number of nicotinic receptors (L-[3H]nicotine and alpha-[125I]bungarotoxin (BTX) binding) was unchanged by chronic DFP treatment. Sprague-Dawley rats injected chronically with lower doses of DFP than were used in mice exhibited a greater reduction in AChE activity, as well as accompanying decreases in [3H]QNB and [3H]nicotine binding. Neither species exhibited changes in alpha-[125I]BTX following chronic DFP injection. The effects of chronic DFP treatment on sensitivity to DFP and to nicotine were also assessed in the two mouse strains using a battery of behavioral and physiological tests that included rotarod performance, Y-maze crossing and rearing activity, heart rate, and body temperature. No tolerance to DFP was observed in either mouse strain after 2 weeks of treatment. Following 4 weeks of treatment, DFP-treated DBA mice exhibited modest tolerance to the effect of DFP on body temperature. C3H mice did not survive the 4-week treatment. Some evidence for reduced sensitivity to nicotine's effects was detected in the DFP-treated DBA mice, but cross-tolerance to nicotine was not observed in the DFP-injected C3H mice. Because chronic DFP treatment did not evoke a change in the number of brain nicotinic receptors, the reduced sensitivity to some of nicotine's effects seen in DBA mice must be due to some factor other than receptor downregulation.

Animals↗
PubMedDate not supplied

Heterogeneity of tolerance developed to effects of ethanol on rotarod and accelerod performances in rats.

The ethanol-induced impairment of rotarod and accelerod performances has been investigated in rats. Ethanol (7.2%, v/v) was given orally ad lib to rats in a modified liquid diet for 15 days. Rotarod and accelerod performances were recorded before and at the 2nd, 4th, 7th, and 15th days of ethanol intake. The daily ethanol consumption of the rats ranged from 12.03 to 16.4 g/kg. Mean blood ethanol level was estimated as 282.3 and 242.5 mg/dl on the 7th and 15th days of ethanol consumption, respectively. Ethanol significantly decreased (p < 0.01 rotarod performance on the 2nd and 4th days. But tolerance developed to the ethanol-induced impairment of rotarod performance from the 7th day. It also significantly decreased (p < 0.01) accelerod performance of the rats throughout the 15 days. So no tolerance was seen to this action of ethanol. Our results suggest that rotarod and accelerod performance tests seem to have differential characteristics in the context of tolerance development to ethanol in rats.

Animals↗
PubMed2005

Effect of the cannabinoid ajulemic acid on rat models of neuropathic and inflammatory pain.

There is increasing evidence that cannabinoid agonists alleviate the abnormal pain sensations associated with animal models of neuropathic and inflammatory pain. However, cannabinoids produce a number of motor and psychotropic side effects. In the present study we found that systemic administration of the cannabinoid acid derivative 1',1'-dimethylheptyl-delta-8-tetrahydrocannabinol-11-oic acid (ajulemic acid, IP-751) and the non-selective cannabinoid receptor agonist HU-210 reduced mechanical allodynia in a nerve-injury induced model of neuropathic pain and in the CFA-induced model of inflammatory pain. In contrast, HU-210, but not ajulemic acid reduced motor performance in the rotarod test. These findings suggest that ajulemic acid reduces abnormal pain sensations associated with chronic pain without producing the motor side effects associated with THC and other non-selective cannabinoid receptor agonists.

Analgesics↗
PubMed2002

Induction of hyperlocomotion in mice exposed to a novel environment by inhibition of serotonin reuptake. A pharmacological characterization of diverse classes of antidepressant agents.

This study characterized the influence of acute administration of diverse classes of antidepressant agent upon the spontaneous locomotor activity (LA) of mice in a novel, open-field environment. The selective serotonin (5-HT) reuptake inhibitors (SSRIs), citalopram, fluoxetine, paroxetine, fluvoxamine, litoxetine and zimelidine, dose-dependently enhanced LA. Their actions were mimicked by the mixed 5-HT/noradrenaline (NA) reuptake inhibitors (SNRIs), venlafaxine, duloxetine and S33005. In contrast, clomipramine only slightly elevated LA and two further tricyclics, imipramine and amitriptyline, were inactive. Further, the selective NA vs. 5-HT reuptake inhibitors (NARIs), reboxetine, desipramine, maprotiline, nisoxetine and nortriptyline all failed to increase LA. The "atypical antidepressants," mianserin and mirtazapine, neither of which modify 5-HT reuptake, as well as the mixed SSRI/5-HT(2) antagonists, nefazodone and trazodone, also failed to increase LA. Doses of SSRI and SNRI which increased LA did not modify motor performance in the rotarod test. Further, they did not enhance LA in rats, suggesting that this response is characteristic of mice. Finally, upon prehabituation of mice to the activity chamber, the SSRI, citalopram, and the SNRI, venlafaxine, failed to increase LA. In conclusion, in mice exposed to a novel environment, inhibition of 5-HT reuptake by SSRIs and SNRIs enhances spontaneous LA in the absence of a generalized influence upon motor function. This response provides a simple parameter for characterization of SSRIs and SNRIs, and differentiates them from other classes of antidepressant agent. Although an influence upon arousal and/or anxiety is likely related to the increase in LA, the functional significance of this response requires additional elucidation.

Adrenergic Uptake Inhibitors↗
PubMed2003

Prepulse inhibition of acoustic startle in aromatase knock-out mice: effects of age and gender.

Estrogen has been suggested to play a neuromodulatory and neuroprotective role on the brain dopamine system. We used aromatase knockout (ArKO) mice that lack a functional aromatase enzyme and are unable to convert testosterone into estrogen, and assessed prepulse inhibition of acoustic startle, locomotor hyperactivity to amphetamine treatment and rotarod performance. Mice were tested at either 1 month, 4-5 months or 12-18 months of age. In male, but not female ArKO mice, there was an age-related reduction of prepulse inhibition. The 12-18 months old male ArKO mice also showed significantly greater amphetamine-induced hyperactivity. Mice heterozygous for the mutation showed no deficits or were in-between wildtype mice and ArKO mice. We postulate that these data indicate a neuroprotective role of estrogen, particularly in male mice, on ageing of brain mechanisms involved in pre-pulse inhibition and locomotor activity regulation. It is likely that these brain mechanisms are or include dopaminergic activity.

Acoustic Stimulation↗
PubMed2001

Involvement of NMDA receptors in the analgesic properties of psychotridine.

We have previously reported that the alkaloid extract of Psychotria colorata (Willd. ex R. & S.) Muell. Arg., had marked dose-dependent, opioid-like activity. Phytochemical analyses of P. colorata flowers and leaves identified several pyrrolidinoindoline alkaloids, including psychotridine. To further investigate the activity and mechanism of action of Psychotria alkaloids, we studied the effects of psychotridine on thermal and chemical models of analgesia. In the tail-flick model, psychotridine presents a dose-dependent analgesic effect; the effect is not reversed by prior treatment with naloxone. Psychotridine dose-dependently decreased capsaicin-induced pain. Performance in the rotarod test showed that psychotridine does not induce motor deficits at doses effective in analgesia models. Psychotridine inhibited [3H]MK-801 (dizocilpine) binding to cortex membranes in a dose-dependent manner. Binding is completely abolished at 300 nM. The data rule out opioid activity, and the inhibition of capsaicin-induced pain and of radioligand binding strongly suggest the participation of NMDA receptors in psychotridine-induced analgesia.

Alkaloids↗
PubMed1981

[Pharmacological action of eptazocine (l-1,4-dimethyl-10-hydroxy-2,3,4,5,6,7-hexahydro-1,6-methano-1H-4-benzazonine). (III) Central action of eptazocine (author's transl)].

Pharmacological actions of eptazocine on the central nervous system were investigated by pharmacological and behavioral methods. Eptazocine produced sedation at low doses and Straub tail reaction in mice and ataxia in rats at high doses. In mice, eptazocine caused decreases in the spontaneous locomotor activities measured by the wheel cage and Animex methods, but caused an increase of the response in rats as determined by the open-field method. Eptazocine caused impairment of performance in the rotarod test and the traction test in mice, a decrease of activity of EMG, and an inhibition of flexor reflex in rats. Eptazocine decreased body temperature, potentiated pentobarbital-induced sleeping, and convulsion caused by pentylene-tetrazol in mice. Fighting behavior induced by electric shock and central stimulation effect of methamphetamine were inhibited by eptazocine in mice. Eptazocine showed an inhibiton of avoidance behavior in shuttle and skinner boxes in rats. These results suggest that eptazocine produces a non-specific inhibitory action on the central nervous system.

Analgesics↗
PubMed1984

Effects of brotizolam, a new thieno-triazolo-diazepine derivative, on the central nervous system.

The effects of brotizolam, a new thieno-triazolo-diazepine derivative, on the central nervous system were analyzed in mice, rats and rabbits. Diazepam, estazolam and triazolam were used as control drugs. Brotizolam inhibited spontaneous motor activities; performances in the rotarod test, staircase test, and maximal electroshock seizure test; and pentetrazol- or bemegride-induced convulsion. Moreover, catalepsy inducing action and potentiating effect on sleep elicited by pentobarbital or ethanol were observed. Following intraperitoneal or oral administration of brotizolam to rabbits with chronically implanted electrodes, the electroencephalographic profile in spontaneous EEG was characterized by slow waves with high amplitudes in the neocortex. The arousal responses by stimulation of the midbrain reticular formation and posterior hypothalamus were slightly inhibited, but the recruiting responses induced by stimulation of the diffuse thalamic projecting system were not inhibited, and seizure discharges induced by stimulation of the dorsal hippocampus were inhibited markedly. When motor activities and pentetrazol-induced convulsions were observed as indices of tolerance for brotizolam, tolerance was not developed by repeated administration of brotizolam up to 14 days. These results suggested that brotizolam, a new thieno-triazolo-diazepine derivative, is judged to be a safer and stronger sleep inducer than diazepam and estazolam.

Animals↗
PubMed2003

Pharmacological evaluation of garenoxacin, a novel des-F(6)-quinolone antimicrobial agent: effects on the central nervous system.

The effects of garenoxacin (formerly T-3811 or BMS-284756) on the central nervous system (CNS) were compared with various quinolones. Garenoxacin injected intracerebroventricularly into mice caused clonic convulsion at a higher dose (50 micrograms/body) than norfloxacin, ciprofloxacin, sitafloxacin and trovafloxacin. Additionally the convulsant activity of garenoxacin was not potentiated by biphenylacetic acid (BPAA). Garenoxacin did not induce any convulsions at intravenous doses up to 60 mg/kg in combination with 200 mg/kg oral administration of fenbufen in mice, and its convulsant activity was weaker than those of enoxacin, norfloxacin, ciprofloxacin, alatrofloxacin and ofloxacin. In addition, convulsions were not induced by combination administration of garenoxacin (60 mg/kg, i.v.) and any of 9 kinds of nonsteroidal anti-inflammatory drugs (NSAIDs) or BPAA. In a rotarod test, which was performed in order to evaluate the drug-induced dizziness, coordinated locomotor activity of mice was suppressed by alatrofloxacin at an intravenous dose of 60 mg/kg, but not by garenoxacin, ciprofloxacin and norfloxacin at up to 60 mg/kg. In an in vitro study using rat brain synaptic membrane, garenoxacin had no inhibitory effect on GABA binding in the presence or absence of NSAIDs. In conclusion, the effects of garenoxacin on CNS were weaker than those of other quinolones in experimental animals, so it might possess a low potential for CNS adverse reactions such as convulsion and dizziness in clinical use.

Animals↗
PubMed2000

Neuroprotective effects of creatine in a transgenic mouse model of Huntington's disease.

Huntington's disease (HD) is a progressive neurodegenerative illness for which there is no effective therapy. We examined whether creatine, which may exert neuroprotective effects by increasing phosphocreatine levels or by stabilizing the mitochondrial permeability transition, has beneficial effects in a transgenic mouse model of HD (line 6/2). Dietary creatine supplementation significantly improved survival, slowed the development of brain atrophy, and delayed atrophy of striatal neurons and the formation of huntingtin-positive aggregates in R6/2 mice. Body weight and motor performance on the rotarod test were significantly improved in creatine-supplemented R6/2 mice, whereas the onset of diabetes was markedly delayed. Nuclear magnetic resonance spectroscopy showed that creatine supplementation significantly increased brain creatine concentrations and delayed decreases in N-acetylaspartate concentrations. These results support a role of metabolic dysfunction in a transgenic mouse model of HD and suggest a novel therapeutic strategy to slow the pathological process.

Animals↗
PubMed1990

Behavioral changes in rats fed a diet containing 2,4-dichlorophenoxyacetic butyl ester.

Oral administration of 2,4-dichlorophenoxyacetic butyl ester (2,4-Dbe) at a dose of 69 mg/kg/day to nulliparous females had no deleterious effects on either open field (OF) and rotarod performance. By contrast, dams treated with 2,4-Dbe during pregnancy exhibited impairments of OF activity, rotarod performance and improved active avoidance learning (AAL) retention. Administration of 2,4-Dbe to 90-day-old intact male rats depressed spontaneous OF activity, acquisition of conditioned avoidance responses (CARs) and rotarod endurance, but improved AAL performance. Castration itself impaired performance in the rotarod test, and improved AAL, but did not alter OF activity significantly. The effects of castration were reversed by exogenous testosterone. In gonadectomized rats, 2,4-Dbe prevented the reversal of the effect of testosterone on the influence of castration on behavior if given concomitantly with the testosterone. However, when the 2,4-Dbe treatment started seven days after testosterone, the 2,4-Dbe effects on OF, rotarod and AAL behaviors were reinstated. Thus, testosterone appears to be important for causing the toxic effects of 2,4-Dbe in rats.

2,4-Dichlorophenoxyacetic Acid↗
PubMed2003

The influence of diazepam on atropine reversal of behavioural impairment in dichlorvos-treated rats.

Acute effects on the behaviour of the organophosphate insecticide dichlorvos and its standard antidotes possessing behavioural activity, atropine and diazepam, were studied separately and in combinations in male Wistar rats. In the spontaneous locomotor activity test, dichlorvos and diazepam decreased, whereas atropine increased performance. The effect of dichlorvos was obtained at a dose (5 mg/kg) that induced overt intoxication, and could not be reversed during first half hour-period after administration of any combination of drugs. In the other two tests, active avoidance learning and rotarod performance, the effective dose of dichlorvos (2 mg/kg) was devoid of somatic signs of intoxication. In these more sensitive tests, the effective atropine dose (40 mg/kg) completely reversed dichlorvos-induced incapacitation. In the rotarod test, diazepam (0.5 mg/kg) contributed to the incapacitating effect of dichlorvos, and impeded desirable influence of atropine as well. In the active avoidance test, diazepam (2.5 mg/kg) contributed to failure to escape; it did not influence the dichlorvos-induced decrease of avoidance performance, nor did it impair the completely reversing effects of atropine. The results point to the possible summation of acute incapacitating effects of organophosphates and diazepam on motor performance, which seems to be, at least partly, antagonized by sufficiently high doses of atropine. However, taking into account the long-term neuroprotective role of the anticonvulsant diazepam, and hence its delayed beneficial influences on behaviour, the immediate testing of atropine/diazepam treatment of organophosphate intoxication in active avoidance paradigm could possess beside sensitivity the predictive value as well.

Animals↗
PubMed2003

More severe neurologic deficits in SJL/J male than female mice following Theiler's virus-induced CNS demyelination.

Although multiple sclerosis (MS) is more prevalent in women than men, male MS patients develop more severe clinical symptoms and deteriorate faster than female patients. We investigated the differences in CNS demyelinating disease between SJL/J male and female mice following Theiler's murine encephalomyelitis virus (TMEV) infection. Infected female mice had consistently higher serum levels of virus-specific IgG at 14 and 21 days and and 7 months postinfection, which resulted in less infectious virus in CNS. All male mice infected for 6 to 7 months developed paralysis, with 50% displaying bilateral posterior limb paralysis, whereas 77% of age-matched female mice were paralyzed, all displaying unilateral posterior limb paralysis. Male mice infected for 6 to 7 months performed up to threefold fewer spontaneous horizontal and vertical movements (activity box test) compared to infected age-matched females. In addition, infected male mice performed the coordination and balance (Rotarod) test at 27 +/- 4% of the expected level (expressed as a percentage of that of uninfected age-matched mice), whereas infected female mice performed at 41 +/- 5% of the expected level. Male mice had a small increase in the extent of spinal cord white matter demyelination analyzed at both 45 days and between 6 and 7 months postinfection. For individual male and female mice, the extent of demyelination had a negative linear relationship with the neurologic performances. The emergence of a disease paradigm similar to MS supports using the TMEV model to investigate molecular and genetic factors responsible for the gender dimorphism in MS and other autoimmune diseases.

Acute Disease↗
PubMed2000

Quantitative measurement of motor and somatosensory impairments after mild (30 min) and severe (2 h) transient middle cerebral artery occlusion in rats.

We tested the hypothesis that mild and severe ischemic cell damage are reflected in neurological and functional recovery after stroke. Rats were subjected to either 30 min or 120 min of middle cerebral artery occlusion or sham operation. Neurological and functional tests including, gross neurological score, and rotarod and adhesive removal tests were performed at various time points up to 21 days after stroke. Significant differences between groups of animals were detected using the rotarod and adhesive removal test. A significant correlation between lesion volume and adhesive removal test was detected in rats subjected to 30 min of ischemia. Our data indicate that quantitative rotarod and adhesive removal tests measure different aspects of functional recovery after stroke, and both are useful in characterizing functional recovery from an ischemic insult.

Animals↗
PubMed2006

Postnatal inflammatory rat model for cerebral palsy: too different from humans.

OBJECTIVE: In humans, cerebral palsy (CP) may originate from inflammation during the second and third trimesters of gestation when preoligodendrocytes (Pre-OL) are most vulnerable to an inflammatory insult. We studied a postnatal CP model to evaluate injury that would correlate with presence of Pre-OL in human pregnancy. STUDY DESIGN: On postnatal (P) days 2, 3, 4, 5 and 6, pups were treated with (lipopolysaccharide [LPS]) (n = 7; 30, 30, 60, 60, 120 microg/Kg) or saline (n = 7). Neonates were tested for motor and cognitive development. Adult offspring performed beam walking and rotarod for motor activity. White matter damage was assessed with immunohistochemical Pre-OL markers (CNP, PLP). Statistical analysis included Mann-Whitney U and analysis of variance. RESULTS: LPS-treated animals performed negative geotaxis (P = .009) and surface righting (P = .01) earlier than controls. No differences were observed for other neonatal tests. Adult LPS-treated offspring performed better in tests of motor control: rotarod (P = .01) and beam walking (P = .02). Pre-OL markers were altered in LPS-treated animals at both P22 (CNP and PLP increased in LPS, P < .01 and P < .001, respectively) and 12 weeks (CNP and PLP decreased in LPS, P < .0001 and P < .03, respectively). CONCLUSION: Neonatal exposure to LPS induced white matter damage in the brain, accelerated neurodevelopment and motor tasks in adulthood. These are similar to findings from a postnatal hypoxic model suggesting that in the rodent, targeting the Pre-OL does not result in a CP phenotype.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1993

Antinociception induced by CP 96,345, a non-peptide NK-1 receptor antagonist, in the mouse formalin and capsaicin tests.

The non-peptide NK-1 receptor antagonist, CP 96,345, has been evaluated for antinociceptive activity in two chemical pain models in the mouse. CP 96,345, injected intrathecally (i.t.) 5 min prior to 2.0% formalin, produced significant antinociception in both the early and late phases of the formalin-induced paw licking procedure. Antinociception could also be observed during the late phase by treatment with CP 96,345 after formalin. In the capsaicin (CAP) test, i.t. injection of CP 96,345 produced a dose-dependent reduction of the paw-licking response at doses much less than antinociceptive doses in the formalin test. Naloxone did not affect antinociception in either test. CP 96,345 evoked a reversible deficit in motor performance as assayed by the rotarod test. The results indicate that i.t. CP 96,345 is antinociceptive in the capsaicin test at doses showing no overt behavioural effects but there is an overlap in doses producing antinociceptive and motor effects in the formalin test.

Analgesics↗
PubMed2003

Effects of prenatal exposure to methylmercury on dopamine-mediated locomotor activity and dopamine D2 receptor binding.

In the present study we have investigated the neurotoxic effects of the exposure to a low dose (0.5 mg/kg/day) of methylmercury (MeHg) on the developing nervous system. Pregnant rats were treated with MeHg from day 7 of pregnancy to day 7 of lactation. At postnatal day 20 the offspring did not display prominent functional cerebellar alterations, as evaluated by the Rotarod performance. Motor activity (locomotion, rearing and motility) was tested in the 21-day-old rats after administration of apomorphine, an agonist of D(1), D(2), and D(3) dopamine receptors. A low dose of apomorphine (0.1 mg/kg) induced a significantly stronger increase in motility and locomotion in MeHg-treated rats as compared to controls. The same effect was also observed in rats injected with 1 mg/kg apomorphine. No changes were observed in rearing at either doses of the dopamine receptor agonist. The data suggest that changes in dopaminergic transmission are induced by exposure to MeHg in early life. The expression of the striatal dopamine D(1) and D(2) receptors was examined by in situ hybridization in the striatum of the 21-day-old rats. The analysis did not reveal any significant changes at the mRNA level. Ligand autoradiography experiments showed a significant reduction in dopamine D(2) receptor binding in the caudate putamen of MeHg-treated rats. Spatial learning ability was tested in 2-month-old rats using the Morris swim maze test. Changes in retention were shown in MeHg-treated rats, indicating that MeHg induced memory alterations. Taken together, these findings show that exposure to a very low dose of MeHg during development exerts neurotoxic effects on the dopaminergic system and that alterations of brain functions persist in adult life.

Animals↗
PubMed2006

Fluvastatin alters psychomotor performance and daily activity but not the spatial memory in rats.

Statins, inhibitors of cholesterol synthesis for treating dyslipidemia and preventing cardiovascular complications, have been shown to alter central nervous system functions. Our aim was to investigate the effects of the fluvastatin, a member of statin family, on psychomotor performance, daily activity and spatial memory. Sprague-Dawley rats were treated with fluvastatin (n = 8) or placebo as a control (n = 11) regardless of sex. Fluvastatin (7.5 mg/kg) was administered orally once a day for four weeks, while the control group was administered only placebo. Psychomotor performance was measured by rotarod tests. No significant difference was observed in the fluvastatin group over the course of weeks, but the control group preferred to stay on the device shorter times (p < 0.05). For the first three weeks of the drug administration there was a statistical difference between the groups, however no difference was found after the 4th week. There was no difference in the Barnes maze spatial memory test between the groups and also within the groups over the course of time. Daily activity tests revealed that stereotypical and vertical movements of the fluvastatin group were significantly less than the control group in all four weeks. Ambulatory movements and the distances taken by the fluvastatin group were decreased significantly over the course of time (p < 0.005 and p < 0.001, respectively), but the control group did not reveal any significant change. Our results suggest that fluvastatin altered psychomotor performance and daily activity in rats, but it did not affect the spatial memory. These behavioral changes might be associated with alterations in the composition of the brain lipids caused by fluvastatin.

Animals↗