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PubMed2005

Chronic reduction in dietary tryptophan leads to changes in the emotional response to stress in mice.

Acute depletion of brain tryptophan (TRP) levels in humans has been used as a biochemical model of depression. In this study, we examined the effects of consumption of a diet low in TRP on emotional behavior in mice. Specifically, we assessed various parameters of emotional behavior in mice fed a TRP-limited diet for at least 1 mo. TRP-limited mice showed increased defensive, but not offensive, aggression in the resident-intruder test. In the social dominance tube test, these mice showed enhanced social dominance. Since defensive aggression is thought to be a reflection of not only aggression but also fear, these changes in the social behavior of TRP-limited mice are thought to reflect changes in their emotional status. TRP-limited mice also showed increased locomotor activity and mobility in the open field and forced swim tests, respectively, suggesting that their stress/emotional responsiveness was enhanced. Importantly, these mice displayed normal levels of anxiety and motor performance as determined by the elevated zero maze and open field tests, and the rotarod test, respectively, suggesting that their hyperactivity was not due to a reduction in anxiety levels or to enhancement of their motor performance. Thus, dietary TRP restriction appears to result in alterations in the emotional response to stress, in mice.

Aggression↗

PubMed1981

Comparison of accelerod and rotarod sensitivity in detecting ethanol- and acrylamide-induced performance decrement in rats: review of experimental considerations of rotating rod systems.

The relative sensitivity of two rotating rod techniques in detecting performance decrement in rats was assessed after treatment with either ethanol or acrylamide. Performance on the rod during acceleration at approximately 1 rpm/sec (accelerod) was compared to that obtained on the same rod operated at a constant speed of 20 rpm (rotarod). Rats trained to either task received a single oral dose of ethanol (0.5, 1.0, 1.5, or 2.0 g/kg) or a series of ip doses of acrylamide (25 or 50 mg/kg/day) before testing. Accelerod performance was significantly more disrupted at lower doses and for longer periods of time after ethanol ingestion than was rotarod performance. Likewise, task disruption resulted from repeated injections of acrylamide also appeared at lower cumulative doses using the accelerod. A higher proportion of the native subjects were successfully trained and the mean time for training to minimum performance standards was significantly less using the accelerod. The greater sensitivity of the accelerod technique in detecting neurotoxic effects is attributed primarily to the fact that this test provides a continuous measure of the upper limit of performance rather than the quantal or arbitrarily truncated measure that one usually obtains from the rotarod. In light of these findings, a review is presented of the primary experimental variables that affect the reliability of data obtained in neurotoxic evaluations using the accelerod and rotarod procedures.

Acrylamides↗

PubMed2002

Effects of raw garlic on physical performance and learning behaviour in rats.

The effects of garlic (Allium sativum Linn.) on physical performance and learning behaviour were evaluated in male rats (7-8 months old, weighing 250-400 g) by comparison with the effects of pentoxifylline, a haemorheological agent with antiplatelet activity. The tests were designated as experiment A and experiment B, both conducted in two consecutive 4-week sessions. In experiment A, the rats performed in a learning maze model during the first 4 weeks then followed by moving along the rope model for another 4 weeks. In experiment B, the rats were first tested in a rotarod treadmill for 4 weeks and then a step down test model for another 4 weeks. Each experiment consisted of four groups with 6-8 rats per group. Aqueous garlic homogenate at doses of 1 and 2 g (of raw garlic)/kg/day were given orally to group 1 and group 2, respectively, while pentoxifylline dispersion at a dose of 200 mg/kg/day was given to group 3. Group 4 served as the control group and was given water. All tests (maze model, rope model, rotarod model and step down model) were performed three times a week. The number of successful tasks and the acquisition time in 1 week intervals were used for the statistical analysis. The present results demonstrated that neither aqueous garlic homogenate at both doses nor pentoxifylline exhibited any benefit in the maze model or the rotarod model. Garlic only at the lower dose and pentoxifylline however, showed benefit in the rope model and step down model. These findings may provide some evidence to support the beneficial effect of long-term garlic consumption on physical performance and learning behaviour in normal subjects.

Animals↗

PubMed1983

Motor performance achievements in rats of different ages.

Motor performance of rats of different ages was determined in a cross sectional study. The design includes a test battery of seven motor tasks of graduated complexity. The results show a hierarchical order of impairments of motor functions in aging rats; that is, the more complex the task requirement, the earlier and more pronounced is the susceptibility to deterioration of motor coordination. In spontaneous activity and swimming no difference could be observed between young and old rats. With increasing requirements for the tilting-plane, horizontal wire, climbing and chimney tests as well as the rotarod test, the older rats show a differentiated decrease in performance. The findings are discussed in respect to the theory that aging is a reverse process of early development.

Aging↗

PubMed1975

Compartive behavioral effects of dibutyryl cyclic AMP and prostaglandin E1 in mice.

Three behavioral tests, spontaneous locomotor activity (SLMA), exploratory behavior (EB) and rotarod performance (RP), a measure of neuromuscular coordination, were used to stuey the interaction of PGE1 (1 mg/kg i.p., 10 min. pretreatment) with DBcAMP (25 mg/kg i.p., 25 min. pretreatment) in mice. A dose-response relationship of PGE1 (0.01-5.0 mg/kg) to SLMA was determined, with a significant decrease in SLMA produced by a dose of 0.1 mg/kg. decreases in SLMA were produced by PGE1 (79%), DBcAMP (41%) and DBcAMP-PGE1 combination (71%). Similar decreases in EB were observed. Although no significant difference between controls and DBcAMP was observed in RP, 52% of mice tested were RP failures following PGE1 and a 100% failure rate was induced by the combination. Mice were treated with a second injection of DBcAMP or PGE1 or the combination 24 hr following the first injection. Behavioral activity of these mice was observed 25 min (DBcAMP) or 10 min (PGE1) after the second dose was administered. A second injection of DBcAMP failed to decrease SLMA and EB from controls; moreover, SLMA began to return towards control levels as early as 2 hr between injections. The second injection of PGE1 or DBcAMP+PGE1 produced the same behavior as that produced by the first injection. On the basis of these results, the relationship of cyclic nucleotides and PGs to behavioral activity is discussed.

Animals↗

PubMed1991

Assessment of antinociceptive drug effects in the presence of impaired motor performance.

The hot-plate (HP) and tail-flick (TF) tests are widely used to assess analgesic activity of drugs. These tests do not directly measure the intensity of the noxious stimulus perceived by the animal, but only the animal's response to it, and so may be affected by non-analgesic drugs. Sedatives and muscle relaxants, for example, may impair the ability to respond and hence be wrongly considered to have analgesic activity. We examined response of rats in the HP (55 degrees C, cutoff time 25 sec) and TF (cutoff time 5 sec) tests following administration of pentobarbitone, diazepam or pancuronium. These drugs all impaired motor performance as assessed by reduction in mean rotarod performance times to 6-32% of predrug values. However, HP and TF latencies were not appreciably prolonged. We also found that pancuronium did not alter effects of morphine on HP or TF latencies, despite reduction in rotarod performance to 38% of predrug values. Our results support the validity of HP and TF tests as analgesic assays even in the presence of substantial impairment of motor performance.

Analgesics↗

PubMed2001

A comparative assessment of the efficacy and side-effect liability of neuroprotective compounds in experimental stroke.

There are many examples of compounds showing neuroprotective efficacy in animal models of stroke but not in clinical trials. It is possible that some or all of these compounds possess poor therapeutic ratios, which results in the administration of sub-efficacious doses in order to avoid the emergence of side-effects. In order to explore this possibility, this study compared the therapeutic ratios of a number of neuroprotective agents that have undergone clinical trials. Neuroprotective efficacy was established using the mouse permanent (24 h) middle cerebral artery occlusion model. Side-effect liability was determined by assessment of motor coordination using the rotarod test. The therapeutic ratio was calculated as the ratio between the minimum effective dose (MED) for significant impairment in rotarod performance and the MED for significant neuroprotection. Compounds were administered i.p. 30 min prior to rotarod testing or onset of ischemia. Drugs such as Ifenprodil, Cerestat and Selfotel, that have failed in clinical trials, were found to have very low therapeutic ratios of < or = 1, whereas compounds with more tolerable clinical side-effect profiles were found to have higher therapeutic ratios (2, 10 and 10 for Sipatrigine, Remacemide and sPBN, respectively). It is concluded that the lack of efficacy of a number of neuroprotectants in clinical trials may well be a consequence of their poor therapeutic ratios.

Animals↗

PubMed1999

Paradoxical locomotor behavior of dopamine D1 receptor transgenic mice.

The behavioral effects of augmenting dopamine D1 receptor expression in the brain were investigated in mice incorporating additional copies of the mouse D1 receptor gene. Two transgenic lines showed increases in brain D1 receptor binding sites, which were greatest in extrastriatal regions. The full D1 agonist SKF 81297, when administered systemically to control animals, stimulated a dose-dependent increase in locomotor activity. In contrast, in D1 receptor overexpressing transgenic mice, this drug caused a marked suppression of locomotion due to a decrease in the frequency of movement initiation. Amphetamine and cocaine induced comparable locomotor activation in both transgenic animals and their control littermates. In the transgenic animals, D1 agonist-induced rearing and climbing behaviors were suppressed. However, on rotarod testing, the agonist-treated transgenic and control mice performed comparably, indicating that sensorimotor coordination was unaffected. These studies demonstrate that altering the levels of D1 receptor expression reverses the effects of D1 agonism on locomotor initiation and rearing.

Animals↗

PubMed1984

Toxicity of anticholinesterases: interactions of pyridostigmine and physostigmine with soman.

This investigation was conducted to assess the potential of carbamate pretreatment to exacerbate the ill effects of low doses of soman. Ambulatory Activity in a photocell cage (AA) and performance time on an accelerating rotarod (ARR) were used to test for interactions between pyridostigmine or physostigmine and soman. ED50s (i.e., dosages sufficient to reduce ARR time and AA to 50% of control level) of each carbamate (IM) and soman (SC) were determined. The ED50 values (mg/kg) in the ARR test were 3.2, 0.21, and 0.072 for pyridostigmine, physostigmine and soman, respectively, while in the AA test the corresponding values were 1.8, 0.072 and 0.060. The matrix of 16 combinations of 0, 1, 2/3, and 1/3 ED50 each of carbamate and soman was studied in each test system, as well as the effect of behavioral deficit free (BDF) dosages of each carbamate on the ED50s of soman. In both the AA and ARR tests the matrix of combinations of pyridostigmine and soman indicated an additive effect. In contrast, physostigmine produced one instance of potentiation in each test system and anatagonism in two combinations in the AA procedure. A BDF dosage of each carbamate (0.056 mg/kg of pyridostigmine and 0.026 mg/kg of physostigmine) gave no evidence of adding to the deficit in AA induced by soman. In the ARR test, the ED50 of soman was lower by 11% with pyridostigmine pretreatment and by 14% with physostigmine; the latter just reached statistical significance (p less than 0.05). Although additivity was most often found at higher dosages of pyridostigmine and physostigmine, at the BDF dosages little or no adverse interaction was found between Pyridostigmine or Physostigmine and low levels of soman.

Acetylcholinesterase↗

PubMed1999

Characterization of progressive motor deficits in mice transgenic for the human Huntington's disease mutation.

Transgenic mice expressing exon 1 of the human Huntington's disease (HD) gene carrying a 141-157 CAG repeat (line R6/2) develop a progressive neurological phenotype with motor symptoms resembling those seen in HD. We have characterized the motor deficits in R6/2 mice using a battery of behavioral tests selected to measure motor aspects of swimming, fore- and hindlimb coordination, balance, and sensorimotor gating [swimming tank, rotarod, raised beam, fore- and hindpaw footprinting, and acoustic startle/prepulse inhibition (PPI)]. Behavioral testing was performed on female hemizygotic R6/2 transgenic mice (n = 9) and female wild-type littermates (n = 22) between 5 and 14 weeks of age. Transgenic mice did not show an overt behavioral phenotype until around 8 weeks of age. However, as early as 5-6 weeks of age they had significant difficulty swimming, traversing the narrowest square (5 mm) raised beam, and maintaining balance on the rotarod at rotation speeds of 33-44 rpm. Furthermore, they showed significant impairment in prepulse inhibition (an impairment also seen in patients with HD). Between 8 and 15 weeks, R6/2 transgenic mice showed a progressive deterioration in performance on all of the motor tests. Thus R6/2 mice show measurable deficits in motor behavior that begin subtly and increase progressively until death. Our data support the use of R6/2 mice as a model of HD and indicate that they may be useful for evaluating therapeutic strategies for HD, particularly those aimed at reducing the severity of motor symptoms or slowing the course of the disease.

Acoustic Stimulation↗

PubMed1982

[Behavioral effects of flutoprazepam (KB-509) and its metabolites].

The behavioral effects of KB-509 and its metabolites were investigated and compared with those of diazepam in mice and rats. The locomotor activity of mice measured by an Animex test was decreased with relatively large doses of KB-509 and diazepam. The anticonflict effect of KB-509 in rats was approximately as potent as that of diazepam. The lever pressing responses in the unpunished period were reduced by diazepam at a dose of 50 mg/kg p.o., while they were not affected by KB-509 even at a large dose such as 100 mg/kg p.o. KB-509 inhibited conditioned avoidance responses of the rat in a shuttle box at an extremely large dose such as 1000 mg/kg p.o. This effect of KB-509 was much less potent than that of diazepam. KB-509 was more potent than diazepam in inhibiting footshock-induced fighting behavior in mice. KB-509 and diazepam prevented maximal electroshock, pentetrazol, and strychnine induced convulsions in mice. KB-509 was more potent than diazepam in potentiating barbital anesthesia, in impairing rotarod performance, and in muscle relaxant activity measured by a traction test in mice. The pharmacological activity of desalkyl-KB-509 was more potent than that of KB-509 and that of desalkyl-3-OH-KB-509 was approximately as potent as that of KB-509. These results indicate that KB-509 possesses pharmacological properties similar to that of diazepam, and it is slightly greater in potency and is much longer in duration of action than diazepam.

Aggression↗

PubMed1988

On the role of endogenous GABA in the forced swimming test in rats.

GABA content was reduced in the nucleus accumbens, cortex and brainstem of rats after 5 but not after 45, 120 min or 24 hr, from the termination of the pretest session. This reduction was not observed in rats performing on rotarod. Intraperitoneal AOAA (25 mg/kg; 24, 5 and 1 hr before the test), reduced at the same extent immobility time regardless whether the animals had been exposed to a pretest session. In pretested animals, reduction in immobility time produced by AOAA (25 mg/kg X 3 times) was similar to that observed following 50 mg/kg, 5 hr before testing. This reduction was not antagonized by GABA antagonists bicuculline (2 mg/kg) or picrotoxin (2 mg/kg), given intraperitoneally 30 and 20 min before the test respectively. Intraperitoneal sodium valproate (200 or 400 mg/kg; 24, 5 and 1 hr before the test) and isoniazide (200 mg/kg) or 4-deoxypyridoxine (400 mg/kg), administered 1 or 1.5 hr before the test, were ineffective. AOAA (25 mg/kg X 3 times) gave a similar increase in GABA levels to 50 mg/kg only once in the brainstem, nucleus accumbens and hypothalamus and a greater increase in the other brain areas. After 5 hr from single dosing, 25 mg/kg AOAA increased GABA levels less than 50 mg/kg AOAA in the brainstem, nucleus accumbens, frontal cortex and striatum, and increased it to same extent in the other areas. Sodium valproate (400 mg/kg X 3 times) increased GABA levels in all brain areas, except hippocampus, although to a lesser extent than AOAA.

Aminooxyacetic Acid↗

PubMed2001

Therapeutic benefit of intracerebral transplantation of bone marrow stromal cells after cerebral ischemia in rats.

We tested the hypothesis that bone marrow stromal cells (MSCs) transplanted into the ischemic boundary zone, survive, differentiate and improve functional recovery after middle cerebral artery occlusion (MCAo). MSCs were harvested from adult rats and cultured with or without nerve growth factor (NGF). For cellular identification, MSCs were prelabeled with bromodeoxyuridine (BrdU). Rats (n=24) were subjected to 2 h of MCAo, received grafts at 24 h and were euthanized at 14 days after MCAo. Test groups consisted of: (1) control-MCAo alone (n=8); (2) intracerebral transplantation of MSCs (n=8); (3) intracerebral transplantation of MSCs cultured with NGF (n=8). Immunohistochemistry was used to identify cells from MSCs. Behavioral tests (rotarod, adhesive-removal and modified neurological severity score [NSS]) were performed before and after MCAo. The data demonstrate that MSCs survive, migrate and differentiate into phenotypic neural cells. Significant recovery of somatosensory behavior (p<0.05) and NSS (p<0.05) were found in animals transplanted with MSCs compared with control animals. Animals that received MSCs cultured with NGF displayed significant recovery in motor (p<0.05), somatosensory (p<0.05) and NSS (p<0.05) behavioral tests compared with control animals. Our data suggest that intracerebral transplantation of MSCs may provide a powerful autoplastic therapy for stroke.

Animals↗

PubMed1991

Anticonvulsant activity of the imidazoline 6,7-benzoidazoxan.

The effects of the imidazoline 6,7-benzoidazoxan on seizure threshold were assessed using standard tests of anticonvulsant activity. Benzoidazoxan (10-30 mg/kg i.p.; 100 mg/kg p.o.) prevented tonic, but not clonic, convulsions induced by electroshock in mice. The increase in seizure threshold was of rapid onset, and, although of short duration, was comparable with that obtained using phenytoin and sodium valproate. Moreover, unlike sodium valproate, benzoidazoxan was an efficacious anticonvulsant at doses (20, 30 mg/kg i.p.) which did not impair rotarod performance. The anticonvulsant effects of benzoidazoxan were confirmed using the maximal electroshock test in mice (median effective dose, 13.2 mg/kg i.p.) and rats (anticonvulsant at 30 mg/kg i.p.). In addition, benzoidazoxan (10, 30 mg/kg i.p.) prevented tonic, but not clonic, seizures induced by bicuculline in mice. Thus, the imidazoline benzoidazoxan was found to be a novel anticonvulsant agent against electrically and chemically induced seizures in mice and rats with a profile of action similar to that of phenytoin.

Animals↗

PubMed1993

Dextrorphan attenuates the behavioral consequences of ischemia and the biochemical consequences of anoxia: possible role of N-methyl-d-aspartate receptor antagonism and ATP replenishing action in its cerebroprotecting profile.

The acute anti-ischemic and anti-anoxic effects of dextrorphan (DX) were compared with those of dizocilpine (MK-801) in a variety of animal models, and in vivo and in vitro testings under anoxic conditions. DX reduced the incidence of death in ischemic mice and improved the rotarod performance of mice with brain ischemia. The ischemically-impaired memory of mice treated with DX markedly improved, as shown in the step-through type passive avoidance test, Morris water maze and in the habituation of exploratory behavior test. MK-801 likewise improved the water maze performance of the ischemically-impaired mice, but to a lesser extent. The step-through type passive avoidance performance of ischemic mice was not improved by MK-801. In the passive avoidance task with normal mice, DX, like MK-801, produced anterograde amnesia at doses higher than those needed to attenuate the behavioral effects of ischemia. DX, intravenously or centrally administered, markedly and dose-dependently reduced the incidence of death in mice receiving potassium cyanide (KCN). DX lessened the reduction in adenosine triphosphate (ATP) and increased lactate contents in mice dosed with KCN and also lessened the reduction in ATP in the TCA cycle and oxidative phosphorylation reactions caused by KCN (0.58 mmol/l), whereas MK-801 failed to show any effect on ATP formation pathways in vivo and in vitro, and failed to protect mice against KCN-induced lethal toxicity in vivo. In the in vitro studies, DX increased the adenylate kinase activity of the rat brain homogenate. DX was found to be a cerebroprotectant with anti-ischemic and anti-anoxic actions, the effects probably stemming from its N-methyl-d-aspartate receptor antagonistic property in cooperation with its ATP replenishing action.

Adenosine Triphosphate↗

PubMed1994

The rotarod test: an evaluation of its effectiveness in assessing motor deficits following traumatic brain injury.

The purpose of the present experiment was to examine the effectiveness of a modified rotarod test in detecting motor deficits following mild and moderate central fluid percussion brain injury. In addition, this investigation compared the performance of the rotarod task with two other commonly used measures of motor function after brain injury (beam-balance and beam-walking latencies). Rats were either injured with a mild (n = 14) or moderate (n = 8) level of fluid percussion injury or were surgically prepared but not injured (n = 8). All rats were assessed on all tasks for 5 days following their respective treatments. Results revealed that both the mild and moderate injury levels produced significant deficits in the ability of the animals to perform the rotarod task. Performance on the beam-balance and beam-walking tasks were not significantly impaired at the mild injury level. It was only at the moderate injury level that the beam-balance and beam-walking tasks detected deficits in motor performance. This result demonstrated that the rotarod task was a sensitive index of injury-induced motor dysfunction following even mild fluid percussion injury. A power analysis of the three tasks indicated that statistically significant group differences could be obtained with the rotarod task with much smaller sample sizes than with the beam-balance and beam-walking tasks. Performance on the rotarod, beam-walk, and beam-balance tasks were compared and evaluated by a multivariate stepdown analysis (multiple analysis of variance followed by univariate analyses of covariance). This analysis indicated that the rotarod task measures aspects of motor impairment that are not assessed by either the beam-balance or beam-walking latency. These findings suggest that compared to the beam-balance and beam-walking tasks, the rotarod task is a more sensitive and efficient index for assessing motor impairment produced by brain injury.

Animals↗

PubMed2005

Early behavioral deficits in R6/2 mice suitable for use in preclinical drug testing.

Huntington's disease (HD) is a neurodegenerative disorder caused by an elongated glutamine repeat in huntingtin. Improved understanding of the molecular effects of the mutation opens new avenues for treatment. High-throughput automated behavioral tests that produce well-defined markers of disease progression are necessary for in vivo drug screening. We have identified early behavioral deficits in tests of motor function that are amenable to cost effective automated analysis in a mouse model of HD. Running wheel activity and climbing behavior were reduced in R6/2 HD transgenics from as early as 4.5 weeks of age, at a time when rotarod performance and grip strength were still normal. Power calculations showed that the running wheel test was appropriate for efficient, high-throughput drug screening at this early age. Furthermore, the data extend the range of behavioral deficits observed in 1-month-old R6/2 mice, an age when synaptic dysfunction can already be detected in the striatum.

Age Factors↗

PubMed2002

Evaluation of changes in methylmercury accumulation in the developing rat brain and its effects: a study with consecutive and moderate dose exposure throughout gestation and lactation periods.

Methylmercury (MeHg) can be transferred to the fetus through the placenta and to newborn offspring through breast milk. The higher mercury (Hg) accumulation and susceptibility to toxicity in the fetus than in the mother during the gestation period is well known. However, the contribution of MeHg exposure through breast milk to the brain Hg concentration in offspring is not clear. The purposes of this study were to evaluate the changes in Hg concentration in the brain of offspring and its effects on the developing rat brain, based on consecutive and moderate doses of MeHg throughout gestation and lactation. Adult female rats were given a diet containing 5 ppm Hg (as MeHg) for 8 weeks. The administration level was thought not to cause adverse effects in adult rats. The rats were then mated and subsequently given the same diet throughout gestation and after parturition. The newborn offspring were placed with the mothers until postnatal day 30. The offspring were exposed to MeHg throughout their intrauterine life through the placenta, and during the postnatal developing phase via contaminated milk. Furthermore, they were given the same diet containing MeHg for 2 months following weaning. On the day of parturition, the concentration of Hg in the brains of newborns was 1.4 times higher than that in the mothers. During the suckling period the concentration in the brain of the offspring rapidly declined to 1/5 of that at birth, suggesting that MeHg transport by milk was limited while the brain and body volumes increased rapidly. The concentration increased gradually again after the offspring started the contaminated diet. In behavioral tests performed at 5 and 6 weeks of age, MeHg-exposed rats showed a significant deficit in motor coordination in the rotarod test and a learning disability in the passive avoidance response test, compared with controls. Histopathologically, focal cerebellar dysplasia, including the heterotopic location of Purkinje cells and granule cells, was observed. These abnormalities may be induced by the effect of highly accumulated MeHg in the brain during the gestation period. Thus, although offspring are subjected to consecutive and moderate dose MeHg exposure throughout both the gestation and suckling periods, the risk is especially high during gestation but may decrease during lactation.

Animals↗