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PubMed2001

Role of 5-HT6 receptors in memory formation.

Mice lacking the 5-HT(6) receptor presented neither gross anatomical or behavioral abnormalities nor obvious changes in microscopic brain morphology, and their performance in rotarod, open field and novel object testing paradigms revealed no differences compared with wild-type animals. Nevertheless, an association between the 5-HT(6) receptor polymorphism C267T and Alzheimer's disease has been reported. Interestingly, the 5-HT(6) antisense oligonucleotide decreased 5-HT(6) gene expression and enhanced spatial learning acquisition in the water maze. Similarly, injection of the 5-HT(6) receptor antagonist Ro-04-6790 improved learning consolidation in an autoshaping task, while mCPP, scopolamine and dizocilpine decreased performance. The effect induced by scopolamine or dizocilpine, but not that induced by mCPP, was completely or partially reversed by Ro-04-6790. Ro-04-6790 did not modify the 8-OH-DPAT facilitatory effects on learning consolidation. Since Ro-04-6790 facilitatory effect was unaffected by 5-HT(1A), 5-HT(2A/2B/2C), 5-HT(3), 5-HT(4) or 5-HT(7) receptor blockade, the facilitatory effect induced by Ro-04-6790 involved specifically 5-HT6 receptors. Similarly, the 5-HT(6) receptor antagonist SB-271046 improved retention in the water maze and produced a significant performance improvement in aged rats in an operant-delayed alternation task. A series of Ro-04-6790 analogues that penetrate the brain and specifically bind to 5-HT(6) receptors reversed scopolamine-induced retention deficit in a passive avoidance learning test. Collectively, these data provide further support to the notion that 5-HT systems, via 5-HT(6) receptors, also play a significant role in memory formation under normal and dysfunctional memory conditions.

Journal Article↗
PubMed2000

Enoxaparin, a low molecular weight heparin decreases infarct size and improves sensorimotor function in a rat model of focal cerebral ischemia.

Possible neuroprotective effects of the low molecular weight heparin (LMWH) enoxaparin sodium (Lovenox) were evaluated in a rat model of focal ischemia. Male Sprague-Dawley rats were subjected to 90 min of occlusion of the right middle cerebral artery using the intraluminal suture method. Enoxaparin at doses of 0, 10 or 15 mg/kg was administered to groups of rats 1, 8, 24 and 32 h after artery occlusion. Motor impairment was evaluated by performance on the traverse beam and accelerating rotarod tests. Animals were sacrificed 48 h after occlusion and brain sections were stained with 2% 2,3,5-triphenyltetrazolium chloride for determination of infarct volume. Forty percent of the rats receiving 15 mg/kg enoxaparin died as a result of intracranial hemorrhage. Untreated rats exhibited large lesions involving the caudate putamen and much of the cortex. In enoxaparin - treated rats the damage was mainly confined to the caudate putamen. The sensorimotor behavior of the 10 mg/kg enoxaparin group was significantly better than that of untreated animals. Motor performance of the survivors in the 15 mg/kg group was poor due to hypoactivity and weakness resulting from excessive bleeding. These results suggest that LMWH may have a neuroprotective function.

Animals↗
PubMed1982

Assessment of the effects of acrylamide, methylmercury, and 2,5-hexanedione on motor functions in mice.

Neurotoxic effects of acrylamide, methylmercury, and 2,5-hexanedione were studied in forth female BALB/c mice. The chemicals were dissolved in distilled water and administered via light-tight drinking bottles. Three control groups were used. The first received distilled water, the second received concentrated saccharin solution to assess the effects of reduced water intake, and the third was maintained on a reduced food diet. Motor functions were quantified by measuring landing foot-spread and rotarod performance. Baseline data were collected before dosing started. Mice were placed, twice weekly, on an accelerating rotarod, and their retention time was recorded. In the landing foot-spread test, the experimenter dropped mice from 15 cm onto a flat, smooth surface once a week. The hindlimb splay was then measured by the examiner. Both experimenter and examiner were unaware of the identity of each group (except of the food deprived group, in the case of the experimenter) during the first exposure. Decreased retention time and increased hindlimb splay were observed in mice after 12 d of exposure to acrylamide. Recovery followed treatment cessation. Increased hindlimb splay preceded an obvious decline of rotarod performance in the group receiving the 10 ppm of methylmercury solution. Mice receiving the 20 and 40 ppm of methylmercury solutions did not display any change in these tests before overt signs of toxicity. 2,6-Hexanedione produced a small decline in performance to a constant level after 85 d of exposure. After dosing termination, performance returned to baseline values. Control groups showed no change in performance on either the rotarod or the landing foot-spread test. Our data show that the rotarod and hindlimb splay tests in mice are about equal in sensitivity to the effects of the neurotoxic chemicals tested.

Acrylamides↗
PubMed2001

Intravenous administration of human umbilical cord blood reduces behavioral deficits after stroke in rats.

BACKGROUND AND PURPOSE: Human umbilical cord blood cells (HUCBC) are rich in stem and progenitor cells. In this study we tested whether intravenously infused HUCBC enter brain, survive, differentiate, and improve neurological functional recovery after stroke in rats. In addition, we tested whether ischemic brain tissue extract selectively induces chemotaxis of HUCBC in vitro. METHODS: Adult male Wistar rats were subjected to transient (2-hour) middle cerebral artery occlusion (MCAO). Experimental groups were as follows: group 1, MCAO alone (n=5); group 2, 3x10(6) HUCBC injected into tail vein at 24 hours after MCAO (n=6) (animals of groups 1 and 2 were killed at 14 days after MCAO); group 3, MCAO alone (n=5); group 4, MCAO injected with PBS at 1 day after stroke (n=8); and group 5, 3x10(6) HUCBC injected into tail vein at 7 days after MCAO (n=5). Rats of groups 3, 4, and 5 were killed at 35 days after MCAO. Behavioral tests (rotarod and Modified Neurological Severity Score [mNSS]) were performed. Immunohistochemical staining was used to identify cells derived from HUCBC. Chemotactic activity of ischemia brain tissue extracts toward HUCBC at different time points was evaluated in vitro. RESULTS: Treatment at 24 hours after MCAO with HUCBC significantly improved functional recovery, as evidenced by the rotarod test and mNSS (P<0.05). Treatment at 7 days after MCAO with HUCBC significantly improved function only on the mNSS (P<0.05). Some HUCBC were reactive for the astrocyte marker glial fibrillary acidic protein and the neuronal markers NeuN and microtubule-associated protein 2. In vitro, significant HUCBC migration activity was present at 24 hours after MCAO (P<0.01) compared with normal brain tissue. CONCLUSIONS: Intravenously administered HUCBC enter brain, survive, migrate, and improve functional recovery after stroke. HUCBC transplantation may provide a cell source to treat stroke.

Animals↗
PubMed2003

Tongue protrusion: a simple test for neurological recovery in rats following focal cerebral ischemia.

A simple tongue protrusion (TP) test is described for rats following focal ischemia induced by middle cerebral artery occlusion (MCAO). MCAO resulted in a dramatic decrease in TP that correlated with a concomitant decline in neurological performance in standard 5- and 20-point tests and deficits in performance in the Morris water maze and the accelerating rotarod. TP values also correlated with infarct size at 7 and 24 days following MCAO. This simple and inexpensive test, that monitors the ability of rats to lick food out of a glass tube, is easily administered, can be administered frequently without changing baseline performance, is not susceptible to behavioral compensation and should not interfere with other tests used concurrently to evaluate neurological deficit. The TP test may, therefore, serve as a useful addition to the battery of tests commonly used to assess neurological damage in rats, particularly in models of stroke.

Animals↗
PubMed2004

Impaired passive avoidance learning in mice lacking central neuronal nicotinic acetylcholine receptors.

The nicotinic cholinergic system influences cognition, anxiety, locomotion, and addiction by acting upon nicotinic acetylcholine receptors (nAChRs). To date, there are 12 known neuronal mammalian nAChR subunits leading to a rich pharmacological diversity that is difficult to attribute to specific subunits. We generated alpha7-beta2 nAChR double mutant mice by breeding to investigate the effect of a minimal number of nAChRs in the CNS. These mice have been used to determine the role these receptor subunits play in a variety of behaviors. A battery of behavioral tests was used to determine the effect of the mutation in anxiety, locomotor activity, startle response, pre-pulse inhibition, motor coordination and learning and memory. Mice lacking both the alpha7 and the beta2 nAChR subunits displayed impaired learning and memory performance in a passive avoidance test and showed enhanced motor performance on the rotarod.

Analysis of Variance↗
PubMed1997

Anticonflict effect of alpidem as compared with the benzodiazepine alprazolam in rats.

A comparative study between two drugs acting on the GABAA receptor, alprazolam and alpidem was undertaken, using simple tests such as measurement of spontaneous locomotor activity, four plates test and rotarod in mice. Additional conflict test was further performed using a new conflict paradigm where the opportunity existed for rats to choose during punished periods between immediate, punished reinforcement and delayed non-punished reinforcement. The benzodiazepine alprazolam, demonstrated, as expected, strong anxiolytic effects in mice and increased punished response in rats at non sedative doses (0.5, 1 mg/kg). High doses of alprazolam decreased spontaneous locomotor activity and induced myorelaxant effects in mice. Alpidem, an imidazopyridine derivative, induced motor impairment in mice and only very weak anxiolytic effects in the four plates test in mice (4 mg/kg) and in punished procedure in rats (32 mg/kg). As alprazolam is a full agonist for the GABAA receptor complex and alpidem is a partial agonist acting with specificity on omega 1 GABAA receptor subtypes, the results are discussed. Activity on omega 1 receptor subtypes is perhaps not sufficient in order to obtain a true anti-conflict effect and compounds such as alpidem only relieve some of the symptoms of anxiety disorders.

Alprazolam↗
PubMed2003

Motor behaviour deficits and their histopathological and functional correlates in the nigrostriatal system of dopamine transporter knockout mice.

Chronic dysregulation of dopamine homeostasis has been shown to induce behavioural impairment in dopamine transporter knockout mutant mice arising from the dysfunction of the mesolimbic and hypothalamo-infundibular system. Here, we assessed whether there are also any motor consequences of a chronic and constitutive hyperdopaminergia in the nigrostriatal system in dopamine transporter knockout mutant mice. For this, we analysed motor performances using tests assessing balance, coordinated motor skills (rotarod, pole test), stride lengths and locomotor activity. Dopamine transporter knockout mutant mice were markedly hyperactive in the open field with central compartment avoidance, as previously shown. However, sensorimotor integration was also found to be altered in dopamine transporter knockout mutant mice which displayed a reduced fore- and hind-limb mean stride length, impaired motor coordination on the pole test and reduced rearings in the open field. Moreover, dopamine transporter knockout mutant mice showed a slower task acquisition on the rotarod. Six-week-old dopamine transporter knockout wild type mice having the same femur size as adult dopamine transporter knockout mutant mice ruled out a possible size-effect bias. Whilst there was no significant difference in the striatal volume, we found a slight but significant reduction in neuronal density in the striatum but not in the nucleus accumbens of dopamine transporter knockout mutant mice. There was a reduced binding in the striatum and nucleus accumbens of dopamine(1) receptors ([(3)H]SCH 23390) and dopamine(2) receptors ([(3)H]YM-09151-2). There was no significant difference in the number of dopaminergic neurons in the substantia nigra between dopamine transporter knockout mutant mice and dopamine transporter knockout wild type mice. These results suggest an impaired functioning of the nigrostriatal system in dopamine transporter knockout mutant hyperdopaminergic mice, as illustrated by motor and sensorimotor integration deficits, despite their apparent hyperactivity. These dysfunctions may arise from combined striatal cell loss and/or functional changes of dopaminergic neurotransmission.

Animals↗
PubMed2005

Loss of wild-type huntingtin influences motor dysfunction and survival in the YAC128 mouse model of Huntington disease.

Huntington disease (HD) is an adult-onset neurodegenerative disease caused by a toxic gain of function in the huntingtin (htt) protein. The contribution of wild-type htt function to the pathogenesis of HD is currently uncertain. To assess the role of wild-type htt in HD, we generated YAC128 mice that do not express wild-type htt (YAC128-/-) but express the same amount of mutant htt as normal YAC128 mice (YAC128+/+). YAC128-/- mice perform worse than YAC128+/+ mice in the rotarod test of motor coordination (P = 0.001) and are hypoactive compared with YAC128+/+ mice at 2 months (P = 0.003). Striatal neuropathology was not clearly worse in YAC128-/- mice compared with YAC128+/+ mice. There was no significant effect of decreased wild-type htt on striatal volume, neuronal counts or DARPP-32 expression but a modest worsening of striatal neuronal atrophy was evident (6%, P = 0.03). The testis of YAC128+/+ mice showed atrophy and degeneration, which was markedly worsened in the absence of wild-type htt (P = 0.001). YAC128+/+ mice also showed a male specific deficit in survival compared with WT mice which was exacerbated by the loss of wild-type htt (12-month-male survival, P < 0.001). Overall, we demonstrate that the loss of wild-type htt influences motor dysfunction, hyperkinesia, testicular degeneration and impaired lifespan in YAC128 mice. The mild effect of wild-type htt on striatal phenotypes in YAC128 mice suggests that the characteristic striatal neuropathology in HD is caused primarily by the toxicity of mutant htt and that replacement of wild-type htt will not be an adequate treatment for HD.

Animals↗
PubMed1989

Effects of carbamate, BPMC, on the central cholinergic functions and behavior of mice.

O-sec-butylphenyl methylcarbamate (BPMC), an anticholinesterase carbamate, was injected once (100 mg/kg, s.c.) or repeatedly (50 mg/kg/day for 10 days) into mice. Animals were examined for their behavior and for parameters of cholinergic activity in the forebrain. Mice that received only a single injection exhibited reduced ambulation, hypothermia, and impairment of rotarod performance for up to 3 hr after a single injection. BPMC increased levels of acetylcholine (ACh) in the forebrain for up to 6 hr, and decreased acetylcholinesterase (AChE) activity for up to 24 hr. Both high-affinity choline uptake (HACU) and binding of [3H]quinuclidinyl benzilate (QNB) were reduced 20 min after a single injection without any effect on choline acetyltransferase (ChAT) activity. In behavioral tests conducted 10 min prior to the daily injections, rotarod performance and ambulation were slightly impaired for a few days before and after cessation of injection. Repeated treatment decreased HACU and binding of [3H]QNB for 24 hr after the final injection without any changes in levels of ACh content, AChE activity and ChAT activity. BPMC may reversibly impair cholinergic functions through effects not only on AChE activity but also on HACU and binding of [3H]QNB.

Acetylcholine↗
PubMed1986

A strain comparison of physiological and locomotor responses of mice to diisopropylfluorosphosphate.

The effects of acute treatment with the organophosphate, diisopropylfluorophosphae (DFP), were studied in three inbred mouse strains. C57BL, DBA and C3H. A battery of physiological and locomotor tests including respiratory rate, heart rate, body temperature, Y-maze activity and rotarod performance was used. Dose-response and time course studies were carried out. Approximately 15 min after injection the animals were markedly affected by the drug with maximal effects occurring approximately 2 hours after injection. Strain comparisons were made at the 2 hr time point. In all strains, males and females were affected about equally except for respiratory rate and rotarod performance in which females were slightly more affected. Strain comparisons revealed that for most of the tests the C57BL mice were most affected by the DFP and the C3H mice were least affected. For the heart rate test the DBA mice were the most sensitive. Previous studies from our laboratory have demonstrated a similar rank ordering of the strains in their responses to oxotremorine and nicotine. The strain differences in response to these agents is not easily explained by differences in number or affinity of brain muscarinic or nicotinic receptors. The genetic influence on cholinergic drug response may involve receptor coupling mechanisms.

Animals↗
PubMed2005

Inflammatory-mediated model of cerebral palsy with developmental sequelae.

OBJECTIVE: Cerebral palsy (CP) is characterized by motor deficits. There is increasing evidence that CP may result from inflammatory and infection-mediated white matter damage. Our objective was to develop an inflammatory model for CP based on chronic lipopolysaccharide (LPS) exposure with a recognizable phenotype in offspring. STUDY DESIGN: On gestational days 15, 17, and 19 (approximately 28-36 wks human gestation; rat length of gestation is 21 days), pregnant rats were intracervically injected with 0.15 mg/kg LPS (in 0.1 mL saline) or 0.1 mL saline for controls. Neonatal tests for sensory-motor milestones were performed on postnatal days 1 to 21 (LPS n = 25; control n = 26). Adult males were tested at 8 weeks on open field and rotarod for motor activity. Immunohistochemistry studies were performed to assess olygodendrocyte (OL) damage. Statistical analysis included Mann-Whitney U and analysis of variance (ANOVA) with P < .05 considered significant. RESULTS: Immunohistochemistry revealed a decrease in the immature OL marker PLP on day 21 (P = .03) in LPS-exposed offspring, and an increase of the mature OL marker CNP on day 21 and at 8 weeks (P < .01, P < .001). LPS-exposed offspring were delayed achieving 3 motor milestones: negative geotaxis (P < .05), cliff aversion (P < .01), and surface righting (P = .05). They were also delayed in eye opening (P < .01). There was no difference between the 2 groups for the other tests. There was a trend towards decreased mean speed in LPS-exposed adults in open field testing (P = .08), but no differences observed in rotarod testing. CONCLUSION: Using an animal model for CP that mimics a chronic intrauterine inflammation that results in decreased levels of PLP, a marker for early oligodendrocytes consistent with white matter damage, we have demonstrated a phenotype relevant to the human CP manifestations in the neonatal period. Nevertheless, adult animals were able to compensate to the damage. Further refinement is needed to improve the understanding of pathogenesis, as well as allow for testing preventative therapies.

Age Factors↗
PubMed1985

Comparison of anorexia and motor disruption by cyclazocine and quipazine.

The mixed narcotic agonist-antagonist cyclazocine and the 5-HT agonist quipazine disrupt food-rewarded fixed ratio-40 (FR-40) operant behavior in rats as a dose-dependent decrease in the number of reinforcers obtained and a reciprocal increase in the number of 10-second intervals between responding ("pausing"). This disruption has been shown to result in part from interaction with 5-HT neuronal systems, and may be a consequence of: (1) disruption of cognitive processes, (2) motivational impairment, or (3) motor deficits. To identify which of these components is (are) involved in the disruption of operant responding, female Sprague-Dawley rats were tested for food consumption, spontaneous locomotor activity, or rotarod performance following intraperitoneal injection of cyclazocine, quipazine, or both. Cyclazocine decreased food consumption at doses larger than those required to disrupt operant behavior, while quipazine decreased consumption at doses disruptive to operant responding. Little effect was exerted by either drug on spontaneous locomotor activity, while rotarod performance was disrupted only by very large doses of either drug relative to effects of FR-40 behavior. These data indicate that neither drug appears to disrupt operant behavior by causing gross motor deficits. Thus, cyclazocine may disrupt operant responding by impairing cognition, while quipazine may act through food satiation mechanisms.

Animals↗
PubMed2003

Close relationship between motor impairments and loss of functional motoneurons in a Charcot-Marie-Tooth type 1A model.

Charcot-Marie-Tooth disease type 1A is the most frequent hereditary neuropathy affecting the peripheral nervous system. A partial duplication of chromosome 17 (17p11.2) involving the PMP22 gene is responsible for dysmyelination-demyelination processes leading to motor and sensory impairments. Murine models of this disease are now widely used to investigate the mechanisms occurring at the behavioural and physiological levels. In this study, adult transgenic mice (6 months old) having integrated 7 copies of the human PMP22 gene were used to compare the motor performance, evaluated by using a complex locomotor test (the rotarod test), with both the number of functional motoneurons innervating the soleus muscle and the level of myelination in the sciatic nerve. Two levels of motor deficits were detected and led us to divide the population into two subgroups. In both impaired groups, the level of motor deficit was strongly correlated with the number of functional motoneurons evaluated by retrograde labeling from the muscle, but not with the number of myelinated fibers or the thickness of the myelin sheath (g-ratio). It therefore appears that the number of motor units may be a key element in motor impairments observed in Charcot-Marie-Tooth disease type 1A disease. These findings may have implications for therapeutic procedures, which should focus on the survival of the motoneuronal pool and/or the maintenance of functional neuro-muscular connexions to reduce motor impairments in humans.

Animals↗
PubMed2006

Effects of toluene exposure during brain growth spurt on GABA(A) receptor-mediated functions in juvenile rats.

Toluene is a commonly abused inhalant. Its neurobiological effects are, at least in part, mediated by gamma-aminobutyric acid (GABA(A)) receptors. Since GABA(A) receptor function is critical during brain development, the long-term effects of toluene exposure during brain growth spurt were investigated. Spargue-Dawley male rats were administered with toluene (500 mg/kg, i.p.) on postnatal day (PN) 4-9. Behavioral and electrophysiological measures and the levels of messenger RNA (mRNA) expression of GABA(A) receptor subunits were examined on PN 28-32. The seizure sensitivity induced by bicuculline (a GABA(A) receptor antagonist), methyl beta-carboline-3-carboxylate (inverse agonists of the GABA(A)/benzodiazepine receptor) but not 3-mercaptopropionic acid (a glutamate decarboxylase inhibitor) was enhanced by toluene exposure. Toluene exposure had no effect on the performance in the elevated plus-maze and rotarod test but reduced the responses to diazepam in these two tests. In vitro intracellular electrophysiological recordings employing brain slices from rats treated with toluene demonstrated a significant decrease in GABA(A) receptor-mediated inhibitory postsynaptic currents in CA1 neurons but an increased response to GABA perfusion. The relative abundance of the mRNAs encoding various subunits of GABA(A) receptor (alpha1, alpha2, alpha4, alpha5, alpha6, beta2, beta3, gamma2S, gamma2L) was examined in four brain regions (hippocampus, striatum, cortex, and cerebellum) by semiquantitative reverse transcription-PCR. These results demonstrated that subunit- and brain area-selective alterations in GABA(A) receptors after toluene exposure during brain growth spurt. The alterations in GABA(A) receptors might be associated with the neurobehavioral disturbance in offspring of toluene-abusing women.

Animals↗
PubMed1978

[Behavioral and EEG effects of triazolam in comparison with those of diazepam (author's transl)].

Triazolam was 4 to 5 times as potent as diazepam in reducing hyperemotionality of either septal-lesioned or olfactory bulbectomized rats (O.B. rats), and in suppressing muricide in O.B. rats. This agent was equipotent with diazepam in inhibiting fighting behavior of long-term isolated mice, but was longer in duration of action. Triazolam was approximately 4 times more potent than diazepam in preventing pentetrazol convulsion, but was 10 times less potent in inhibiting maximal electroshock convulsion in mice. The muscle relaxant effect of triazolam as assessed by the inclined screen test was 34 times, and the effect on rotarod performance was 17 times more potent than that of diazepam in mice. Triazolam (0.2 approximately 0.5 mg/kg i.v.) changed the EEG to a drowsy pattern in unanesthetized rabbits with a chronic electrode implant, and suppressed the EEG arousal response to auditory stimulation and electrical stimulation given to either the mesencephalic reticular formation or posterior hypothalamus. The limbic afterdischarges induced by either hippocampal or amygdaloid stimulation were also markedly inhibited by triazolam. These EEG effects of triazolam were qualitatively similar to, but were 4 to 5 times more potent than those of diazepam. These results indicate that triazolam is a potent tranquilizer with a longer duration of action, and the muscle relaxant effect is considerable as compared with diazepam.

Aggression↗
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↗
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↗