Biomedical subjects

R Lalonde

Publications and source records attributed to R Lalonde.

At least 109 records · Page 6Linked to original sources

PubMed1997

The effect of neutron-moderating materials in high-energy linear accelerator mazes.

A study was undertaken to examine the effect of lining high-energy linear accelerator mazes with neutron-moderating materials in order to reduce scattered neutron dose at the accelerator room door. Polyethylene alone reduced neutron dose by no more than 27% and did not significantly reduce gamma ray dose. Polyethylene combined with flexboron panels reduced neutron dose by 50% at most, reducing gamma ray dose by a maximum of 32%. Much greater reductions in both neutron and gamma ray dose (by 92% and 55% respectively) can be obtained by incorporating polyethylene and boron into either internal or external maze doors. Our results support the conclusion that neutrons directly incident on the maze from the accelerator contribute little to the neutron dose at the door, and that the majority of neutron dose is due to scattered and thermal neutrons.

Boron↗

PubMed1997

Quantitation of cytomegalovirus (CMV) DNA in leukocytes of human immunodeficiency virus-infected subjects with and without CMV disease by using PCR and the SHARP Signal Detection System.

We report the development of a simple and rapid PCR assay for quantitation of the cytomegalovirus (CMV) DNA load in polymorphonuclear leukocytes. Using this system, a very good correlation was found between a high number of CMV copies in the blood and the presence of CMV disease in subjects with AIDS.

AIDS-Related Opportunistic Infections↗

PubMed1996

Effects of midline and lateral cerebellar lesions on motor coordination and spatial orientation.

Rats were lesioned in the midline cerebellum, comprising the vermis and fastigial nucleus, or the lateral cerebellum, comprising the cerebellar hemispheres and dentate nucleus, and evaluated in a series of motor and non-motor learning tests. Rats with midline lesions had difficulty in maintaining their equilibrium on a bridge and were slower before turning upward and traversed less squares on an inclined grid. They were not impaired for muscle strength when suspended from a horizontal wire. Rats with lateral lesions had milder deficits on the bridge and were not affected in the other two tests. In the Morris water maze test, rats with lateral lesions were deficient in spatial orientation, whereas rats with midline lesions were deficient in visuomotor coordination. Lateral lesions had no effects on visual discrimination learning. These results illustrate the differential influence of midline as opposed to lateral cerebellar regions on both motor and non-motor behaviors. Fastigial nucleus lesions decreased the time spent in equilibrium and latencies before falling on the bridge and the distance travelled along the inclined grid but had no effect on muscle strength when suspended from the horizontal string. Quadrant entries and escape latencies were higher in rats with fastigial lesions during the hidden platform condition of the Morris water maze but not during the visible platform condition. It is concluded that fastigial-lesioned rats are impaired in equilibrium and spatial orientation but with repeated trials learn to improve their performances.

Analysis of Variance↗

PubMed1996

Effects of MPTP on lever-pressing for light extinction in rats.

Rats were daily treated for seven days with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP) at a dose of 20 mg/kg/day, i.p. Seven days after treatment withdrawal, the rats were individually tested in a brightly lit apparatus containing two levers: an active lever allowing periods of darkness, and an inactive one. The test was performed over two consecutive days, in 20-min sessions. While control rats had a higher number of total active lever pressings than inactive lever pressings, this was not the case for MPTP-treated rats. Control rats decreased their useless active lever pressings and inactive lever pressings across the two sessions, but MPTP-treated rats did not do either. The absence of the differential effect in rats injected with MPTP may be due to a reduction in reinforcement mechanisms caused by the mild depletion of dopamine in the striatum.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1996

Sensorimotor learning in three cerebellar mutant mice.

Cerebellar damage occurs during developmental stages in three mutant mice (staggerer, hot-foot, and lurcher), causing disturbances in posture and equilibrium. During three tests of motor coordination, the performances of staggerer mutants was inferior to that of normal mice and did not improve with extended practice for up to 7 days of training. The sensorimotor performance of hot-foot mutants and of lurcher mutants was also lower than that of normal mice. Nevertheless, hot-foot mutants showed evidence of learning in two of the three tests and lurcher mutants in all three tests. Cerebellar atrophy in the latter two mutants did not prevent sensorimotor learning, but instead impaired their ability to reach the same level of performance as that of normal mice.

Animals↗

PubMed1996

Spontaneous alternation, motor activity, and spatial learning in hot-foot mutant mice.

Hot-foot mutant mice, characterized by defective innervation of Purkinje cells and an ataxic gait, were less active than normal mice in a T-maze. In spontaneous alternation testing with either single or multiple trials, hot-foot mutants, contrary to normal mice, did not alternate above chance. Moreover, the mutants had a higher number of errors and higher escape latencies in a water-filled Z-maze. These results indicate that in addition to motor coordination deficits, these cerebellar mutants have deficits in spatial learning and perseverate choices of maze arms.

Animals↗

PubMed1996

Effects of the light--dark cycle on a water tank social interaction test in mice.

Mice were exposed to a water tank interaction test in which food could be obtained either by wading in the water or by attacking littermates. A tank with progressively rising water levels caused mice in groups of four to differentiate into those willing to wade (carrier mice) from those unwilling to wade (noncarrier mice). Noncarrier mice could only obtain food by stealing it from carrier mice or from other noncarrier mice. It was found that mice during the dark period of the light--dark cycle were more willing to wade in the search for food rather than attempt to steal food from other mice. Because mice are generally more active during the dark period, this result suggests that higher activity levels increase the willingness to share the work load, a form of altruism, rather than promote parasitic behavior and aggression.

Altruism↗

PubMed1996

Spatial learning in a Z-maze by cerebellar mutant mice.

Two types of cerebellar mutant mice (staggerer and lurcher) were evaluated during 5-day acquisition of a spatial learning task in a Z-maze filled with water. Although the number of errors and escape latencies decreased in normal mice, the acquisition of the cerebellar mutants was impaired but not abolished. These results indicate that the cerebellum has a role in spatial learning. Mice with cerebellar dysfunction take a more indirect route toward a goal during the course of swimming, when ataxic symptoms are no longer in evidence.

Animals↗

PubMed1996

Beam sensorimotor learning and habituation to motor activity in lurcher mutant mice.

Lurcher mutant mice lose cerebellar granule cells and Purkinje cells. The mutants were compared to normal mice in a beam-walking task. Normal mice were placed on a slippery bridge while lurchers, because of their severe ataxia, were placed on a bridge with the same diameter, but enveloped with surgical tape to improve traction. The performance of both groups improved with repeated trials. In an activity box, lurcher mutants were as active as normal mice, showed normal intrasession habituation, and emerged from a toy object as easily as normal mice. These results indicate that the cerebellar damage in lurchers does not prevent the acquisition of a motor skill task requiring balance in an immobile apparatus. Ataxia was not accompanied by hypoactivity, inhibition or disturbances in intrasession habituation.

Animals↗

PubMed1996

Regional distribution of the 5-HT innervation in the brain of normal and lurcher mice as revealed by [3H]citalopram quantitative autoradiography.

The neurological cerebellar mutant lurcher is characterized by a primary degeneration of Purkinje cells as well as retrograde secondary partial degeneration of cerebellar granule cells and inferior olivary neurons. Since serotonin (5-HT) has been implicated in the modulation of excitatory amino acid systems of the cerebellum, the 5-HT innervation of the normal and lurcher mice was examined by quantifying uptake sites using [3H]citalopram autoradiography, and by biochemical assays of the indoles 5-HT, 5-hydroxy-L-tryptophan and 5-hydroxyindole-3-acetic acid using high-performance liquid chromatography. Comparable results were found between [3H]citalopram binding and 5-HT tissue concentrations in different brain regions. The highest [3H]citaslopram labelling was observed in defined structures of the mesencephalic and upper pontine regions, in limbic strutures, in hypothalamus and in discrete thalamic divisions, while the lowest labelling of uptake sites was documented in cerebellum and brainstem reticular formation. In lurcher mutants, the histology confirmed cell degeneration and the reduction in width, leading to 65%, 45% and 25% atrophies of total cerebellum, deep nuclei and inferior olivary nucleus, respectively. The [3H]citalopram labelling corrected for surface loss was 45% and 20% higher to cerebellar deep nuclei and red nucleus, respectively, but remained unchanged in the cerebellar cortex and inferior olivary nucleus. Moreover, higher labelling was found in nucleus raphe dorsalis, ventral tegmental area, inferior colliculus, locus coeruleus, pontine central grey and anterior thalamic nuclei, areas known to be part of cerebellar afferent and efferent systems. The present results indicate that in such pathological conditions as described for the lurcher mutant, the 5-HT system may modulate motor function not only at the level of the cerebellum, but also in other forebrain structures functionally related to the motor system.

Animals↗

PubMed1996

Climbing sensorimotor skills in Lurcher mutant mice.

Lurcher mutant mice, characterized by massive degeneration of cerebellar granule and Purkinje cells, were compared to normal mice of the same background strain in three sensorimotor learning tasks requiring climbing skills. In the coat-hanger test, Lurcher mutants were deficient in forepaw contact time and four paw latencies. Improvement over time was weak for both groups. For latencies before reaching the halfway point or the top of the diagonal bar in the same apparatus, Lurcher mutants showed gradual improvement while normal mice appeared to lose motivation to perform the task. In a rope-climbing test, a slight reduction in movement time was detected in Lurcher mutants with repeated trials, whereas the performance of normal mice was stable over time. In a water escape pole-climbing test, Lurcher mutants were impaired relative to controls. Both groups decreased the time required before grasping the pole across days of testing. The number of segments climbed was increased in Lurcher mutants across days. These results illustrate that massive cerebellar damage does not eliminate the possibility of acquiring climbing skills, but under some conditions limit performance.

Animals↗

PubMed1996

Dorsal striatal lesions in rats. 1: Effects on exploration and motor coordination.

Rats with small dorsal striatal lesions were compared to sham-operated controls in a series of test measuring their exploratory behavior in a T-maze, a hole-board, and an elevated plus-maze. Motor coordination was evaluated in the inclined grid and in the square bridge tests and grip strength in the wire suspension test. The rats with dorsal striatal lesions were not impaired in the motor coordination tests, the grip strength test, nor in spontaneous alternation. By contrast, an increase of emergence latencies in the elevated plus-maze and a reduction of motor activity in the hole-board confined space during the early part of testing were observed in rats with dorsal striatal lesions. These results are ascribed to a lesion-induced situation-specific increase in inhibition.

Animals↗

PubMed1996

Dorsal striatal lesions in rats. 2: Effects on spatial and non-spatial learning.

Rats with small electrolytic lesions of the dorsal striatum were evaluated in acquisition of spatial learning, sensorimotor learning, and a straight runway food approach response and its extinction. No differences were detected between rats with dorsal striatal lesions and sham-operated controls during acquisition of hidden and visible trials in the Morris water maze. Neither was an intergroup difference observed during acquisition of the rotorod test of motor coordination. Lesioned rats were not impaired in running for a food reward, but their running latencies on day 2 of extinction were lower than those of controls, an indication of perseveration. These results indicate that perseverative responding may occur in dorsal striatal lesioned rats in the absence of spatial or sensorimotor defects.

Analysis of Variance↗

PubMed1996

Amantadine hydrochloride treatment in heredodegenerative ataxias: a double blind study.

OBJECTIVE: A group of 27 patients with Friedreich's ataxia and another group of 30 patients with olivopontocerebellar atrophies were each randomly divided into two subgroups, one receiving placebo and the other amantadine hydrochloride (AH; 200 mg daily) for three to four months. METHODS: The effect of double blind treatment was evaluated by simple visual and auditory reaction time (RT) and movement time (MT) for both right and left hands. RESULTS: The subgroup with olivopontocerebellar atrophies receiving AH showed significant improvement on seven out of eight variables studied by analysis of covariance. In patients with Friedreich's ataxia, improvement was definitely less. Treatment remained contraindicated for those with cardiomyopathies or drug intolerance. CONCLUSION: The rationale of AH use in heredodegenerative ataxias can be explained by its replacement effect (dopamine release) and by direct involvement of N-methyl-D-aspartate (NMDA) in glutamate mediated neurotoxicity in cerebellar granular cells; memantine, an AH analogue, is a potent blocker of NMDA receptors.

Adult↗

PubMed1995

Elevated (+)-maze and hole-board exploration in lurcher mutant mice.

The behavior of lurcher mice, a mutant with degeneration of cerebellar cells, was compared to that of normal mice for three days in two tests of exploration; an elevated (+)-maze and a 4 x 4 hole-board. In the elevated (+)-maze, lurcher mutants visited fewer closed arms than normal mice only on the first test day. Lurcher mutants were slower to emerge from the first closed arm but did not differ from normal mice for entry latencies into the first open arm. The time spent by the mutants in the open arms was higher than that of normal mice, an indication of decreased inhibition to open spaces. In the hole-board, lurcher mutants visited fewer holes than normal mice only on the first day of testing. In proportion to the total number of holes explored, lurcher mutants visited fewer center holes and fewer holes situated next to each other. These results may be due to a lesion-induced tendency to explore a more restricted region of a novel spatial environment and to explore it in a more haphazard fashion.

Animals↗

PubMed1995

Spatial navigation of staggerer and normal mice during juvenile and adult stages.

Staggerer mutant mice were compared to normal mice of two different ages (2-6 mo) in two tasks requiring navigational skills in a circular maze visible platform condition and a T-maze. Staggerer mutants had higher latencies than normal mice in both tests. The performance of normal mice worsened with age for both tests. The aging factor interacted with the genotype factor only in the circular maze, where the mutant-nonmutant differential was wider among juvenile animals. In neither task was there evidence of a more pronounced impairment with aging in staggerer mutants. It remains to be determined in this mutant at more advanced stages of aging or in other models of chronic neural disease whether early neuropathology accelerates brain aging.

Aging↗

PubMed1995

Rotorod sensorimotor learning in cerebellar mutant mice.

Lurcher mutant mice, characterized by degeneration of cerebellar granule and Purkinje cells, were compared to normal littermate controls in a rotorod test, consisting of a wheel turning at constant speed which required on the part of the animal postural adjustments in order to maintain equilibrium. Identical baseline rates for the two groups were assured by changing the speed and size of the rotating rod. Although both groups were able to learn the task, the fall latencies of normal mice exceeded those of lurchers. These results indicate that cerebellar cortical atrophy does not abolish this form of sensorimotor learning. However, brain-damaged animals are unable to reach the same level of performance as normal animals. In contrast to the results in lurcher mutants, no sensorimotor learning was displayed by hot-foot mutants and staggerer mutants.

Animals↗

PubMed1995

Exploratory drive, frontal lobe function and adipsia in aging.

Aging in animals in accompanied by a decrease in exploratory drive, as assessed by hole poking and spontaneous alternation tests. This decrease is caused either by increased fear of the novel testing environment (neophobia) or by apathy. Either cause may be related to dysfunction of prefrontal cortex-related pathways. The myelination of the prefrontal cortex appears late in ontogeny. In accordance to the last-in first-out principle, this brain region seems to be affected early during aging. It remains to be determined whether this decrease of exploratory behavior is reversible by behavioral intervention, by dietary changes or by the administration of psychotropic drugs. One hypothesis worth testing is whether the decrease in exploration is associated to the well-described adipsia in human aging, whose neurobiological basis has not yet been determined. It is possible to consider that the maladaptive response to thirst is responsible for some senescent changes in the brain and that reversal of adipsia by behavioral, dietary or pharmacological means improves the quality of life in the elderly.

Affect↗