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Biomedical subjects

A Barbeau

Publications and source records attributed to A Barbeau.

At least 91 records · Page 5Linked to original sources
PubMed1980

Influence of substance P on the behavioral changes induced by haloperidol in rats.

Locomotor activity and grooming behavior of rats were recorded for a period of 30 min following intraventricular injections of substance P(SP) in doses of 0.60 and 2.50 microgram/rat. The lower dose of the peptide significantly increased locomotion for 10 min and time spent grooming for 25 min. The effects of the same two doses of SP on the hypokinesia induced by various pharmacological treatments modifying catecholaminergic systems were then examined. SP did not affect the behavioral depression produced by alpha-methyl-para-tyrosine (250 mg/kg), FLA-63 (25 mg/kg) and phenoxybenzamine (20 mg/kg). However, SP, in dose of 0.60 microgram/rat, systematically reversed the decrease in locomotor activity induced by a relatively small dose of haloperidol, 0.1 mg/kg. The dame dose of the peptide significantly counteracted the rigidity but not the hypokinesia and catalepsy resulting from the previous administration of a higher dose of haloperidol, 3 mg/kg. The results support the hypothesis that SP may exert direct or indirect function in motor behavior, possible via a modulatory action on brain dopaminergic systems.

Animals↗
PubMed1980

Effects of taurine and gamma-aminobutyric acid on akinesia and analgesia induced by D-Ala2-Met-enkephalinamide in rats.

Effects of taurine or gamma-aminobutyric acid (GABA) on akinesia and analgesia induced by D-Ala2-Met-enkephalinamide were investigated in rats. Administration of taurine (dose range: 2.375 X 10(-2) M-9.5 X 10(-2)-Met-enkephalinamide were investigated in rats. Administration of taurine (dose range: 2.375 X 10(-2) M-9.5 X 10(-2) M/10 microliters) into the left lateral ventricle 10 min prior to the injection of D-Ala2-Met enkephalinamide (50 microgram/10 microliter) produced a dose-dependent reduction in the duration of akinesia and to some extent of analgesia, as estimated at 30 min and 60 min following the enkephalinamide injection; at the first estimation-time (10 min), taurine did not alter the duration of akinesia or that of analgesia. The median effective dose (ED50) for akinesia determined at 60 min after D-Ala2-Met-enkephalinamide was 5 times greater and that for analgesia assessed at the same time was 1.7 times greater in taurine-treated rats than the respective doses in control animals. Administration of GABA under similar experimental conditions produced a dose-dependent reduction in the duration of analgesia from the initial estimation time (10 min) following the injection of D-Ala2-Met-enkephalinamide. The ED50 for analgesia determined at 30 min after D-Ala2-Met-enkephalinamide was 3 times greater in GABA-treated rats than in control animals. Unlike the effects of taurine, GABA did not alter the duration of akinesia. Neither the duration of akinesia nor that of analgesia was modified by taurine or GABA alone in rats tested 9 min after the injection of each amino acid. These findings suggest that taurine may promote a recovery from both akinesia and analgesia, while GABA decreases only the analgesia induced by D-Ala2-Met-enkephalinamide.

Analgesia↗
PubMed1980

Field testing of an ataxia scoring and staging system.

The authors present a simple system for disability scoring and functional staging of an ataxic patient, based on modifications of a previous scheme advocated by De Falco and collaborators (1979). This system was tested under field conditions in 47 ataxic subjects and found to be useful and functional.

Ataxia↗
PubMed1980

Friedreich's ataxia in the south of Italy: a clinical and biochemical survey of 23 patients.

We report a clinical and biochemical survey of 23 patients with Friedreich's ataxia from southern Italy. They were studied clinically and by means of a clinical rating scale devised by us (Inherited Ataxias Clinical Rating Scale). Laboratory tests, based on the Quebec Cooperative Study, were also performed on our patients. No major clinical or biochemical differences were found between Italian and Canadian patients. Investigation of CSF monoamine metabolites showed that HVA decreased after probenecid and metoclopramide loading.

Adolescent↗
PubMed1980

Hypertrophic cardiomyopathy in Friedreich's ataxia: symmetric or asymmetric?

We evaluated 15 patients with Friedreich's ataxia (FA) to define the incidence of myocardial involvement and the type of cardiomyopathy observed. All patients with FA had either ECG, vectocardiographic or echocardiographic abnormalities, suggesting some degree of myocardial involvement. In contrast to reports indicating that asymmetric septal hypertrophy (ASH), often obstructive, is associated with FA, symmetric, concentric hypertrophic cardiomyopathy (SCH) was the predominant abnormality (sixty-seven percent of patients). Echocardiograms should be performed periodically in all FA patients since this technique allows the detection of cardiac hypertrophy.

Adolescent↗
PubMed1980

Friedreich's ataxia and oral glucose tolerance: I. The effect of ingested glucose on serum glucose and insulin values in homozygotes, obligate heterozygotes and potential carriers of the Friedreich's ataxia gene.

Glucose tolerance and insulin release were evaluated in 16 families with Friedrich's ataxia. Impaired glucose tolerance differed in incidence according to the method of evaluation, but was increased in number in parents and siblings of Friedreich's cases. Insulin output was not quantitatively different from normal, although the insulin peak was often delayed. This finding, in association with impaired glucose tolerance, suggest a defect in glucose entry into cells.

Adolescent↗
PubMed1980

Friedreich's ataxia and oral glucose tolerance: II. The effect of ingested glucose on serum growth hormone in homozygotes, obligate heterozygotes and potential carriers of the Friedreich's ataxia gene.

Homozygotes, obligatory heterozygotes and potential carriers of the Friedreich's Ataxia gene were tested with an oral glucose tolerance in order to assess a. the prevalence of abnormalities in glucose handling, b. the secretory pattern of two "diabetogenic" hormones, growth hormones and prolactin and c. to evaluate the possibility for detection of an abnormal trend in these hormones to be used as a genetic marker. Despite the high prevalence of glucose abnormalities horizontally and vertically in these families, the basal output and responses of these metabolic hormones to a glucose challenge were appropriate and thus not characteristic of any of the above groups.

Adolescent↗
PubMed1980

Leucocyte glutamate dehydrogenase in various hereditary ataxias.

Leucocyte Glutamate Dehydrogenase (GDH) activity was measured in 44 patients with various forms of ataxia and 44 age and sex-matched normal controls. The only significant change found was a moderate decrease in activity in Friedreich's ataxia and a few patients with OPCA. This decreased activity is not primary to the disease but probably reflects a regulatory defect affecting mitochondrial membranes in these patients.

Ataxia↗
PubMed1980

Protein kinase activity of human erythrocyte membranes in Friedreich's ataxia.

Proteins of human erythrocyte membranes of Friedrich's ataxia patients and controls were examined by SDS-polyacrylamide gel electrophoresis before and after reduction with beta-mercaptoethanol. No difference could be detected in the composition of their state of aggregation. The protein kinase activity of human erythrocyte membranes of eleven Friedreich's ataxia patients and six controls was determined. No difference in their protein kinase activity could be detected. These results are discussed with respect to an involvement of a generalized membrane defect in Friedreich's ataxia.

Electrophoresis, Polyacrylamide Gel↗
PubMed1980

Lecithin: cholesterol acyltransferase activity and fatty acid composition of erythrocyte phospholipids in Friedreich's ataxia.

In a study of the fatty acid composition of erythrocyte membrane phospholipids in Friedreich's ataxia, a lower percentage of linoleic acid in phosphatidylcholine was demonstrated. An enzyme involving the exchange of lipids between plasma and erythrocyte membrane, lecithin: cholesteryl acyltransferase (LCAT) was also studied. It was found that the LCAT activity had a trend towards low values. However, crossing-over studies indicated that when the LCAT enzyme of patients was exposed to its own substrate it gave low activity values but that the result reverted to normal when control substrate was used.

Acyltransferases↗
PubMed1980

Taurine decreases lesion severity in the hearts of cardiomyopathic hamsters.

Cardiomyopathic Syrian hamsters develop necrotic lesions consequent upon calcium overload from 60 days of age onward. Taurine, given as a 0.1 M solution in place of drinking water for one month prior to sacrifice of animals of initial age 35 days, decreased the severity of subsequently developing cardiac lesions by 40%. Calcium concentration in the heart was decreased by 57%. Magnesium and iron concentrations were unaltered. Taurine given in a similar manner for 4 months had a protective effect, decreasing lesion severity by 21% and calcium concentration by 35%. Magnesium concentrations were increased by 12%. Compared to random-bred animals, cardiomyopathic hamsters at one and two months of age have the same concentrations of calcium, magnesium and iron in the quadrants of the heart, except in the left ventricle, which has significantly higher concentration of calcium. Calcium concentrations are 70%, 1320% and 2100% higher respectively in one month, two month and five month old animals. Five month old animals differ slightly but significantly in iron (17% decrease) and magnesium concentrations (17% increase). Cardiomyopathic hamsters have insignificant differences in beta-adrenergic receptor density compared to random-bred animals and have a significantly higher rate of taurine influx.

Adult↗
PubMed1980

Effect of asparagine, glutamine and insulin on cerebral amino acid neurotransmitters.

Treatment of rats with asparagine or glutamine caused substantial increases in glutamine concentrations in cerebellum and medulla oblongata. Insulin treatment caused a diminution of glutamate and GABA in these regions of brain. Since it is now well-established that glutamine is a very efficient precursor of the neurotransmitter pool of glutamate in mammalian brain, treatment with asparagine or glutamine could be of therapeutic (replacement) value in the treatment of neurological disorders such as Friedreich's ataxia, in which cerebral glutamate concentrations have been found to be diminished.

Animals↗
PubMed1980

Effects of glutamate and aspartate on ataxic gait induced by 3-acetyl pyridine in rats.

The main purpose of this study was to examine the effects of intraventricular injections of glutamate and aspartate on the walking gait of rendered ataxic by the administration of 3-acetyl pyridine. Both amino acids significantly improved the walking gait of these animals. The effects of other substances known to have a stimulatory influence on locomotor activity in rats were also investigated. Amphetamine, apomorphine and thyrotropin releasing hormone (TRH) had no effect on the ataxic gait of 3-AP treated animals. Substance P significantly improved the gait of ataxic animals, but to a lesser extent than that seen with glutamate and aspartate.

Amphetamine↗
PubMed1980

Friedreich's ataxia 1980. An overview of the physiopathology.

Phase three of the Quebec Cooperative Study of Friedreich's Ataxia was devoted to an understanding of the physiopathology of individual symptoms on the basis of previously discovered biochemical leads. The present paper attempts to pull these results together by presenting, as a hypothesis, a unifying scheme of possible interactions and relationships. The central core of this hypothesis is the demonstration in Friedreich's ataxia of a state of mitochondrial energy deprivation. This is indirectly responsible for such associated and important symptoms as muscle weakness, dying-back neuropathy, scoliosis and hypertrophic cardiomyopathy. Secondarily, and possibly as an independent but linked-event, the entry of glucose into cells and pyruvate oxidation, are slowed down, favoring the development of diabetes. As a consequence, tissue concentrations of glutamic acid and aspartic acid are decreased, particularly in more vulnerable areas such as the cerebellum, brain stem and dorsal root ganglia. This tissue deficiency in putative excitatory neurotransmitters is directly responsible for the symptom of ataxia. This conclusion is reinforced by the correction of the ataxia in experimental animals, by the intraventricular injection of the same amino acids, and not by the injection of other stimulants of motricity. The observed mitochondrial energy deprivation could be the metabolic consequence of major changes in the linoleic acid (18.2) composition of inner mitochondrial membrane phospholipids, such as cardiolipin. Such decreases in membrane 18:2 could be the result of interference with the normal incorporation of this fatty acid to lipoproteins and/or cell membranes. It is at this level that the search for the specific enzyme defect in Friedreich's ataxia is continuing.

Cardiomyopathy, Hypertrophic↗
PubMed1980

Lecithin in Parkinson's disease.

Pathological and biochemical evidence reviewed favours the hypothesis that the dementia seen in Parkinson's disease, particularly after long-term levodopa therapy, is akin to Alzheimer's disease. We postulate, in late Parkinson's disease, the development of a relative cholinergic deficiency due to the accelerated process of aging and the presence of neurofibrillary tangles (with choline acetyl transferase deficiency.) This process would be enhanced by the imbalance in favour of dopaminergic predominance caused by chronic levodopa therapy, and would partially explain the increase in dementia. As a test of this hypothesis we have given 10 levodopa-treated parkinsonian patients with dementia, a regimen of lecithin (average 20 gms/day). A clear improvement in Kohs block design test of constructive ability was noted with a decrease in the toxic symptoms of confusion, hallucinations and nightmares. In another study lecithin produced a decrease in levodopa-induced abnormal movements, but at the expense of motor performance. These preliminary investigations indicate that the progressive dementia of Parkinson's disease may not be irreversible.

Humans↗