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Biomedical subjects

S Gauthier

Publications and source records attributed to S Gauthier.

At least 217 records · Page 12Linked to original sources
PubMed1983

Origin of insulin-receptive nerve terminals in rat median eminence.

The origin of insulin-receptive axon terminals in the rat median eminence was determined by combining surgical and chemical ablation techniques and the in vivo radioautographic approach, in which labeling of the median eminence with blood-borne [125I]insulin served as a quantifiable marker for the presence of receptive axonal elements. Whereas unilateral deafferentation of the median eminence from the ipsilateral brain produced as much as a 50% ipsilateral loss of insulin-binding sites, transection of axonal projections to median eminence from neurons located lateral to the ventromedial hypothalamic nucleus produced no detectable loss in insulin-binding capacity. Unilateral electrocoagulation of various regions of the medial basal hypothalamus indicated that insulin-receptive axon terminals arise primarily from neurons in and about the hypothalamic arcuate nucleus and from the posterior ventrolateral subdivision of the hypothalamic ventromedial nucleus. A primary site of origin from the arcuate nucleus was confirmed in rats treated neonatally with monosodium L-glutamate, which, in addition to a selective destruction of arcuate neurons, produced a profound reduction in the insulin-specific binding capacity of the median eminence. The results of this study indicate that insulin-binding axon terminals arise from a unique class of tuberoinfundibular neuron with hormone-receptive capacity. These neurons may function to mediate direct interaction of circulating insulin with central autonomical, behavioral, and neuroendocrine systems.

Animals↗
PubMed1982

Effect of folic acid and vitamin B12 deficiencies on 5-hydroxyindoleacetic acid in human cerebrospinal fluid.

Indoles were measured in cerebrospinal fluid (CSF) from control patients, from patients suffering from folate deficiency, and from patients with vitamin B12 deficiency. The folate-deficient patients were classified according to whether they exhibited a neuropsychiatric syndrome, consisting of organic mental changes, polyneuropathy, and depression, which responded to folate administration. CSF 5-hydroxyindoleacetic acid was low in the vitamin B12-deficient patients and in those folate-deficient patients whose symptoms were not related to folate deficiency. CSF 5-hydroxyindoleacetic acid returned to normal with folate treatment in the patients exhibiting folate-responsive neuropsychiatric signs. The data indicate a close association between folate-responsive neuropsychiatric symptoms and changes in 5-hydroxytryptamine metabolism in the central nervous system.

Adolescent↗
PubMed1982

The effect of carbidopa and benserazide on human plasma 5-hydroxytryptophan levels.

Peripheral aromatic amino acid decarboxylase inhibitors increase human plasma 5-hydroxytryptophan (5-HTP) levels. However the 5-HTP, which is synthesized in the intestine, is not present in a sufficient quantity to influence brain 5-HT to any significant degree. Thus, peripheral decarboxylase inhibitors are unlikely to affect brain 5-HT function via 5-HTP which is synthesized peripherally.

5-Hydroxytryptophan↗
PubMed1982

Anatomical and biochemical basis of the extrapyramidal disorders.

1. Degeneration of various components of the extrapyramidal system has been correlated with specific clinical syndromes. 2. In Parkinson's disease, loss of ascending nigrostriatal fibers is associated with reduction of presynaptic dopamine binding and increase of postsynaptic dopamine binding. The latter is reversed by treatment with dopamine agonists. 3. In Huntington's disease, multiple types of striatal neurons are lost, with their corresponding enzymes and receptors. 4. In tardive dyskinesias, there are no specific neuropathological findings, but increased amounts of striatal dopamine receptors. 5. Knowledge of the chemical nature of the pallidal outflow to the thalamus may be the next most important step in the pharmacological control of extrapyramidal function.

Basal Ganglia Diseases↗
PubMed1982

Precursors and metabolites of phenylethylamine, m and p-tyramine and tryptamine in human lumbar and cisternal cerebrospinal fluid.

Phenylacetic acid, p-hydroxyphenylacetic acid, m-hydroxyphenylacetic acid, phenylalanine, indoleacetic acid, 5-hydroxyindoleacetic acid and tryptophan were measured in lumbar and cisternal cerebrospinal fluid (CSF) taken during pneumoencephalography. The data suggest that the concentration of the acid metabolites of the trace amines tryptamine, phenylethylamine, p-tyramine and m-tyramine in lumbar CSF are influenced by the system that transports these acids out of CSF. In cisternal CSF this mechanism does not operate and more information can be obtained on the metabolism of the parent amines in the CNS. Our data indicate that (1) m-tyramine is relatively unimportant quantitatively (2) the rate of metabolism of phenylethylamine in human brain is similar to that of 5-hydroxytryptamine (3) the most important variable controlling the synthesis of phenylethylamine is the activity of aromatic amino acid decarboxylase (4) p-tyramine is synthesised at about half the rate of phenylethylamine and is thus quantitatively important in metabolic terms.

Adolescent↗
PubMed1982

Thiamine deficiency and cerebrospinal fluid 5-hydroxyindoleacetic acid: a preliminary study.

In three out of five patients with low cerebrospinal fluid thiamine concentrations, the 5-hydroxyindoleacetic acid (5HIAA) values also were low. All patients received thiamine replacement therapy; they underwent a second lumbar puncture after 13, 6, 7, 5 and 45 days of treatment. In all patients blood and cerebrospinal fluid thiamine values rose after treatment. In those patients with initially low CSF 5HIAA, thiamine treatment increased 5HIAA markedly.

Adult↗
PubMed1981

Tryptophan availability and the control of 5-hydroxytryptamine and tryptamine synthesis in human CNS.

The data presented here suggest that control of human brain 5HT synthesis by precursor availability is similar to that in the rat. Plasma tryptophan controls the brain level, although the plasma-brain relationship is modified by other large neutral amino acids in plasma. In normal circumstances brain tryptophan is an important factor controlling the synthesis of 5HT and tryptamine in human brain. However, the elevated brain tryptophan in patients with chronic liver disease does not lead to an increase in the rate of 5HT metabolism. In human brain the rate of tryptamine synthesis is normally aobut 10-20% of the rate of 5HT synthesis. Tryptamine metabolism is more sensitive than 5HT metabolism to changes in brain tryptophan. This is especially apparent after a tryptophan load. Our results suggest that tryptophan administration increases indoleamine function, as well as indoleamine synthesis, in depressed patients. Whether physiological variations in brain tryptophan in normal people are responsible for variations in indoleamine function is an open question.

Animals↗
PubMed1981

Effect of tryptophan administration on tryptophan, 5-hydroxyindoleacetic acid and indoleacetic acid in human lumbar and cisternal cerebrospinal fluid.

Tryptophan 5-hydroxyindoleacetic acid and indoleacetic acid were measured in cerebrospinal fluid taken during pneumoencephalography from patients, some of whom took a 3 g or 6 g tryptophan load at various times before. Measurements were made on both lumbar and cisternal cerebrospinal fluid and the results showed similarities between indoleamine metabolism in human brain and spinal cord. Our data suggested that (1) the blood-brain barrier active transport system for tryptophan is not far from saturation with tryptophan and the rate-limiting enzyme in 5-hydroxytryptamine (5HT) synthesis, tryptophan hydroxylase, is about half saturated. Therefore, both 3 g and 6 g tryptophan loads produced the same maximum rise in 5HT synthesis of just under 100%, (2) tryptamine differs from 5HT in two respects. It is more sensitive to changes in tryptophan availability than 5HT and the 6 g load increased brain tryptamine metabolism more than the 3 g load; also some of the tryptamine in brain is derived from peripheral sources and diffuses from blood to brain, (3) although the brain tryptamine content is much lower than that of 5HT, its rate of metabolism as indicated by CSF metabolite levels is not. In controls the rate of tryptamine metabolism is 15% of the rate of 5HT metabolism and this can increase to 40% after a 6 g tryptophan load.

Adolescent↗
PubMed1981

Alzheimer disease: lack of effect of lecithin treatment for 3 months.

Eleven outpatients with Alzheimer disease of moderate severity completed a double-blind placebo-controlled crossover trial of lecithin. Each patient received 10 gm three times daily of a placebo for 3 months. Plasma choline levels rose threefold and remained at that level throughout the lecithin administration period. A significant difference between mean baseline scores and treatment scores was found on tests of new learning ability, indicating a practice effect in these tests. However, there were no differences between mean placebo and lecithin scores on any of the psychological test measures.

Aged↗
PubMed1981

[Palatal myoclonus associated with a decrease in 5-hydroxy-indole acetic acid in cerebrospinal fluid and responding to clonazepam].

A patient representing with palatal myoclonus was diagnosed as suffering from possible multiple sclerosis. A reduction of cerebrospinal 5-hydroxy-indole-acetic acid suggested a decreased central serotonergic turnover. A therapeutic trial with clonazepam, a serotonergic agonist, improved the myoclonus symptomatically. The possible involvement of serotonergic inhibitory systems in the expression of palatal myoclonus is discussed.

Benzodiazepinones↗
PubMed1980

Development of a scleroderma-like illness during therapy with L-5-hydroxytryptophan and carbidopa.

A scleroderma-like illness developed in a patient treated with L-5 hydroxytryptophan (L-5HTP) and carbidopa for intention myoclonus. The patient had high plasma kynurenine levels that remained high when the L-5HTP-carbidopa combination was discontinued, However, levels rose futher on drug rechallenge, suggesting that the drug unmasked an abnormality in one of the enzymes that catabolize kynurenine. Plasma kynurenine was also determined to be high in seven of 15 patients wth idiopathic scleroderma, but not in eight patients with intention myoclonus treated with L-5HTP and a decarboxylase inhibitor and in whom scleroderma did not develop or in 10 patients with Parkinson's disease treated wth L-dopa and carbidopa. Our data and studies in the literature suggest that two factors may be important in the pathogenesis of some scleroderma-like illness: high plasma serotonin and the abnormality associated with elevated kynurenine.

5-Hydroxytryptophan↗
PubMed1980

Tryptophan, 5-hydroxyindoleacetic acid and indoleacetic acid in human cerebrospinal fluid: interrelationships and the influence of age, sex, epilepsy and anticonvulsant drugs.

Tryptophan, 5-hydroxyindoleacetic acid and indoleacetic acid were measured in cerebrospinal fluid, taken during pneumoencephalography, from a large series of patients, the majority of whom were epileptics, most of them receiving anticonvulsants. CSF indoleacetic acid reflects CNS tyrptamine metabolism in the same way that CSF 5-hydroxyindoleacetic acid reflects CNS 5-hydroxytryptamine metabolism. Our data suggest that (i) the brain tryptophan content is an important factor in the control of both 5-hydroxytryptamine and tryptamine synthesis (ii) brain 5-hydroxytryptamine metabolism exhibits a U-shaped relationship with age (iii) the mean brain tryptophan content and rate of 5-hydroxytryptamine metabolism are greater for women than men (iv) indoleamine metabolism is unaffected in untreated epileptics compared with non-epileptics, but anticonvulsant drugs decrease the rate of 5-hydrosytryptamine metabolism.

Adult↗