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Biomedical subjects

S Gauthier

Publications and source records attributed to S Gauthier.

At least 199 records · Page 11Linked to original sources
PubMed1985

Descending spinal pathways mediating the responses of adrenal tyrosine hydroxylase and catecholamines to insulin and 2-deoxyglucose.

We investigated the bilateral organization of the descending spinal sympathetic projections that subserve adrenomedullary stimulation caused by insulin hypoglycemia or 2-deoxyglucose (2DG) cellular glucopenia in adult rats with right-sided hemisection of the cord at C6-C7 (i.e. above the site of origin of the adrenal innervation). Cord hemisection alone caused a minor rise of adrenal tyrosine hydroxylase activity (ATHA) on the intact side as compared to sham-operated animals, but there was no change on the operated side. Catecholamine levels were marginally affected. In rats with hemisection the drugs elevated ATHA significantly in both glands; the response on the intact side was similar to that in sham-operated rats, but the effect on the sectioned side was reduced by one-half. 2DG affected the adrenaline content differently in the two glands: on the intact side it provoked a decrease comparable with that in non-lesioned rats, but had no significant effect on the lesioned side. 2DG acts through higher CNS structures, for complete transection of the cord at T2-T3 prevents the effects of 2DG on ATHA and adrenal adrenaline. We conclude that adrenal tyrosine hydroxylase induction by insulin and 2DG in hemisectioned rats, just as in the case of immobilization stress, is mediated by ipsilateral and, to a lesser degree, contralateral pathways generating net excitatory effects on ATHA; the latter fibers decussate below the low cervical level. The same organization may prevail for control of the concentration of adrenal adrenaline.

Adrenal Medulla↗
PubMed1985

Differential effects of transection of the spinal cord and splanchnic nerve on adrenal tyrosine hydroxylase and catecholamines.

The role of spinal pathways in the regulation of adrenal medullary tyrosine hydroxylase and catecholamines was studied in adult rats subjected to spinal cord transection at the third thoracic level. In these animals the sympathoadrenal preganglionic neurons were isolated from their supraspinal afferents. This treatment led after three days to a progressive reduction of tyrosine hydroxylase activity and dopamine content (as compared to unoperated controls) until at least the 10th day. The results of the administration of dexamethasone or adrenocorticotropic hormone to spinalized rats suggest that in these animals glucocorticoid hypersecretion is not involved in the decline of adrenal tyrosine hydroxylase and that in fact adrenocorticotropic hormone supplementation can prevent it. A neurogenic origin for the depression of adrenomedullary function is favoured because unilateral splanchnicotomy (which by itself does not affect adrenal tyrosine hydroxylase), prior to cord section, prevented the diminution of tyrosine hydroxylase activity in the denervated gland. The decline of adrenal tyrosine hydroxylase and dopamine after spinal section may result from a decrease of modulatory impulses to the adrenal from decentralized sympathoadrenal preganglionic neurons in the isolated cord, following the loss of a descending facilitation of these neurons and/or the release of a segmental interneuronal inhibition of these neurons from a descending inhibitory influence. Such descending pathways may decussate partially below the low cervical level because rats with hemisection of the cord at C6-C7 exhibited no decline of adrenal tyrosine hydroxylase or of dopamine measured on either side seven days postoperatively.

Adrenal Medulla↗
PubMed1985

Akinetic mutism and parkinsonism associated with obstructive hydrocephalus.

We report the case of a patient with idiopathic aqueductal stenosis and hydrocephalus who had several episodes of akinetic mutism, each preceded by shunt malfunction, that resolved with shunt revision. She also developed a parkinson's syndrome resistant to shunt revision but responsive to antiparkinsonian medications. The parkinson's syndrome and the episodes of akinetic mutism may be related to a reduction of dopaminergic input to the striatum and to the cingulate and frontal cortex brought about or worsened by ventricular dilatation.

Adult↗
PubMed1985

NH2-terminal specificity and axonal localization of adrenocorticotropin binding sites in rat median eminence.

Adrenocorticotropin binding sites in the rat median eminence have been localized in vivo. These binding sites occur in the basalar zone, which is rich in axonal endings. Using competitive binding and quantitative light-microscope radioautography, we found that the median-eminence binding site, in contradistinction to the adrenal receptor, binds specifically the residue 4-10 region of the adrenocorticotropin molecule. Using quantitative electron-microscope radioautography and median-eminence deafferentation, we localized the binding sites to axon terminals in this region. In time-delayed uptake studies using light-microscope radioautography, we failed to observe concentration of radiolabel in neurons of the medial basal hypothalamus after the direct injection of radioiodinated adrenocorticotropin(1-24) into the median eminence.

Adrenal Glands↗
PubMed1984

CSF acetylcholinesterase in dementia and in sequential samples of lumbar CSF.

Acetylcholinesterase (AchE) activity (nmol/ml/min) was measured in lumbar CSF from 11 patients with dementia of the Alzheimer type (DAT), 8 patients with Korsakoff psychosis and 33 patients with low back pain who were undergoing myelography (controls). There was no significant difference in enzyme activity between the three groups. There was no significant correlation between age and AchE activity. AchE was also measured in 20 two-ml samples of CSF collected sequentially by lumbar puncture in two neurosurgical patients who had been recumbent for at least 8 hours. Variations in AchE between samples were small. In neither patient was there an increase in AchE activity with progressive sampling. These data indicate that (1) AchE is unchanged in Korsakoff psychosis (2) decreases in brain AchE which are found in DAT are not readily reflected in lumbar CSF (3) AchE in lumbar CSF has a diffuse origin including spinal cord (4) CSF AchE activity is unlikely to be a useful clinical marker for DAT.

Acetylcholinesterase↗
PubMed1984

Effect of oral melatonin administration on melatonin, 5-hydroxyindoleacetic acid, indoleacetic acid, and cyclic nucleotides in human cerebrospinal fluid.

Melatonin was given orally to patients undergoing diagnostic pneumoencephalography and various compounds were measured in the lumbar and cisternal CSF. Melatonin markedly increased plasma and CSF melatonin concentrations. The plasma: CSF melatonin ratios were similar in patients who received, and in those who did not receive, melatonin. This supports the idea that melatonin is released from pineal to blood and gets into the CSF via the blood. Melatonin did not affect CSF 5-hydroxyindoleacetic acid, which indicates that it has no effect on 5-hydroxytryptamine metabolism. Melatonin increased CSF indoleacetic acid significantly, indicating increased metabolism of tryptamine. Melatonin did not affect CSF cAMP levels, but increased cGMP levels. The effect on indoleacetic acid and cGMP was seen in both lumbar and cisternal CSF, suggesting that melatonin can have generalized actions throughout the CNS.

Adolescent↗
PubMed1984

Enzyme changes in actively spiking areas of human epileptic cerebral cortex.

Five enzymes involved in glutamic acid, GABA, and catecholamine metabolism were measured in epileptic human brain. Electrocorticographically defined areas of focal spiking were compared with samples from surrounding nonspiking cortex. Comparative enzyme activities were as follows (mumol/h/g wet wt): glutamic acid dehydrogenase (GDH)--spiking 135.77 +/- 10.22 (mean +/- SEM), nonspiking 118.58 +/- 9.42 (p less than 0.001, N = 17); glutamic acid decarboxylase--spiking 10.63 +/- 0.95, nonspiking 9.96 +/- 1.10 (NS, N = 13); GABA-aminotransferase--spiking 36.49 +/- 1.05, nonspiking 36.46 +/- 1.48 (NS, N = 12); glutamine synthetase--spiking 96.94 +/- 3.81, nonspiking 96.52 +/- 4.10 (NS, N = 20); and tyrosine hydroxylase (TH; nmol/h/g)--spiking 16.23 +/- 2.39, nonspiking 10.67 +/- 1.95 (p less than 0.001, N = 14). Increased activity of GDH and TH may prove useful to characterize further areas of active spiking in human focal epilepsy.

Adolescent↗
PubMed1983

Studies on kynurenine in human cerebrospinal fluid: lowered levels in epilepsy.

Kynurenine, tryptophan and 5-hydroxyindoleacetic acid were measured in human lumbar and cisternal cerebrospinal fluid (CSF) taken during pneumoencephalography. The results do not support the hypothesis that any substantial part of the CSF kynurenine is of central origin. However, the results suggest that CSF kynurenine is reduced in some epileptic subjects and this seems to be due to the disease rather than anticonvulsants. This finding is of interest in view of the reported convulsant effect of kynurenine in experimental animals.

Adolescent↗
PubMed1983

A post-mortem comparison of the cortical cholinergic system in Alzheimer's disease and Pick's disease.

Assessment of neurochemical markers in the frontal cortex indicates that choline acetyltransferase is significantly decreased in Alzheimer's and Gerstmann-Straussler dementias but not in Pick's dementia. It therefore appears that the cholinergic innervation of the cortex from the basal forebrain is intact in Pick's disease. Cortical somatostatin was decreased only in Alzheimer's disease (AD), indicating that loss of somatostatin is not a constant feature in different forms of dementia. Muscarinic binding sites were unaltered in Pick's disease and Gerstmann-Straussler syndrome but were decreased in a subpopulation of AD patients. These data suggest that in some cases of AD a significant loss of cholinoceptive neurones in the cortex is evident.

Adult↗
PubMed1983

Participation of spinal monoaminergic and cholinergic systems in the regulation of adrenal tyrosine hydroxylase.

The role of spinal pathways in the regulation of tyrosine hydroxylase activity (ATHA) in the adrenal medulla was characterized in adult rats with surgical transection of the upper thoracic cord. The animals received injections of centrally active agonists, which could then act on the sympathoadrenal preganglionic neurons isolated from their supraspinal afferents. All agonists tested produced distinct increases of tyrosine hydroxylase activity in rats with a surgical sham operation. The injection of quipazine or oxotremorine into spinalized rats led to decreased tyrosine hydroxylase activity. Clonidine and several dopamine agonists did not affect tyrosine hydroxylase activity. Considering the mechanism of the observed changes in tyrosine hydroxylase activity it is concluded that the changes are mediated by neural pathways and that variations in the secretion of adrenocorticotrophic hormone (ACTH) do not play a role. The results suggest (a) that there are serotonergic and cholinergic (muscarinic) receptors in the lower thoracic cord generating a net inhibitory action on tyrosine hydroxylase activity; and (b) that increases of tyrosine hydroxylase activity mediated by dopaminergic drugs probably originate from areas rostral to the thoracic cord. It is possible that an alpha-adrenergic system participates in the regulation of tyrosine hydroxylase activity in the adrenal medulla.

Adrenal Medulla↗
PubMed1983

Lack of cholinergic deficit in the neocortex in Pick's disease.

Choline acetyltransferase activity was decreased in the frontal cortex in Alzheimer's and Gerstmann-Straussler dementias but not in Pick's disease. Cortical somatostatin was only decreased in Alzheimer's dementia. Postsynaptic muscarinic binding sites appeared to be decreased in a subpopulation of Alzheimer's patients. Our data indicate that a loss of cholinergic innervation of the cortex is not common to all dementias.

Choline O-Acetyltransferase↗
PubMed1983

Gilles de la Tourette's syndrome in monozygotic twins.

Concordance is reported of Gilles de la Tourette syndrome in a male twin pair in whom phenotyping revealed a >98·7% probability that they were monozygotic. The development and extent of the illness differed markedly in the two subjects. Our findings are compatible with the view that there is a genetic form of Gilles de la Tourette syndrome.

Adolescent↗