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Biomedical subjects

P Etienne

Publications and source records attributed to P Etienne.

At least 37 records · Page 2Linked to original sources
PubMed1986

Nucleus basalis neuronal loss, neuritic plaques and choline acetyltransferase activity in advanced Alzheimer's disease.

All our advanced, severe cases of Alzheimer's disease have dramatic cholinergic cell losses in the nucleus basalis of Meynert even after correction for cell or nucleoli shrinkage. There is a good correlation between choline acetyltransferase activity and "healthy" cell number in the nucleus basalis of Meynert. Half of the Alzheimer disease cases have markedly reduced cortical choline acetyltransferase activity in spite of preserved nucleus basalis of Meynert choline acetyltransferase activity, suggesting a deficiency of cortical origin and/or of axonal transport in Alzheimer disease. The relationship between cell loss in the various sub-divisions of the nucleus basalis of Meynert and plaque counts in corresponding and non-corresponding projection areas of the cortex has also been examined. Globally, this relation appears more obvious when cell loss in a sub-division of the nucleus basalis of Meynert is compared to plaque counts in its cortical projection area. However, the relation is discontinuous with few or no data to document the intermediary stages of the process, probably reflecting the severity of our Alzheimer disease cases.

Aged↗
PubMed1986

Neurotransmitter and receptor deficits in senile dementia of the Alzheimer type.

Multiple neurotransmitter systems are affected in senile dementia of the Alzheimer's type (SDAT). Among them, acetylcholine has been most studied. It is now well accepted that the activity of the enzyme, choline acetyltransferase (ChAT) is much decreased in various brain regions including the frontal and temporal cortices, hippocampus and nucleus basalis of Meynert (nbm) in SDAT. Cortical M2-muscarinic and nicotinic cholinergic receptors are also decreased but only in a certain proportion (30-40%) of SDAT patients. For other systems, it appears that cortical serotonin (5-HT)-type 2 receptor binding sites are decreased in SDAT. This diminution in 5-HT2 receptors correlates well with the decreased levels of somatostatin-like immunoreactive materials found in the cortex of SDAT patients. Cortical somatostatin receptor binding sites are decreased in about one third of SDAT patients. Finally, neuropeptide Y and neuropeptide Y receptor binding sites are distributed in areas enriched in cholinergic cell bodies and nerve fiber terminals and it would be of interest to determine possible involvement of this peptide in SDAT. Thus, it appears that multi-drug clinical trials should be considered for the treatment of SDAT.

Alzheimer Disease↗
PubMed1986

CCK-8 antagonizes apomorphine-induced growth hormone secretion in normal subjects.

Cholecystokinin octapeptide (CCK-8) (5 ug iv over 10 minutes) administered to normal men had no effect on basal growth hormone (GH) or prolactin secretion but significantly antagonized the GH response to the dopamine (DA) receptor agonist, apomorphine HCI (Apo) (0.5 mg sc), 30 (P less than 0.05) and 45 minutes (P less than 0.01) after Apo injection (n = 8). These results are compatible with an inhibitory effect of CCK-8 on certain DA mechanisms in the hypothalamic-pituitary axis. Whether CCK-8 affects DA function in other brain regions in man is unknown.

Adolescent↗
PubMed1986

Increase in the content of quinolinic acid in cerebrospinal fluid and frontal cortex of patients with hepatic failure.

Quinolinic acid (QUIN), an excitotoxic tryptophan metabolite, has been identified and measured in human cerebrospinal fluid (CSF) using a mass-fragmentographic method. Furthermore, its content has been evaluated in frontal cortex obtained at autopsy from the cadavers of patients who died after hepatic coma. During the coma, the concentration of QUIN in the CSF was 152 +/- 38 pmol ml-1. In contrast, the concentration in control patients affected by different pathologies was 22 +/- 7 pmol ml-1. In the frontal cortex of patients who died after episodes of hepatic encephalopathy, the content of QUIN was three times higher than in controls (2.6 +/- 0.6 versus 0.80 +/- 0.08 nmol/g wet weight). As a result of these investigations we are now able to extend our previous observations on the increase of QUIN in the brains of rats used as experimental models of hepatic encephalopathy to man. QUIN should therefore be added to the list of compounds possibly involved in the pathogenesis and symptomatology of brain disorders associated with liver failure.

Aged↗
PubMed1986

Nucleus basalis neuronal loss and neuritic plaques in advanced Alzheimer's disease.

All our advanced severe cases of Alzheimer's disease had dramatic cholinergic cell loss in the basal forebrain, even after correction for cell or nucleolus shrinkage. We examined the relation between cell loss in the various subdivisions of the nucleus basalis of Meynert and plaque counts in corresponding and noncorresponding projection areas. This relation was not interpretable because of the ambiguity in the data.

Aged↗
PubMed1984

The occurrence of large acetylcholinesterase-containing neurons in human neostriatum as disclosed in normal and Alzheimer-diseased brains.

The human neostriatum was found to contain large neurons (maximum diameter: 30-40 microns) that stain intensely for acetylcholinesterase (AChE). These neurons are few in number, representing less than 5% of the total striatal neuronal population, and appear uniformly scattered throughout the caudate nucleus and putamen. They are morphologically similar to the AChE-containing neurons disclosed in the striatum of rat, cat and monkey after AChE inhibitor (DFP) pretreatment. In Alzheimer-diseased brains the number, morphological characteristics, and staining intensity of the striatal AChE neurons were found to be unaltered despite a marked loss of AChE cells in the adjoining nucleus basalis. These findings suggest that large intrinsic cholinergic neurons exist in human neostriatum and that these elements, in contrast to those of nucleus basalis, are not affected in Alzheimer's disease.

Acetylcholinesterase↗
PubMed1984

CCK-33 antagonizes apomorphine-induced growth hormone secretion and increases basal prolactin levels in man.

Cholecystokinin (CCK-33) (225 Ivy Dog Units intravenously) had no effect on basal growth hormone (GH) secretion but antagonized the GH response to the dopamine receptor agonist, apomorphine HCl (0.5 mg sc) (N = 7), and induced a transient increase in basal prolactin (PRL) secretion (N = 8) in normal men. These findings are similar to those described with neuroleptics and are compatible with an inhibitory effect of CCK-33, or fragments, on dopamine function in man, at least in the hypothalamic-pituitary axis. However, an inhibitory effect of CCK-33 on the release of GH and a stress-induced increase in PRL secretion cannot be excluded.

Adult↗
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 apomorphine, a dopamine receptor agonist, on penile tumescence in normal subjects.

Apomorphine HCl (Apo) (0.25, 0.5 or 0.75 mg sc), a dopamine (DA) receptor agonist, induced penile erections (PEs) (monitored by mercury strain gauges and continuous recording on paper strip charts) in 7 out of 9 normal subjects and placebo in 1 of these 9 (p less than 0.05). Apo-induced PEs recurred in each of the 6 subjects retested. Benztropine (2 mg iv) had no effect on Apo-induced penile tumescence (PT). These data suggest (a) DA mechanisms play a role in normal erectile function (b) DA-mediated PT is not modulated by cholinergic systems (c) evaluation of the erectile response to Apo may provide a simple ancillary test to the investigation of impotence and a way of identifying a subpopulation of impotent subjects with impaired DA function who may respond to long-acting DA agents (d) Apo-induced PT may provide a novel way of studying DA function in man.

Adult↗
PubMed1984

Benzodiazepines and GABAergic regulation of nigrostriatal neurons: lack of tolerance.

Decreases of 40 to 50% in striatal dopamine release by diazepam in doses above 5 mg/kg were elicited. Similar actions were observed with clonazepam and nitrazepam. No tolerance to these actions was evident after 3 weeks of chronic treatment. These data are consistent with a potent inhibitory GABAergic regulation of nigrostriatal dopaminergic neurons.

Animals↗
PubMed1984

[Isolated arterial hypertension during pregnancy disclosing a malignant tumor of the kidney. Apropos of a case].

The authors report an observation of isolated hypertension during pregnancy; this hypertension has revealed a cancer of kidney. As hypertension has regressed after ablation of the tumor, the authors evoke physiopathological hypothesis. They insist about X Ray of kidney after pregnancy, for hypertensive pregnancy. It seems to be the best exam to discover an uropathy.

Adenocarcinoma↗
PubMed1983

Buspirone: a potential atypical neuroleptic.

Buspirone produces a dose-dependent but short-lived elevation in striatal dopamine (DA) metabolites in the rat. In vitro, buspirone possesses an affinity similar to sulpiride for DA receptors (3H-spiperone). A moderate affinity for alpha 1 receptors was also observed while buspirone was inactive at alpha 2, beta, muscarinic and serotonin2 receptors. This pharmacological profile as well as previous behavioral data indicate that buspirone may be a potential "atypical" neuroleptic.

Animals↗
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↗