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Biomedical subjects

J Constantinidis

Publications and source records attributed to J Constantinidis.

At least 91 records · Page 5Linked to original sources
PubMed1984

The basal nucleus of Meynert in patients with progressive supranuclear palsy.

The neuronal number and nucleolar volume of the magnocellular population of the basal nucleus of Meynert in 6 patients with progressive supranuclear palsy (PSP) - one associated with Alzheimer's disease - were compared with those of 5 controls. In the 5 typical PSP cases, an age-dependent neuronal loss was demonstrated ranging from 12.6% to 54.1%. In the PSP-Alzheimer patient, the loss of cells amounted to 73.8% and the surviving neurons exhibited a reduction in the nucleolar volume, suggesting a reduced protein synthetic capability. The involvement of the basal nucleus is therefore a usual anatomical feature of PSP. The damage is less severe than generally observed in Alzheimer's disease and biochemical studies are required to state whether this is accompanied by a substantial cholinergic deficit.

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PubMed1984

Mapping of enkephalins in human brain. An immunohistofluorescence study on brains from patients with senile and presenile dementia.

The results of this study of the distribution of enkephalin-like immunoreactivity in four human "senile" and "presenile" brains by immunofluorescence microscopy (Coons' Method) showed specifically fluorescing varicosities containing fibres in the following areas: nucleus accumbens, nucleus caudatus, pallidum (mainly the external segment), septal nuclei, substantia innominata, hypothalamus, hypophysis, substantia nigra, nucleus interpeduncularis, locus coeruleus and other nuclei of the brain stem, most of the nuclei of the cranial nerves (mainly the sensitive) and spinal cord (mainly the substantia gelatinosa of the posterior horn). Fibres were observed surrounding cell bodies in the substantia nigra, in the nucleus raphe and in the anterior horn of the spinal cord (motor cells). Cylindrical ("pipe-shaped") structures formed by enkephalin-like immunoreactive fibres were seen in the pallidum, between the pallidum and the nucleus accumbens, and in the substantia nigra. A complete map of enkephalin-like immunoreactivity, based on Riley's Atlas of the human brain, is included. The distribution of enkephalin-like immunoreactivity showed many similarities to that in animal species that have been studied by immunohistochemistry (rat, primate) except for a lack of detectable enkephalin immunoreactivity in the amygdala in our material. No conclusions about the possible relationship of this finding to the clinical condition of dementia can be drawn without further work.

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PubMed1984

The basal nucleus of Meynert in idiopathic Parkinson's disease.

The basal nucleus of Meynert (bnM) was examined in 6 patients with idiopathic Parkinson's disease and in 5 age-matched controls. The histopathological study was followed by a quantitative analysis of the magnocellular population of the nucleus, with the determination of the number of neurons and their nucleolar volume. In Parkinson's disease, there was a neuronal loss ranging from 29.9% to 68.3% (mean 45.8%) and numerous surviving cells containing Lewy inclusion bodies. The percentage loss of cells did not display a significant correlation with the age of the patients, the duration of the illness, the mental state or the drug regime. On the other hand, no significant differences in nucleolar volume of bnM neurons were detected between patients and controls. The damage of the basal nucleus of Meynert in Parkinson's disease is less severe than that generally observed in Alzheimer's disease, and is slightly more pronounced than that reported for progressive supranuclear palsy.

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PubMed1983

Delta sleep-inducing peptide in the rat brain: an immunohistological microscopic study.

The authors have developed a method which makes it possible, for the first time, to visualize the delta sleep-inducing peptide in histological preparations and study it under the light and fluorescence microscope. Their research builds on Monnier 's discovery, in 1963, of a humoral hypnogenic factor in rabbits which was subsequently isolated and identified as a nonapeptide. Dubbed delta sleep-inducing peptide (DSIP), this factor was later detected in rat brain by radioimmunoassay but has eluded histological visualization until recently. In their work, the authors used an anti-DSIP antiserum suitable for immunohistological purposes. Two indirect immunohistological methods (PAP and immunofluorescence) allowed them to visualize, for the first time, structures containing specific DSIP-like immunoreactivity in some areas of the rat brain: indusium griseum, nucleus septi lateralis, hippocampus, striae longitudinales of Lancisi , bandeletta diagnalis of Broca, pallidum, hypothalamus, hypophysis and neocortex. Some DSIP pathways seem likely: (1) indusium griseum - striae longitudinales - hippocampus; (2) nucleus septi lateralis - striae longitudinales , bandeletta diagonalis - hippocampus; (3) neurons of the pyramidal layer of the hippocampus - gyrus dentatus; (4) pallidum - commissura of Ganser - hypothalamus. The possible correlations between DSIP neurons and neurons with other neurotransmitters are discussed. In preliminary clinical trials, DSIP has shown promise for the treatment of insomnia and the opiate and alcohol withdrawal syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Putative peptide neurotransmitters in human neuropathology: a review of topography and clinical implications.

In Huntington's disease, there is a decrease of the neuropeptides, substance P, enkephalins, and cholecystokinin in the striatonigral system, whereas in Parkinson's disease an increase of substance P is found in the substantia nigra. Several neuropeptides should be involved in Alzheimer's disease: substance P, endorphins, vasopressin, ACTH, somatostatin, vasoactive intestinal peptide, cholecystokinin, neurotensin, delta sleep-inducing peptide. Alterations of substance P, vasoactive intestinal peptide, cholecystokinin, somatostatin, and endorphins may be related to the pathophysiology of schizophrenia. Delta sleep-inducing peptide may interfere in addiction pathology.

Alzheimer Disease↗
PubMed1981

Antidepressants and serotonin neurons of the raphe.

Reserpine + nialamid administration to the rat induces a strong yellow fluorescence of the neuronal bodies of the raphe, due to serotonin (5-HT) accumulation. Under these conditions, administration of clomipramine (an antidepressant drug acting preferentially on 5-HT-mediated neurons) induces a decrease of intraneuronal fluorescence and its interneuronal diffusion. On this pattern we administered new antidepressant drugs which act on 5-HT neurons in a much more intensive way than clomipramine (fluvoxamine, clovoxamine, LM 5008, citalopram, Ro 11-2465). To varying degrees, we observed in the raphe, in addition to a decrease in intraneuronal fluorescence and interneuronal diffusion, the presence of a yellow fluorescence in capillary walls. It seems that under these antidepressants, 5-HT, which is outside neuronal bodies because of uptake blockade, is partly caught by the capillary walls. In these walls rich in monoamine oxydase, 5-HT would be catabolized, 5HIAA dispersed in the blood and thus, this 'capillary effect' could correspond to a loss of 5-HT in the raphe. Antidepressant drugs preferentially acting upon noradrenaline (NA) neurons do not, in this model, induce analogous phenomena in NA cell bodies of the locus coeruleus. So the 'capillary effect' differentiates antidepressant drugs acting specifically on 5-HT or NA neurons. It may be considered together with other parameters which also indicate asymmetries on the modes of action of antidepressant drugs, such as effects on monoamine turnover (increase for NA and decrease for 5-HT) and on receptor sensitivity (decrease for NA and increase for 5-HT).

Animals↗
PubMed1980

[The morphology of substance P in the human brain as determined by an immuno-histo-fluorescence study].

The application of Coon's indirect method, using antisubstance P antibodies, has permitted the immuno-histo-fluorescence study of the distribution of SP positive structures in 6 human brains. Several areas of the hemispheres and of the brainstem have shown axons of various sizes and densities exhibiting SP positive varicosities. Their topographic distribution was established for the human brain and compared with the distribution observed in the brain of the rat. Both distributions appeared very similar in the somato-sensorial systems of the spinal cord, medulla and pons, in the structures of the midbrain tectum and tegmentum as well as in those of the thalamus and hypothalamus. Substantia nigra and globus pallidus showed a large amount of substance P, in human brain as well as in the rat, but in human brain, substance P positive axons were arranged in a longitudinal peridendritic "pipe" shaped manner, particularly in the antero-external and superior part of the substantia nigra as well as in the internal segment of the globus pallidus; such "pipes" were rarely seen in the rat. Moreover, in man, the pallidal substance P was almost exclusively seen in the internal segment while it spreads to the external segment in the rat. Substance P was found to be scarce in the rhinencephalic and limbic structures, the amygdala and the olfactory bulb of man, contrary to their abundance in the rat, but this peculiarity could be due more to some pathological changes associated with the advanced age of the patients whose brains were studied than to an interspecific difference.

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PubMed1979

[Senile plaques, neuro-fibrillar degeneration and other associated cerebral lesions (morphology and pathogenetic theory].

A brief review about present knowledge on morphology of brain degenerative alterations in the elderly, their topography, their correlations and the various pathogenic theories. The particular pathoclisis of some areas is reported, i.e. the pathoclisis of some hippocampal areas for neurofibrillary tangles and senile plaques, the pathoclisis of the IVth layer of calcarinian cortex for dyshoric angiopathia. These morphological pecularities must be correlated to more recent data concerning alterations of neurotransmitters and their enzymes.

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PubMed1979

[Mechanisms of action of the antidepressants (author's transl)].

The tricyclic and related antidepressants reduce monoamine uptake at the synapses, block the presynaptic receptors and, after chronic administration, act upon the synthesis of the monoamines and the sensitivity of the post-synaptic receptors. The NA and 5-HT synapses are influenced to different degrees by the antidepressants: for example, desipramine has a preponderance of activity at NA synapses and clomipramine at 5-HT synapses. By combining these findings and by highlighting one or other of these properties, it is possible to come to diametrically opposite conclusions upon the effect of the antidepressants upon monoamine performance (activation or inhibition) and to develop many models of the mechanisms of antidepressant action. The authors describe some of these and stress the model which is at the basis of the studies being carried out at the Department of Psychiatry of the University of Geneva.

Animals↗
PubMed1978

The malignancy of dementias.

Sruvival times were determined for 982 patients admitted over a ten-year period to the Geneva Psychiatric Clinic. Patients with dementia had one-third the life expectancy of controls. Among patients classed as having Alzheimer disease, the longest survival times were in those with neurofibrillary tangles involving the neocortex, while those lacking this anatomical abnormality had the shortest survival times. Except for women with Alzheimer disease, patients with dementia had less than 10% life expectancy from the time of their admission to the clinic compared to the life expectancy of Geneva's population.

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PubMed1978

[Pallido-dentate calcifications (apropos of 7 anatomo-clinical case reports)].

"Fahr's Disease" is characterized by bilateral and symmetrical calcifications of the Globus Pallidus (systematically extending to the Commisura Anterior and the Capsula Interna, and less commonly to the Putamen, the Centrum Semi-Ovale and the Cerebral Cortex), and of the Cerebellar Nucleus Dentalus (with spreading to the White Matter and the Cortical Lamellae). Lesions or absence of Parathyroids are frequently related, with subsequent metabolic disorders of Phosphorus and Calcium, but idiopathic cases without hypoparathyroid disturbances are also found. A Morgagni-Morel Hyperostosis Frontalis Interna is often associated with "Fahr's Disease", and there could be a relationship between these two affections. We found in three cases the association between "Fahr's Disease" and Morel's Nodular Dysgenesis of the Frontal Cortex. Most of the cases are sporadic, but observations with a clear familial incidence are also found. Clinically, various Neurological Disorders (cerebellar, extrapyramidal, pyramidal, dysarthria, epileptic seizures) are often but not always observed; the Psychiatric Disorders found in some cases could be fortuitious associations (psychoses), connected to hypothyroidism (oligophrenia), and in aged patients, to unrelated cerebral vascular or degenerative lesions; very seldom, a dementing state could be connected to the spreading of calcifications to the Cerebral Cortex.

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PubMed1977

Paradoxical sleep and brain catecholamines in the rat after single and repeated administration of alpha-methyl-paratyrosine.

This study is concerned with the role of catecholamines (CA) in the regulation of paradoxical sleep (PS) in the rat. Alpha-methyl-paratyrosine (alphaMPT), an inhibitor of tyrosine hydroxylase, was used in a multiple administration schedule in order to avoid toxic effects. From 2 to 10 doses of 75 mg/kg of alphaMPT, a progressive reduction of green fluorescence occurred in CA cell bodies as well as in terminals. The green fluorescence reduction was faster in dopaminergic than in noradrenergic neurons, and faster in cell bodies than in terminals. Sleep recordings showed a slight increase of PS after one or two doses of 75 mg/kg of alphaMPT, and a dose-related decrease after 3-7 injections. After two doses of 75 mg/kg, the number of PS phases was significantly increased. This can be due to the release of a non-CA PS primer mechanism. These experiments support the view that an intact synaptic transmission in CA neurons is necessary for the realization of PS.

Adrenergic Fibers↗