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C Bouras

Publications and source records attributed to C Bouras.

At least 109 records · Page 6Linked to original sources
PubMed1990

Substance P immunoreactivity in Alzheimer disease: a study in cases presenting symmetric or asymmetric cortical atrophy.

Substance P-like immunoreactivity was visualized by immunohistochemical methods in 20 postmortem brains: 6 senile, 4 presenile Alzheimer dementia (AD), 3 AD with interhemispheric asymmetric cortical atrophy, and 7 control cases. For all pathological cases, the SP-like immunoreactivity was significantly reduced in the neocortical areas and in the hippocampus. This contrasted with an enhanced SP-like immunoreactivity in the pallidum and the substantia nigra in AD brains and a more pronounced SP-like immunoreactivity in the more atrophic side in the asymmetrically atrophied brains.

Aged↗
PubMed1989

Balint's syndrome in Alzheimer's disease: specific disruption of the occipito-parietal visual pathway.

Previous quantitative neuropathologic analyses have shown that the association cortices of the temporal and frontal lobes are more damaged than the visual regions of the occipital lobe in Alzheimer's disease. In the present paper, we report on a subpopulation of Alzheimer's disease patients presenting a visual defect referred to as Balint's syndrome, and displaying a global caudal shift in pathology. Balint's syndrome is a defect in visuospatial skills, and the distribution of pathology suggests that the connections underlying this functional component of the visual system are devastated, whereas they are normally spared in Alzheimer's disease. These results suggest that multiple subtypes of Alzheimer's disease exist with differential distribution of pathology and corresponding neurologic symptomatology, and that neuritic plaque and neurofibrillary tangle formation involve the loss of specific corticocortical projections associated with specific functional deficits and identifiable neurologic syndromes.

Aged↗
PubMed1989

An improved immunohistostaining procedure for peptides in human brain.

Floating sections from human brains immersed for more than forty years in formalin, or from brains freshly fixed for a short time are treated by KMnO4-Pal's modified solutions to suppress the endogenous peroxidase activity before using the peroxidase-antiperoxidase method (PAP), or to remove the autofluorescence of lipofuscin, which is very intense in brains from old patients, before using the immunofluorescence method. Following this, immersion of sections in NaOH and H2O2 allows for the demasking of antigenic sites. These treatments enhance the immunolabelling considerably, with results comparable to those obtained with freshly fixed tissues, and facilitate the discrimination between specifically and unspecifically stained structures.

Aged↗
PubMed1989

Down patients: extracellular preamyloid deposits precede neuritic degeneration and senile plaques.

Using anti-SP28 (a polyclonal antibody to a 28 residue synthetic peptide homologous to the NH2-terminal region of the Alzheimer amyloid beta-protein) to investigate the cerebral cortex of 6 Down patients aged 6-55 y, we found that, besides senile plaques and congophilic vessels, extracellular deposits unrelated to degenerating neurites, tangle-bearing neurons or congophilic vessels were labelled. These deposits were similar to the extracellular deposits previously observed in the cerebral cortex of Alzheimer patients and non-demented individuals. The material accumulated in the deposits did not react with Congo red, thioflavine S or, on some occasions, silver salts and therefore might have been constituted by beta-protein precursors lacking the molecular conformation of amyloid fibrils. Age-related analysis of the cortical lesions in Down patients suggested that such extracellular deposits precede degenerating neurites and evolve into senile plaques.

Adult↗
PubMed1989

Immunohistochemical colocalization of delta sleep-inducing peptide and luteinizing hormone-releasing hormone in rabbit brain neurons.

The anatomical distributions of luteinizing hormone-releasing hormone and delta sleep-inducing peptide immunoreactivity in the rabbit brain were studied by indirect immunofluorescence technique. The comparison of adjacent serial sections, one being immunolabeled with an antiserum to luteinizing hormone-releasing hormone, the other with an antiserum to delta sleep-inducing peptide, showed that the respective distribution patterns of immunoreactivity exhibited a remarkable overlap through the basal forebrain and hypothalamic regions. A sequential double-immunolabelling (elution-restaining method) clearly indicated that all the luteinizing hormone-releasing hormone-immunoreactive cell bodies displayed delta sleep-inducing peptide immunoreactivity. These cell bodies were sparse and mainly located throughout the septal-preoptico-suprachiasmatic region and the ventrolateral hypothalamus. The colocalization of luteinizing hormone-releasing hormone and delta sleep-inducing peptide immunoreactivity was also observed in many fibres supplying all these brain regions and terminal areas such as the organum vasculosum of the lamina terminalis, the subfornical organ, the median eminence and the pituitary stalk. These neuroanatomical findings are suggestive of interaction between delta sleep-inducing peptide and luteinizing hormone-releasing hormone in various brain areas including some circumventricular organs.

Brain↗
PubMed1989

Immunohistochemical distribution of delta sleep inducing peptide in the rabbit brain and hypophysis.

The distribution of delta sleep inducing peptide (DSIP) in the rabbit brain has been studied with immunohistochemical techniques. DSIP-like immunoreactivity was predominantly detected in the basal forebrain, hypothalamus and hypophysis. Even in colchicine-pretreated animals, immunolabeled cell bodies were relatively few. They were mostly scattered through the ventrolateral septum, the diagonal band of Broca and preoptic areas. Clusters of positive cell bodies were also found in the arcuate nucleus and adjacent lateral hypothalamic areas. Large populations of varicose fibers and terminal-like structures were observed in the juxtaventricular zone of the ventrolateral septum, in the preoptic areas and lamina terminalis especially around the preoptic recess of the third ventricle and more caudally, in the ventromedial nucleus of the hypothalamus. Dense networks of immunolabeled fibers were visualized in the median eminence and pituitary stalk where many fibers could be seen in close apposition to the capillaries. Many DSIP-immunoreactive fibers were observed in the subfornical organ. Other extra-hypothalamic regions displaying a low-to-moderate density of immunoreactive fibers were the indusium griseum, the hippocampus, the fimbria of the fornix, the subcommissural organ, the medial habenula and, occasionally, the medial periaqueductal gray. Most cells of the pars intermedia and a few cells of the pars distalis of the anterior pituitary were DSIP-immunoreactive. Taken together these results in the rabbit brain emphasize the predominant localization of DSIP-like immunoreactivity in areas related to the hypothalamic neurosecretory systems.

Animals↗
PubMed1988

Distribution and colocalization of delta sleep inducing peptide (DSIP) with corticotropin-like intermediate lobe peptide (CLIP) in the human hypophysis.

DSIP and CLIP [ACTH(18-39)] immunoreactive (IR) neurons and fibers were examined in the human hypophysis and pituitary stalk using immunmohistofluorescence and peroxidase-antiperoxidase methods. Double-stained and adjacent stained sections demonstrate that DSIP is colocalized in about 75% of CLIP-IR-like cells in the anterior pituitary and in residual intermediate lobe cells. Only few CLIP-IR-like fibers are observed in the posterior lobe. On the contrary, a high density of DSIP-IR fibers is visualized in the stalk. It is suggested that DSIP acts as a sleep promoting factor (one of many other actions) and that CLIP increases the paradoxical sleep, so that these two peptides could play a role in the regulating system of the sleep-waking cycle.

Adrenocorticotropic Hormone↗
PubMed1988

[Distribution of the delta sleep-inducing peptide in the brain of rabbits: study by immunofluorescence].

Using the indirect immunofluorescence method, the distribution of the Delta Sleep Inducing Peptide (DSIP)-containing neurons was studied in the rabbit brain. DSIP antisera were raised in rat by multiple injections of synthetic DSIP conjugated to thyroglobulin. Some DSIP immunoreactive cell bodies were detected in the diagonal band of Broca and anterior part of the hypothalamus. Large populations of immunofluorescent fibers and terminals were visualized mainly through the organum vasculosum of the lamina terminalis, the preoptic areas, the subfornical organ, the thalamus, the ventromedial hypothalamus and infundibulum. Further, most of the cells of the intermediate lobe of the hypophysis displayed DSIP-immunoreactivity. The predominant localization of DSIP-immunoreactive fibers and terminals in certain circumventricular organs suggests that DSIP could play a specific role in the neurohumoral regulation.

Animals↗
PubMed1987

A monoclonal antibody to non-phosphorylated neurofilament protein marks the vulnerable cortical neurons in Alzheimer's disease.

Various cytoskeletal proteins have been implicated in the formation of neurofibrillary tangles in Alzheimer's disease. A monoclonal antibody to non-phosphorylated neurofilament protein labels a distinct subset of pyramidal cells in the normal human cortex which have a distribution very similar to that of neurofibrillary tangles in brains from patients with Alzheimer's disease. In addition, regions and layers that normally contain a high density of such cells, in Alzheimer's disease, have large numbers of neurofibrillary tangles and few remaining immunoreactive cells.

Aged↗
PubMed1987

An immunohistochemical study of pro-somatostatin-derived peptides in the human brain.

The distribution of pro-somatostatin-derived-peptide-positive profiles was examined by indirect immunohistofluorescence in nine post-mortem human brains (age 58-73 years). Three specific antisera were used for this study which recognize, respectively, somatostatin-28, somatostatin-28 (1-12) and somatostatin (1-14). Pro-somatostatin-derived-peptide-positive immunoreactive profiles were observed throughout the neuraxis. Cell bodies were found within archeo-, paleo- and neocortical areas, the subcortical white matter, in the nucleus accumbens, caudate nucleus and putamen, as well as in the hypothalamus, the reticular thalamic nucleus and the reticular formation of the brainstem. Fibers and terminals were seen in the same areas as well as in various thalamic nuclei, in the brainstem and spinal cord. Pro-somatostatin-derived-peptide-positive fibre tracts include the bed nucleus of the stria terminalis, the diagonal band of Broca, the stria medullaris, the inter-thalamic adhesion, the posterior commissure and the spinothalamic tract. Furthermore, differences between human and animal brains were noted and some somatostatin systems reported which may be implicated in certain human neuropathological states.

Aged↗
PubMed1986

Substance P neuronal cell bodies in the human brain: complete mapping by immunohistofluorescence.

The localization of substance P-immunoreactive (SP-IR) cells was studied in 5 postmortem brains from aged human subjects using technical improvements combined with the indirect immunofluorescence method. The presence of various forms of SP-IR cells was observed in paleocortical and neocortical areas as well as in the basal ganglia, the brainstem and the spinal cord. The distribution of these SP-IR cell bodies was transposed onto our previous mapping of SP-IR fibers and terminals. The morphological differences between SP-containing cell bodies or areas of human and rat central nervous systems and the SP-changes in various states of human pathology are shortly discussed.

Aged↗
PubMed1986

Neuropeptides in Alzheimer's disease: a review and morphological results.

The anatomic distribution of classical neurotransmitters, i.e. NA, DA, 5HT, ACH and GABA in the post-mortem autopsied brain of Alzheimer's disease (AD) has been reviewed. In addition, the results and reviews reported in this paper give evidence for the change of a large number of neuropeptides in AD on the basis of immunohistochemical criteria. Among numerous peptidergic systems, abnormalities in SP, SS, NT and VIP have been observed. Therefore, no changes in the concentrations of CCK and TRH were reported. In this study, using immunohistochemical methods for SS changes in post-mortem brain material of three cases of AD and two controls, the following changes were observed: An important reduction of the SS-positive cell bodies and fibres in the cortex, the hippocampus, parahippocampic cortex, and neocortex, particularly in the parietal and frontal areas, as well as a reduction of SS cell bodies and fibres in the sub-cortical white matter. An amorphous SS-positive material in or close to the corona of a number of senile plaques. An important decrease of SS fibres and cell bodies in the lateral septi nuclei. An increase of the number and immunoreactive intensity of SS-positive fibres in the substantia innominata. In animal studies, an interaction between SS- and ACH turnover in the substantia innominata is reported. The GABA decrease as well as the SS deficit in the cortex area and sub-cortical white matter may lead to the interaction between SS and other neurotransmitters in AD.

Aged↗
PubMed1986

Differential effects of acute and chronic administration of haloperidol on substance P and enkephalins in diverse rat brain areas.

Rats received 10 mg/kg/day of haloperidol during up to 9.5 weeks. Substance P, Leu- and Met-enkephalins, were studied in brain using immunohistochemical methods. Haloperidol modified the peptides immunoreactivity in most brain areas. The time necessary to observe the effects of haloperidol on the peptides varied individually, depending on the peptide and the brain area. Moreover, inversions of these effects were often observed, generally occurring between in 5th and 7th day of drug administration. Substance P was increased after haloperidol in the hypophysis, a finding hereto not described. This descriptive study identified none of these three peptides as a single and specific target for dopaminergic receptor blockade. Methodological issues in evaluating the effects of neuroleptics on brain peptides are discussed.

Amygdala↗
PubMed1986

An immunohistochemical study of six biologically active peptides in the human brain.

The morphological characteristics and distribution patterns of neurons immunoreactive for antisera against six biologically active peptides were examined by indirect immunofluorescence in the human brain. The peptides studied were: met-enkephalin, leu-enkephalin, substance P, somatostatin, cholecystokinin and vasoactive intestinal peptide. The tissue samples for this study were removed, dissected and placed into fixative within 4 h post-mortem. Regional differences throughout the entire neuraxis were observed in the localization of cell bodies, fibers and terminals for the various peptides. The observations reported in this article demonstrate certain distribution patterns for peptide immunoreactivities that appear to be specific to the human brain when compared to other species. These morphologic studies establish a valuable framework for the further analysis of the role of peptide-containing neuronal circuits in normal and diseased human brain.

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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.

Aged↗
PubMed1984

Evaluation of the levels of free and total amitriptyline and metabolites in the plasma and brain of the rat after long-term administration of doses used in receptor studies.

This study was conducted in order to investigate the level of amitriptyline (AT) and its metabolites. Three separate experiments were carried out. In two of these experiments, rats were treated over 7 days with IP doses of AT (10 mg/kg in experiment A and 2 X 20 mg/kg in experiment C). The rats were sacrificed either 2 (experiment C) or 12 h (experiments A and C) after the last dose. In experiment B, rats were sacrificed 2 or 12 h after a single dose of 20 mg/kg AT. The results of these experiments showed the following: in experiment A only AT was measurable in the brain and in the plasma, in contrast to experiments B and C, where NT and the hydroxylated metabolites AT-OH and NT-OH reached significant levels in the plasma and in the brain. The concentrations of AT-OH, NT-OH, and NT (12-h values) that were found in the brain are probably not pharmacologically relevant. The 12-h plasma values of all compounds tested were, even with the highest dose, lower than those expected to be clinically effective in man. Our results suggest that AT, at higher doses, may induce its own metabolism. The free plasma levels of this drug and its metabolites are higher in man than in the rat. The possible implications of these results in the use of antidepressants in the treatment of depression are discussed.

Amitriptyline↗
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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