PubMed Health⌕ Search

Biomedical subjects

P Anglade

Publications and source records attributed to P Anglade.

At least 37 records · Page 2Linked to original sources
PubMed1995

Plasticity of nerve afferents to nigrostriatal neurons in Parkinson's disease.

Clinical symptoms in Parkinson's disease do not appear until almost total depletion of dopamine has occurred in the striatum, suggesting the existence of compensatory mechanisms to offset the loss of nigrostriatal dopaminergic neurons. This compensation has been attributed mainly to an increased turnover of dopamine in the remaining dopaminergic neurons. Besides this biochemical phenomenon intrinsic to dopaminergic neurons, we tested whether morphological changes in the nerve afferents to the dopaminergic neurons could participate in these compensatory mechanisms. The afferents to the dendrites of dopaminergic neurons were analyzed ultrastructurally in the substantia nigra of parkinsonian patients and matched controls, using simultaneous histochemical detection of acetylcholine-like cation and tyrosine hydroxylase. The size of acetylcholine-like cation-containing terminals in contact with dopaminergic dendrites increased significantly by 38% in the substantia nigra of parkinsonian patients; whereas their number per section of dopaminergic dendrite showed an increase of 60%, although not reaching statistical significance. The number of the terminals devoid of acetylcholine-like cation per section of dopaminergic dendrite decreased significantly by 52% in the substantia nigra of parkinsonian patients. These results suggest (1) a plasticity of excitatory cholinergic neurons targeting nigral dopaminergic neurons and (2) an involution of noncholinergic nerve terminals, mostly originating from inhibitory nigral, pallidal, and striatal GABAergic neurons. The findings provide evidence of a capacity for neuronal plasticity in the elderly human brain, even in the presence of neurodegenerative disorders.

Acetylcholine↗
PubMed1995

New data on the proteins of rabbit (Oryctolagus cuniculus) milk.

The main rabbit milk proteins have previously been prepared by reversed-phase HPLC of the acid-precipitated material ('whole casein') and of its supernatant (acid whey). Most of them were nearly homogeneous on SDS-PAGE. Among those isolated from whole casein, alpha s1-, beta- and kappa-caseins, as well as whey acidic protein (WAP) were identified by N-terminal sequencing. After further internal sequencing, two unknown proteins were found to be the putative products, alpha s2a- and alpha s2b-caseins of two recently sequenced transcripts from rabbit mammary gland. Each whole casein component gave several bands on IEF. For kappa-casein, this was probably due to uneven glycosylation as in all kappa-caseins studied so far. For the other whole casein components, including WAP, the number of bands roughly reflected the number of potential phosphorylation sites predicted from the sequences. For alpha s1- and alpha s2-caseins polymorphism could be detected. From acid whey, in addition to WAP, which was a minor component, reversed phase HPLC separated three proteins. These were alpha-lactalbumin, transferrin and serum albumin, on the basis of their apparent molecular weights deduced from SDS-PAGE. WAP was a major component of the native whey obtained by ultracentrifugation of rabbit milk. It was found to consist of two identical subunits linked by at least one disulfide bridge.

Amino Acid Sequence↗
PubMed1994

Monoamine vesicular uptake sites in patients with Parkinson's disease and Alzheimer's disease, as measured by tritiated dihydrotetrabenazine autoradiography.

The monoaminergic innervation of the caudate nucleus, putamen and ventral striatum was investigated post mortem, in patients with Parkinson's and Alzheimer's disease as compared to control subjects, by autoradiographic detection of tritiated dihydrotetrabenazine (3H-TBZOH), a specific high affinity ligand of the vesicular monoamine transporter. The binding of 3H-TBZOH was specific and saturable (Kd 5.3 nM). In control striatum, the pattern of distribution of 3H-TBZOH binding was heterogeneous, with higher binding levels in the 'matrix' than in the 'striosome' compartment. Changes in ligand binding levels were observed in the pathological brains compared to controls. In Parkinson's disease (PD), characterized by a severe damage of mesostriatal dopaminergic neurons, the density of 3H-TBZOH binding was reduced. A severe decrease in 3H-TBZOH binding was observed in all parts of the striatum (caudate nucleus: -80%, putamen: -86%, ventral striatum: -94%) in PD brains. The data corroborate the deficiency in striatal dopaminergic transmission and suggest that in PD brains dopaminergic terminals have disappeared and/or no longer contain synaptic vesicles. In Alzheimer's disease (AD), 3H-TBZOH binding was significantly reduced by 57% in the ventral striatum and not in the caudate nucleus and putamen. The specific decrease of monoaminergic transporter levels in the ventral striatum confirm that this nucleus is a target area in AD.

Aged↗
PubMed1994

Immunocytochemical analysis of tumor necrosis factor and its receptors in Parkinson's disease.

Activated glial cells observed in the substantia nigra in Parkinson's disease may participate in the mechanism of nerve cell death by providing toxic substances such as cytokines. Among these compounds, tumor necrosis factor-alpha (TNF) is of interest because it can provoke cell death. We detected TNF-immunoreactive glial cells in the substantia nigra of parkinsonian patients but not in those of control subjects. Immunoreactivity for TNF receptors was found in cell bodies and processes of most dopaminergic neurons of control and parkinsonian subjects, suggesting that nigral dopaminergic neurons might be sensitive to TNF produced in Parkinson's disease. These results suggest that TNF may participate in the degenerative processes occurring in Parkinson's disease, at least after a primary insult inducing a reactive gliosis.

Aged↗
PubMed1994

Morphological and molecular characterization of the response of differentiated PC12 cells to calcium stress.

The mechanisms that lead ultimately to neuronal death in pathological ageing of the brain remain mostly unknown as in the case of Parkinson's disease where there is a progressive and selective loss of dopaminergic neurons within the substantia nigra. Dopamine-expressing PC12 cells that were neuronally differentiated by nerve growth factor treatment were chosen as a culture model in which to study some of the changes that may occur during the course of the degenerative process. They were exposed to the calcium ionophore A23187 in order to produce a sustained rise in cytoplasmic calcium, a phenomenon related to various pathological conditions. The degenerative effects of the ionophore were dose- and time-dependent. They were characterized by early fragmentation of the neurites followed ultimately by a loss in cell viability. Biochemical changes, such as a decrease in [3H]dopamine uptake and modulations of the tyrosine hydroxylase gene, were detected before macroscopic evidence of cell suffering (e.g. neurite fragmentation) could be observed. Although an ongoing degenerative process was occurring in cell somata, PC12 cells were able to recover upon ionophore withdrawal. Characteristics of apoptosis such as chromatin condensation and DNA fragmentation were detectable in a small population of dying cells. DNA fragmentation could be prevented by the endonuclease inhibitor aurintricarboxylic acid. New protein synthesis was not required, as cycloheximide failed to prevent degeneration. Taken together, these results suggest that differentiated PC12 cells react to calcium stress through a sequence of regulatory processes which appears to be independent of the apoptotic pathway.

Animals↗
PubMed1994

Distribution of manganese-dependent superoxide dismutase in the human brain.

The distribution of manganese-dependent superoxide dismutase, an enzyme that transforms superoxide radicals into hydrogen peroxide, was studied in the human brain post mortem using a sheep polyclonal antiserum raised against the enzyme from liver mitochondria. One band, corresponding to a protein of 22,000 mol. wt was detected in the human brain by western blot analysis. At the light-microscopy level, a punctate immunostaining was observed in the neuropil and in some but not all, glial and neuronal cell bodies. Electron-microscopy revealed that the staining was exclusively confined to the inner mitochondrial membrane. A heterogeneous distribution of manganese-dependent superoxide dismutase was observed in the human brain. In the forebrain, numerous immunostained neurons were detected in the striatum, thalamus, pallidal complex and the nucleus basalis of Meynert. In the cerebellum, only granular and Purkinje cells were immunostained. Various nuclei from the brainstem displayed superoxide dismutase immunoreactivity, including the cranial nerve nuclei, the nucleus supratrochlearis, the red nucleus, the substantia nigra, the nucleus cuneiformis and subcuneiformis, the nucleus parabigeminal, the nucleus centralis superior, the nucleus supraspinalis, the nucleus of the medullae oblongata and the gigantocellularis nucleus. Large pyramidal neurons containing superoxide dismutase were detected in the CA subsectors, the hilus of the hippocampus and the cerebral cortex. Smaller immunostained neurons were also observed in layers I, IV and VI of all cortical regions studied. The distribution of immunostained glial cells was more limited, and restricted to the internal and external capsules, the hypothalamus, the red nucleus, the pyramidal white matter and surrounding areas, the cerebral cortex and the sub-ependymal layer, the alveus and the stratum oriens of the hippocampus. This heterogeneous but not ubiquitous distribution of cells expressing manganese-dependent superoxide dismutase suggests that not all cells in the human brain are protected to the same extent against the deleterious effects of superoxide.

Aged↗
PubMed1994

Immunohistochemical study of catechol-O-methyltransferase in the human mesostriatal system.

The cellular localization of catechol-O-methyltransferase was analysed in the mesostriatal system of human brain post mortem by means of immunohistochemistry. In the human nigral complex, catechol-O-methyltransferase immunostaining was not detected in melanized dopaminergic neurons, except in the ventral tegmental area and substantia nigra pars lateralis, where few neurons displayed intense immunolabelling. In the striatum, catechol-O-methyltransferase immunostaining was found in numerous cell bodies and in the neuropile. Observations at the electron microscope level revealed that catechol-O-methyltransferase immunoreactivity was present in the cell bodies of neurons and their processes, including the dendritic spines. No catechol-O-methyltransferase immunolabelling was observed in striatal nerve terminals in contact with dendritic spines, indicating that dopaminergic nerve terminals do not exhibit catechol-O-methyltransferase immunoreactivity. Catechol-O-methyltransferase-immunoreactive cell bodies and processes of glial cells were also detected in the striatum. The data suggest that catechol-O-methyltransferase is either not expressed or only slightly expressed by the dopaminergic nigrostriatal neurons, whereas it is clearly present in striatal neurons and glial cells. Thus, the catabolic degradation of striatal released dopamine by its O-methylation may involve postsynaptic neurons rather than dopaminergic presynaptic neurons. The presence of catechol-O-methyltransferase in some dopaminergic neurons of the ventral tegmental area and substantia nigra pars lateralis suggests that methylation of dopamine may occur in these neurons, which may consequently be better protected against dopamine auto-oxidation than those of the substantia nigra pars compacta.

Animals↗
PubMed1993

Even in culture, oligodendrocytes myelinate solely axons.

Cerebral hemispheres from mouse embryos at 15 days of gestation were dissociated and maintained in culture for several weeks in a medium which permitted homochronic and homotypic oligodendrocytes and neurons to interact in the presence of other central nervous system cells. After 13-14 days in culture a few oligodendrocytes changed from highly branched, "sun-like," nonmyelinating cells to sparcely branched myelinating cells. The number of fibers myelinated per oligodendrocyte ranged from 1 to 10, similar to that described previously in vivo in the corpus callosum. When an oligodendrocyte began to myelinate, it immediately myelinated a maximum number of fibers, suggesting that the number of axons to be myelinated by the oligodendrocyte was predetermined. When only one fiber was in the vicinity of a myelinating oligodendrocyte, whorls of myelin-like figures were seen at the tip of oligodendrocyte processes that had not reached an axon. Myelinated fibers were unambiguously identified as axons both by immunostaining and by electron microscopy. Myelin was not observed around astrocyte processes or around dendrites. The exclusive myelination of axons suggests the existence of a specific axonal recognition signal which attracts oligodendrocyte processes.

Animals↗
PubMed1993

Biochemical characterization of the bovine genetic kappa-casein C and E variants.

Analysis of elution profiles of enzymatic and CNBr digests of kappa-caseins C and E, and sequencing of most relevant peptides allowed the chemical characterization of both genetic variants. They differ from their B and A allelic counterparts by a single substitution, His97/Arg and Gly155/Ser, respectively. Electrophoretic behaviour of the investigated C and E variants was in good agreement with the observed amino acid replacements.

Alleles↗
PubMed1993

Ultrastructural relations between nigrostriatal dopaminergic neurons and cholinergic nerve endings in the human brain.

The connections between cholinergic nerve endings and nigrostriatal dopaminergic neurons were studied in the substantia nigra pars compacta of the human brain. Immunocytochemistry of tyrosine hydroxylase followed by ionic fixation of acetylcholine-like cation in synaptic vesicles allowed dopaminergic neurons and cholinergic nerve endings to be visualized on the same ultrathin section. Numerous contacts, some of them with synaptic structures, were observed between nerve endings, with or without precipitates of acetylcholine-like cation and dendrites or cell bodies of tyrosine hydroxylase-immunoreactive neurons. These results, which agree with previous studies performed in the rat, suggest that cholinergic nerve endings control the activity of the nigrostriatal neurons at the level of the dendrites and cell bodies in the substantia nigra.

Aged↗
PubMed1992

Cryoultramicrotomy: electrostatic transfer of dry ultrathin frozen sections on grids applied to the central nervous system.

Due to the extreme fragility of ultrathin frozen sections of brain tissue, the cryoultramicrotomy of non-embedded tissue has not been sufficiently used for immunocytochemical studies of the central nervous system. Sections are easily disrupted by the liquid surface tension when a droplet of sucrose is used (method by Tokuyasu, 1973) for their transfer on the grids. Use of silicotungstic acid (Tsuji, 1986) in place of sucrose improved the preservation of the ultrastructure but still could not resolve the difficulty. This report describes a new procedure for transferring dry ultrathin frozen sections by means of electrostatic attraction induced on the membrane covering the grids. Once attached electrostatically to the membrane, the sections were retained by van der Waals' forces. The dry ultrathin frozen sections obtained from both fresh and fixed brains displayed good preservation of their ultrastructures over a large surface. This new method which electrostatically transfers dry ultrathin frozen sections, avoiding the use of any liquid, is expected to serve for the immunocytochemical identification of neuronal cell bodies and terminals as well as their neurotransmitters and enzymes in both fresh and fixed brains.

Animals↗
PubMed1992

Peristaltic movement evoked in intestinal tube devoid of mucosa and submucosa.

Computerized analysis of video-recorded peristalsis was made in a preparation of guinea-pig ileum tube from which both mucosa and submucosa were mechanically scraped off. Threshold value for provoking peristalsis was higher, conduction velocity of peristalsis was slower, and peristaltic force was weaker in comparison with the ileum tube from which only mucosa was scraped off and with the normal ileum tube. A histological control of the preparation proved that there was no nerve cell body of submucous plexus on the surface of separated circular muscle. It was concluded that peristalsis, though impaired, could be provoked by way of activation of the reflex arch consisted by neural circuit of myenteric neurons which should be produced by excitation of stretch receptors in the muscularis externa.

Animals↗
PubMed1991

Primary structure of bovine lactoperoxidase, a fourth member of a mammalian heme peroxidase family.

Much is known about bovine lactoperoxidase but no data are available on its primary structure. In this work its main active fraction was isolated from cow's milk and sequenced using a conventional strategy. A clear similarity was found with human myeloperoxidase, eosinophil peroxidase and thyroperoxidase, the sequences of which were recently elucidated from those of their cDNAs and/or genes. The single peptide chain of bovine lactoperoxidase contains 612 amino acid residues, including 15 half-cystines and 4 or 5 potential N-glycosylation sites. The corresponding peptide segments of human myeloperoxidase, eosinophil peroxidase and thyroperoxidase display 55%, 54% and 45% identity with bovine lactoperoxidase, respectively, with 14 out of the 15 half-cystines present in each of the four enzymes being located in identical positions. The occurrence of an odd number of half-cystines in bovine lactoperoxidase supports the recent finding of a heme thiol released from this enzyme by a reducing agent, suggesting that the heme is bound to the peptide chain via a disulfide linkage, since the absence of free thiol in the enzyme was reported long ago.

Amino Acid Sequence↗
PubMed1991

Localization of substance P, CGRP, VIP, neuropeptide Y, and somatostatin immunoreactive nerve fibers in the carotid labyrinths of some amphibian species.

Immunohistochemical localization of substance P (SP), CGRP, VIP, neuropeptide Y (NPY), and somatostatin (SOM) in the carotid labyrinth were compared in some species of amphibians using the peroxidase-antiperoxidase method. Immunoreactivity of SP, CGRP, VIP, and NPY was found in the nerve fibers distributed in the intervascular stroma of the carotid labyrinth. SP, CGRP, and VIP immunoreactive varicose fibers were densely distributed in the peripheral portion of the carotid labyrinth. Some SP-immunoreactive fibers were distributed similarly to CGRP-immunoreactive fibers. The density of NPY and SOM immunoreactive varicose fibers was low. No immunoreactivity of enkephalins was observed in the labyrinth. The intensities of these peptides were varied from species to species. No glomus cells showed immunoreactivity for any of the 7 peptides studied. These results suggest that the vascular regulatory function, which is one of the possible functions of the carotid labyrinth, is controlled by the peptidergic mechanisms in addition to regulation through intimate apposition of glomus and smooth muscle cells (g-s connection).

Ambystoma↗
PubMed1990

Identification of the binding sites of benzyl penicilloyl, the allergenic metabolite of penicillin, on the serum albumin molecule.

Tryptic digests of fragment A299-585 of penicilloylated serum albumin obtained from two penicillin-treated patients or prepared by in vitro conjugation, were analyzed by a tandem immunoaffinity reversed-phase HLPC. Determinations of benzyl penicilloyl groups (BPO) were performed on the different fractions. Three BPO containing peptides were identified by their amino acid sequence and the bound BPO were located on lysines 432, 541 and 545. Six major BPO binding sites were thus identified on the whole albumin molecule. All of them are lysine residues and correspond to a limited number of definite structures in which lysine and serine residues appear to be closely associated.

Amino Acid Sequence↗
PubMed1990

Ultrastructural simultaneous localization of vasoactive intestinal polypeptide immunoreactivity and the acetylcholine-like cation in rat endocrine pancreas.

The ultrastructural co-localization of vasoactive intestinal polypeptide (VIP) and acetylcholine (ACh)-like cation was demonstrated in the rat endocrine pancreas. Immunoperoxidase cytochemical procedure for the detection of VIP was followed by ionic fixation of ACh by silicotungstic acid. All the VIP-immunoreactive nerve endings displayed punctiform precipitates revealing ACh-like cations in the small clear vesicles. Almost all the VIP-immunoreactive nerve terminals were in contact with endocrine A, B or D cells, but not in the close vicinity of blood vessels. Nerve endings devoid of VIP immunoreactivity but containing ACh-like cations were seen either in contact with endocrine cells or in close vicinity to blood vessels. These data suggest that VIP might modulate, concomitantly with ACh, the hormonal secretion of the endocrine pancreas, although the possibility of the neurosecretion of ACh and VIP into the blood vessels should not be excluded. ACh might also control some function of the endothelial cells of blood vessels.

Acetylcholine↗