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M Fonseca

Publications and source records attributed to M Fonseca.

36 records · Page 2Linked to original sources
PubMed1995

The expression of alpha 1 adrenoceptor subtypes changes with age in the rat aorta.

Previous studies showed that alpha 1 adrenoceptor-mediated contractile responses change with age in the rat aorta, becoming more sensitive to Ca++ channel blockers and less sensitive to chlorethylclonidine (CEC), suggesting a change in the alpha 1 adrenoceptor subtypes that are present. In this study, alpha 1 adrenoceptor density and alpha 1 adrenoceptor subtypes were measured in the Fischer 344 rat aorta during aging. Aortic alpha 1 adrenoceptor densities, determined by saturation binding of 2-[beta-(4-hydroxy-3-[125I]iodophenyl)ethylaminomethyl] tetralone ([125I]-HEAT), were 47, 41 and 45 fmol/mg protein in 1-,6- and 24-month-old rats, respectively. The noncompetitive antagonist CEC completely blocked [125I]-HEAT binding in aortas from 1-month-old rats but inhibited binding only partially in aortas from older rats. Two binding sites were detected for norepinephrine and for WB4101 in all ages. The low-affinity constants for WB4101 (31-51 nM) were consistent with those for the alpha 1b adrenoceptor subtype, and this binding site decreased with age. The high-affinity constant for WB4101 (1.4 nM) in 1-month-old aorta was consistent with that for alpha 1d adrenoceptor subtype, whereas the high-affinity constants (0.03 nM) in 6- and 24-month-old aortas were consistent with those for the alpha 1a adrenoceptor subtype. At least three alpha 1 adrenoceptor subtypes appear to be colocalized in the rat aorta, so the binding affinities may reflect binding to more than one subtype. This makes it difficult to identify denfinitively the subtypes based on their radioligand binding characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1995

[Intranasal encephalocele].

We present a case of an intranasal encephalocele in a 6-year old girl, that appears as an intranasal mass with CSF rhinorrhea. The surgical treatment is described, specially the extracranial step through a paralateronasal via. The embryogenesis, classification, diagnosis and management of these rare congenital lesions are discussed.

Child↗
PubMed1993

Chandelier cell axons identified by parvalbumin-immunoreactivity in the normal human temporal cortex and in Alzheimer's disease.

Parvalbumin is a calcium-binding protein which is thought to play a role in neuronal excitability. In the cerebral cortex parvalbumin is largely found in two subsets of GABAergic neurons, the chandelier and basket cells. A distinguishing characteristic of the chandelier cell is that the terminal portions of its axon form short vertical strings of boutons resembling candlesticks, which embrace the initial segment of pyramidal cell axon. In the present study, the terminals of chandelier cells in the human temporal cortex were immunostained with an antibody against parvalbumin. These terminals were found more abundantly in layers II and VI, less frequently in layers III and V, were hardly identified in layer IV, and absent in layer I. The relationship of parvalbumin-immunoreactive terminals and axon initial segments was further evidenced by re-sectioning identified rows of boutons into semithin sections. Electron microscopy of both temporal cortex and the somatosensory region of a biopsy sample revealed that these parvalbumin-positive boutons indeed form symmetric synaptic contacts on the axon initial segments of pyramidal cells. As part of an enquiry into the possibility that these specialized interneurons may be involved in degenerative neurological diseases, the temporal lobes from seven patients with Alzheimer's disease were immunostained for parvalbumin. As in the control brains, the specific terminal portions of chandelier cells were recognized and identified in the temporal cortex by parvalbumin-immunocytochemistry. No major difference from normal brains was found, excepting for a lower density of candlesticks (30-35%) in layer II-III. Since we showed in a previous study [Ferrer et al. (1991) J. neurol. Sci. 106, 135-141] that the number of parvalbumin-immunoreactive somata in the same Alzheimer's disease cases was not decreased, the observed reduction of terminals in layer II suggest that only the terminals of chandelier cells, but not the parent neurons, are decreased in Alzheimer's disease.

Aged↗
PubMed1992

Calbindin immunoreactivity in normal human temporal neocortex.

Calbindin immunoreactivity in the temporal neocortex was examined in 4 subjects with no neurological, metabolic or malignant disease. The brains were obtained between 1 and 4 h after death and rapidly fixed by perfusion with 4% paraformaldehyde through the carotid arteries, cut into slabs, cryoprotected and stored at -80 degrees C. Sections of the whole left temporal lobe obtained with a freezing microtome were processed free-floating with a well known monoclonal antibody against calbindin according to the peroxidase-antiperoxidase (PAP) method. Calbindin-immunoreactive (CaBP-ir) neurons were found to be local-circuit neurons (interneurons) mainly distributed in the upper cortical layers (layers I, II and III), and were categorized as small multipolar neurons with ascending dendrites ramifying in the molecular layer, small bitufted cells, pyramid-like cells in layer II, horizontal neurons in the molecular layer, multipolar neurons with long descending dendrites, and large double-bouquet cells, some of them exhibiting a very long dendrite with claw-shaped terminals in layer V. Less than 10% of all CaBP-ir neurons were localized in the remaining cortical layers. Pyramidal cells were only very weakly or not stained at all. In addition, CaBP-ir fibres formed a dense plexus in the molecular layer, and vertical bundles 8-10 microns thick and 500-600 microns long, separated by blank spaces 20-40 microns wide were distributed in layers III and V/VI.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Parvalbumin immunoreactive neurons in normal human temporal neocortex and in patients with Alzheimer's disease.

Parvalbumin-immunoreactive (PARV-ir) neurons were studied in the temporal neocortex of 4 normal subjects and in 7 patients with Alzheimer's disease (AD) whose brains were removed from the skull between 1 and 4 h after death and immediately fixed by perfusion through the carotid arteries to minimize pitfalls related to delayed tissue processing. Freezing microtome sections were immunostained free-floating for PARV using a well characterized monoclonal antibody diluted at 1:5000 and the peroxidase-antiperoxidase method. PARV-ir cells predominated in layers III, IV and V and were classified as bitufted cells and small, medium and large multipolar neurons according to their dendritic arbors. Immunoreactive cell processes surrounding the soma of neighbouring cells and immunoreactive vertical strings of buttons were consistent, respectively, with terminal axons of basket cells and chandelier neurons. The number of PARV-ir cells in the superior (T1), middle (T2) and inferior (T3) temporal gyri was variable from one case to another in both normal and pathological cases. Only 1 of 7 patients with AD had significantly reduced numbers of PARV-ir neurons, thus suggesting that PARV-ir cells in the neocortex are relatively resistant to degeneration in Alzheimer's disease.

Aged↗
PubMed1990

Naturally occurring cell death in the cerebral cortex of the rat and removal of dead cells by transitory phagocytes.

Regressive phenomena are common during the development of the nervous tissue. Among them, naturally occurring cell death has been observed in several regions of the nervous system. Cell death in the somatosensory cortex and medial cortical regions (hind limb, frontal cortex 1, frontal cortex 2, retrosplenial agranular, retrosplenial granular [Zilles K. et al. (1980) Anat. Embryol. 159, 335-360]) as well as in the cortical subplate (future subcortical white matter) in the rat mainly occurs during the first 10 days of postnatal life with peak values of 3.1 dead cells per 1000 live neurons at the end of the first week. Cell death progresses from birth to day 7 with a predominance of dead cells in the subplate and in layers II-III. Later, dead cells are more dispersed in the cerebral cortex, but a significant amount is still present in the subcortical white matter. This pattern correlates with the arrival and settlement of cortical afferents at the different cortical levels, as described in other studies, and points to the likelihood that transitory cellular populations are important clues in the modelling of the cerebral cortex during normal development. Transitory populations of macrophages (amoeboid or nascent microglial cells) that appear in great numbers during the same period and in the same regions are involved in the removal of dead cells.

Aging↗
PubMed1990

Correlation of serum vitamin A and its transport protein (RBP) in malnourished and vitamin A deficient children.

Eighty nine children were studied for retinol (vitamin A) estimation and its transport protein--retinol-Binding Protein (RBP). Serum levels of retinol, RBP and serum protein and albumin were found to be low in children with signs of vit. A deficiency irrespective of their nutritional status. Serum levels of retinol and RBP were risen significantly almost double, after the oral and parenteral administration of vitamin A. PEM interferes with hepatic synthesis of RBP and the release of RBP from the liver depends on vitamin A. Vitamin A is a limiting factor, the presence of which is required for the release of apo-RBP from the liver.

Blood Proteins↗
PubMed1988

Local connections in transplanted and normal cerebral cortex of rats.

Injections of the fluorescent tracer Fluoro-Gold were made in transplanted and normal cerebral cortex of rats in order to investigate and compare the local connectivities of both. In the normal somatosensory cortex, small injections in superficial layers (I to III) produced retrograde cell labeling below the injection site in two bands: in layer V and in the deep part of layer VI. Pieces of embryonic rat neocortical tissue were transplanted into a cavity made in the somatosensory cortex of young adult rats. After a survival period of 2-3 months, small injections of Fluoro-Gold were made in the superficial part of the grafts. These injections revealed multiple clusters of intratransplant-projecting cells. No callosal or thalamic neurons were labeled in these experiments. On occasion, a bilaminated pattern of retrograde cell labeling was observed inside the transplants. In both transplanted and normal cortices, pyramidal and non-pyramidal cells were retrograde-labeled. We conclude that in the neocortical transplants there is a pattern of local connectivity that is reminiscent of the pattern of intracortical connectivity in the normal neocortex in at least two aspects: first, the retrograde-labeled cells tended to form clusters or bands; second, both pyramidal and non-pyramidal cells were labeled.

Animals↗
PubMed1986

Times of generation of glutamic acid decarboxylase immunoreactive neurons in mouse somatosensory cortex.

The birth dates of neurons showing glutamic acid decarboxylase (GAD) immunoreactivity have been determined in mouse somatosensory cortex. Pregnant C57Bl mice received pulse injections of (3H)thymidine from E10 through E17 (E0 being the day of mating). The distributions of thymidine-labeled, GAD-positive and nonimmunoreactive (non-GAD) cells as a function of depth under the pial surface were recorded in adult animals. The maximum rate of generation of GAD-positive neurons occurred at E14, whereas the generation of non-GAD neurons reached its maximum rate at E13. Except for those in layer I, GAD-positive neurons followed an inside-out sequence of positioning. GAD-positive neurons born at E12 and E13 were located in layers VI-IV. GAD-positive neurons born at E14 were found throughout the cortical thickness, with a maximum in layer IV. The GAD-positive neurons labeled after pulses at E15 or E16 or E17 were limited to the superficial strata, forming a band that became narrower as it moved toward the pial surface with increase in age of pulse labeling. GAD-positive neurons in layer I were generated at a constant rate during the whole embryonic period analyzed. Non-GAD neurons also followed an inside-out spatiotemporal gradient. Two partially overlapping phases were distinguished in non-GAD neurogenesis. During the first phase (from E12 to E14) neurons populating adult layers VI and V originated, while neurons located in layers IV through I were generated during the second phase (from E13 to E17). Since GAD-immunoreactive neurons form a heterogeneous population, we envisage further studies in order to test whether differences exist in birth dates among the classes.

Animals↗
PubMedDate not supplied

Increased serum S100B protein in schizophrenia: a study in medication-free patients.

S100B protein, a calcium binding protein produced and released by glial cells, has been used as a sensitive marker of brain damage. Previous studies have found alterations in peripheral S100B levels in schizophrenic patients on medication. We compared serum S100B levels of 20 medication-free DSM-IV schizophrenic patients and 20 age-gender matched healthy controls. Schizophrenic patients presented higher serum S100B levels (mean 0.120 ng/ml+/-S.D. 0.140) compared to controls (mean 0.066 ng/ml+/-S.D. 0.067; P=0.014) and there was a negative correlation with illness duration (r=-0.496, P=0.031). The results of this study indicate that serum S100B levels may be a state marker of a limited neurodegenerative process, particularly in the early course of schizophrenia or, at least, in a subgroup of schizophrenic patients.

Adolescent↗
PubMedDate not supplied

Glutamate-like immunoreactivity and fate of Cajal-Retzius cells in the murine cortex as identified with calretinin antibody.

Cortical layers VI to II develop between two layers of older neurons, the marginal and subplate zones, which are believed to have unique roles in cortical development. While subplate cells have been found essential for the establishment of thalamocortical relationships, the function of the marginal zone and in particular of the neurons of Cajal-Retzius has not been elucidated. Here we show that an antibody against the calcium-binding protein calretinin labels the population of Cajal-Retzius cells throughout their life in the murine cerebral cortex. In prenatal and early postnatal stages, Cajal-Retzius cells were found evenly distributed throughout the murine cerebral cortex. Cajal-Retzius-like neurons were also found in the developing hippocampus and dentate gyrus, which indicates that they may have a general function in cortical development. From P8 onward Cajal-Retzius cells disappeared from the neocortex and hippocampus, at the same time as degenerating immunoreactive neurons were observed. Calretinin-positive Cajal-Retzius cells were glutamate immunoreactive and their presumed axon terminals formed asymmetric synapses. These observations indicate that Cajal-Retzius cells may provide a tonic excitatory input, essential for the maturation of cortical neurons. Furthermore, since neuronal migration has been shown to be dependent on glutamate receptors, we propose that Cajal-Retzius cells releasing glutamate may direct migrating neuroblasts toward the marginal lamina, therefore creating the "inside-out" sequence of cortical development.

Animals↗
PubMedDate not supplied

[Dysgenetic male pseudohermaphroditism].

Dysgenetic male pseudohermaphroditism is the result of a defect of testis development that encompasses a large clinical heterogeneity. It is characterized by bilateral dysgenetic testis, absence of mullerian regression, ambiguous genitalia and/or stigmata of Turner's syndrome in the majority of the cases. Typically, these individuals have either a 46,XY or 45,X/46,XY karyotype. The authors present four cases of dysgenetic male psudohermaphroditism, with ages of diagnosis between 1 month and 17 years old. The first had a male phenotype with stigmata of Turner's syndrome and the others ambiguous genitalia. Two patients were 45,X/46,XY and 45X/47,XYY mosaics and the other two were 46,XY. Gonadal karyotyping showed mosaicism (45,X/46,XY) in all four cases. In the first case was programed orquidectomy; all the others assigned a male gender, with regular follow-up until the puberty.

Adolescent↗
PubMedDate not supplied

Calbindin D-28k immunoreactivity in the temporal neocortex in patients with Alzheimer's disease.

Calbindin D-28k immunoreactivity in the temporal isocortex was examined in seven patients with Alzheimer's disease (AD) and in six controls. In normal brains, calbindin D-28k-immunoreactive cells were bitufted neurons, multipolar cells with ascending dendrites and large double-bouquet cells mainly located in layers II and III. Immunoreactive fibres were seen in the molecular layer and in vertical bundles in layers III and V/VI. Calbindin D-28k immunoreactivity was reduced in patients with AD, although with differences from one patient to another. Immunoreactivity was decreased in the plexus of the molecular layer and in the vertical bundles in the cellular layers in every case. Most patients had, also, decreased immunoreactivity in the dendritic arbors. The number of calbindin D-28k-immunoreactive cells was significantly decreased in three of five patients with moderate or severe dementia, and was normal in two cases with mild dementia.

Aged↗