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Biomedical subjects

A Ruiz-Marcos

Publications and source records attributed to A Ruiz-Marcos.

At least 19 recordsLinked to original sources
PubMed2005

Movements restriction and alterations of the number of spines distributed along the apical shafts of layer V pyramids in motor and primary sensory cortices of the peripubertal and adult rat.

The number and distribution of spines along apical shafts of rapid-Golgi-stained layer V pyramidal cells from visual, motor and somatosensory cortical areas were analyzed in control and movement-restricted (beginning at 20 days old) Wistar rats killed at 30, 40, 80 and 120 days of age (experiment A). In other group of rats, spine density was analyzed when restriction initiates on day 40 and the animals were killed at 50, 60 and 80 days postpartum, or after restriction starting on day 80 and killed at 120 days of age (experiment B). It has been found that the restriction of movements significantly reduces the total number of spines on apical shafts in the three cortical areas, when this condition starts at 20, 40 or 80 days without changing the overall distribution of spines. Also present findings indicate that the effects of movements restriction are attenuated when they were concurrent with maturational brain processes (20-40 days) than when they occurred later in life. The question remains open of which part of the measured reduction on the number of spines is due to the immobilization and which to the stress associated with this maneuver.

Aging↗
PubMed2003

Neonatal food restriction induces hypoplasia in developing facial motor neurons of rats.

The effects of neonatal food restriction upon the dendritic development of facial nucleus (FN) motor neurons of Wistar rats were analyzed. Rats neonatally underfed by daily (12 h) mother-litter separation in an incubator from 5-30 days after birth exhibited, in brain stem Golgi-Cox sections, significant reductions in the number and extension of stellate, triangular and bipolar FN neuronal dendritic prolongations with negligible effects upon perikarya measurements. Data suggest that in the underfed newborn, the ability of FN neurons to establish synaptic contacts with afferent fibers is reduced, which then interferes with their capacities for the integration and triggering of nerve impulses to modulate facial motor expression in response to sensory cues.

Animals↗
PubMed1997

Myelin basic protein immunoreactivity in the internal capsule of neonates from rats on a low iodine intake or on methylmercaptoimidazole (MMI).

Rats fed on low iodine diets (LIDs) result in a normal circulating level of triiodothyronine (T3), a low level of thyroxine (T4) and an elevated thyroid-stimulating hormone (TSH). These changes are similar to those observed in habitants who live in iodine-deficient areas and different from those observed when the hypothyroidism is produced by goitrogens. To study the effects of LID or goitrogens on the myelin basic protein (MBP) immunoreactivity (MBP-ir) during the myelination of the internal capsule, one group of experimental female rats was fed on an LID, and another group received a standard laboratory diet with methylmercaptoimidazole (MMI) added in the drinking water. Animals fed on a standard laboratory diet and animals fed on an LID supplemented with KI were used as controls. At P10, the MMI treatment has produced a more marked decrease in the surface density of MBP-ir processes with respect to controls than that produced in the LID animals. This decrease was correlated with the cerebral concentrations of triiodothyronine (T3) we found. During the postnatal development, a recovery in the levels of the surface density with respect to controls was observed in both experimental groups. The recovery occurred by P20 in the LID group and by P32 in the MMI rats.

Animals↗
PubMed1997

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

The most severe brain damage associated with thyroid dysfunction during development is observed in neurological cretins from areas with marked iodine deficiency. The damage is irreversible by birth and related to maternal hypothyroxinemia before mid gestation. However, direct evidence of this etiopathogenic mechanism is lacking. Rats were fed diets with a very low iodine content (LID), or LID supplemented with KI. Other rats were fed the breeding diet with a normal iodine content plus a goitrogen, methimazole (MMI). The concentrations of -thyroxine (T4) and 3,5,3'triiodo--thyronine (T3) were determined in the brain of 21-d-old fetuses. The proportion of radial glial cell fibers expressing nestin and glial fibrillary acidic protein was determined in the CA1 region of the hippocampus. T4 and T3 were decreased in the brain of the LID and MMI fetuses, as compared to their respective controls. The number of immature glial cell fibers, expressing nestin, was not affected, but the proportion of mature glial cell fibers, expressing glial fibrillary acidic protein, was significantly decreased by both LID and MMI treatment of the dams. These results show impaired maturation of cells involved in neuronal migration in the hippocampus, a region known to be affected in cretinism, at a stage of development equivalent to mid gestation in humans. The impairment is related to fetal cerebral thyroid hormone deficiency during a period of development when maternal thyroxinemia is believed to play an important role.

Animals↗
PubMed1994

Sexual differences in the numerical density of synaptic profiles of developing rat visual cortex.

Axo-dendritic synaptic profiles were quantified along the whole depth of the visual cortex of 10-day-old male and female rats. In both sexes the numerical density of synaptic profiles on spine-like structures was greater than the numerical density of synapses on dendritic shafts. Females had a significantly greater numerical density of synaptic profiles on spine-like structures, than did males at a distance of 200-400 and 500-600 microns from the pia surface, which corresponds to layers II-III and IV of the cortex, respectively. A small percentage (2%-4%) of spine-like structures received two presynaptic terminals. This type of double synapses was three times more abundant in females. No sex differences were found in the numerical density of synapses on dendritic shafts in any cortical layer.

Animals↗
PubMed1994

Thyroxine treatment and the recovery of pyramidal cells of the cerebral cortex from changes induced by juvenile-onset hypothyroidism.

In contrast to the permanent alterations resulting from neonatal hypothyroidism, the effects of juvenile-onset hypothyroidism on the number and distribution of spines along the apical shaft of pyramidal neurons of the visual cortex appeared to be potentially reversible with adequate thyroxine (T4) therapy (Ruiz-Marcos et al., 1980, Brain Res. 185:91-102 and 1982, Brain Res. 239:559-574). Treatment with 0.20 or 1.50 micrograms T4/100 g body weight per day had, however, only partially reversed the changes induced by juvenile-onset hypothyroidism. We here study whether or not a higher dose of T4 would totally reverse these effects. A group of rats were thyroid-ectomized at 40 days of age, and injected once daily with placebo or T4 (1.75 micrograms/100 g BW per day) from 70 to 90 days of age, a group on 1.50 micrograms being included to compare with previous results. Spine number and distribution were measured, as well as the concentrations of T4 and triiodothyronine (T3) in plasma, liver and brain. The activities of two hepatic enzymes were measured as thyroid hormone-sensitive biological end points. The 1.75-micrograms dose restored spine number to 88% of normal values and was markedly more effective than the 1.50-micrograms dose, which increased it to 68%. The degree of restoration appeared related to the concentration of T3. It is concluded that the changes caused by juvenile-onset hypothyroidism in the number and distribution of dendritic spines along the apical shafts of pyramidal neurons are reversible, although complete restoration might require a higher dose of T4, a continuous mode of administration, or longer period of treatment.

Age of Onset↗
PubMed1992

Aging reverts to juvenile conditions the synaptic connectivity of cerebral cortical pyramidal shafts.

Quantitative analysis of the total number and distribution of dendritic spines along the apical shafts of layer V cerebral cortical pyramids has been performed on aging rats (90-120 to 1,135 days old) and on rats during the period of early and late development (10-80 days). As expected from previous work, present results show that the total number of dendritic spines along the shafts increase from 10 to 80 days, after which it starts to gradually decrease until the last age studied (1,135 days). The quantitative analysis of the effect of aging on the relative decrease of dendritic spines shows that this decrease starts being homogeneous along the whole length of the apical shafts and that from a certain age onwards, estimated according to present results in 400 days, this effect is significantly more pronounced in layers IV and III-II than in deep layers. Furthermore, the comparison made between the distribution of dendritic spines along the apical shafts of pyramidal neurons of old and young animals has shown that aging produces a regression of this distribution to juvenile conditions.

Aging↗
PubMed1991

Regional sex differences in spine density along the apical shaft of visual cortex pyramids during postnatal development.

Dendritic spines from the apical shaft of layer V pyramids were counted on Golgi-stained sections of the monocular subfield of the primary visual cortex of 10-, 20-, 40- and 60-day-old male and female rats. Dendritic segments located in layer IV and at 100-300 microns from the soma had a significantly higher spine content in 10-day-old females when compared to males. This sex difference was extended to outer dendritic segments with increasing age, and became restricted to dendritic segments of outer layers (II-III) located at 400-550 microns from the perikaryon in 40-day-old rats. Sex differences in spine content finally disappeared by day 60. These results show the existence of specific laminar and temporal sex differences in the development of dendritic spines in the apical shaft of visual cortex pyramids.

Aging↗
PubMed1990

Developmental sex differences and effect of ovariectomy on the number of cortical pyramidal cell dendritic spines.

Dendritic spines in the apical shafts of layer V pyramidal neurons were quantitatively assessed in Golgi preparations of visual cortex from male and female rats, 10-60 postnatal days old. The number of dendritic spines increased in both sexes from days 10 to 20. However, we found that 10-day-old females had a significantly greater number of dendritic spines than males of the same age. The absolute difference further increased with increasing age, reaching a maximum at 20 days. Then, the number of dendritic spines progressively decreased in females between days 20 and 60, showing a certain tendency to increase in males during the same period. As a result of this different developmental trend, the number of spines was similar in 60-day-old male and female rats. Ovariectomy of females, at day 30, prevented the decrease in the number of dendritic spines. These results indicate that spine development in the rat visual cortex is dependent on sex, suggesting a possible influence of sex steroids on pyramidal cell maturation.

Aging↗
PubMed1988

Rapid effects of adult-onset hypothyroidism on dendritic spines of pyramidal cells of the rat cerebral cortex.

We have previously shown (Ruiz-Marcos et al. 1980, 1982) that thyroidectomy (T) performed in rats at 40 days of age, well past the neonatal period of development, results by 80-90 days of age in a decrease of the number of spines along the shaft of pyramidal neurons with the cell body in layer V in the visual area of the cerebral cortex. We have here studied how soon after the operation an effect on spine number and distribution may be observed. We have found that the response of these neurons to T is very rapid: a decrease in the number of spines/shaft between T and age-paired controls (C) rats is statistically significant by the earliest period of observation, namely 5 days after T. These results may be related to those of Dembri et al. (1983) showing that T performed in adult rats decreases the activity of Type I RNA polymerase by 5 days after the operation. It is possible that T impairs the synthesis of some compound(s) necessary for the formation and maintenance of spines. The present results suggest that spine number is not a fixed structure of the apical shaft once brain development is over, but is in a state of continuous formation and degradation. We have further observed that the effect of T performed at 40 days of age is more pronounced in the distal part of the shaft than on the rest, a result similar to that found after neonatal T (Ruiz-Marcos et al. 1982). However, contrary to findings after early hypothyroidism, T at 40 days of age does not distort the distribution of spines along the shaft.

Animals↗
PubMed1987

Pyramidal cortical cell morphology studied by multivariate analysis: effects of neonatal thyroidectomy, ageing and thyroxine-substitution therapy.

The changes produced on the whole dendritic morphology of layer III cortical pyramidal neurons by neonatal hypothyroidism, induced in rats by thyroidectomy at 10 days of age (T), as well as those changes related to ageing, have been studied in rats at 40 and 80 days of age. For these purposes, the dendritic structure of these neurons was defined by a set of 10 variables whose measurements were analyzed using multivariate methods. The effect of tyroxine (T4) substitution therapies applied to T rats between 12-40 and 30-80 days of age has been further investigated with the same mathematical methodology. The results obtained from the analyses performed show that hypothyroidism affects both the apical tuft and the basal dendritic arborization of these neurons. The observed damage was similar: a decrease of the total length of the dendritic segments of the apical tuft and the basal arborization. This change, however, was detected in these two different subregions with a different timing. These results seem to reinforce our findings concerning the selective effect of T on different sites of these neurons. On the other hand, 3 morphological changes have been revealed regarding the development of the pyramidal neuron studied: (1) the total length of the apical tuft dendritic segments increases from 40 to 80 days of age; (2) the total length of the basal dendritic segments decreases from 40 to 80 days of age; and (3) the perimeter of the cell body decreases from 40 to 80 days of age. Finally, the results obtained did not allow us to detect any recovery of the damage induced by T, as a consequence of the T4 substitution therapies applied.

Aging↗
PubMed1986

The metric analysis of three-dimensional dendritic tree patterns: a methodological review.

Metric analysis methods used to study neuronal arborizations are reviewed and discussed. The analysis methods considered are those examining the spatial orientation and density of the whole dendritic field of a neuron, the metrics of dendritic segments and the bifurcation angles. General variables indicating the size of the soma and the dendritic field are indicated. In addition, the instrumentation used for providing 3-dimensional data for metric analyses and the shrinkage of Golgi-stained neurons are discussed.

Animals↗
PubMed1986

Dendritic structure alterations induced by hypothyroidism in pyramidal neurons of the rat visual cortex.

In order to study the effect that neonatal hypothyroidism has on the whole morphology of pyramidal neurons of the cerebral cortex, the dendritic structure of these cells was defined by a set of 10 variables divided into two subsets, one composed of 7 variables defining the apical shaft and the other composed of 3 variables concerning the basal arborization. The canonical multivariate analysis applied to the measurements of these variables made on two groups of layer III pyramidal neurons belonging to 80-day-old control and thyroidectomized rats revealed that this disease only affects the development of the apical tuft region of those neurons. This result is in agreement with our previous finding concerning the effect of hypothyroidism on the dendritic densities of layer III pyramidal neurons (Dev. Brain Res., 28 (1986) 259-262).

Analysis of Variance↗
PubMed1985

Effect of hypothyroidism on the size of spines of pyramidal neurons of the cerebral cortex.

We have previously shown that hypothyroidism produces a decrease in the number of spines counted along the apical shafts of pyramidal neurons of the cortex. Nevertheless, other authors have found that when an animal is subjected to some adverse living conditions the size of the spines decreases, making them invisible to the light microscope. The question arises then of whether the decrease in the number of spines reported by us in hypothyroid animals is real or is due to a shrinking effect. In order to elucidate this question the cross-surface area of dendritic spines of apical shafts belonging to 20- and 60-day-old rats, thyroidectomized at 10 days of age, as well as those of their corresponding controls were measured in different layers of their cortex, studied using conventional electron microscopic techniques. The application of the three-way analysis of variance model to these data has shown us that while the age of the animal produces a definite increase in the size of the spines, hypothyroidism does not produce any change in their size, leading us to the conclusion that the decrease in the number of spines previously reported is due to an actual loss of these elements.

Animals↗
PubMed1984

Cerebral hypothyroidism in rats with adult-onset iodine deficiency.

Rats fed chronically a low iodine diet may have low serum T4 and high circulating TSH, despite normal serum T3. As the brain depends to a great extent on intracellular generation of T3 from T4 for its total and nuclear T3, we have carried out two experiments to determine whether the brain of iodine-deficient rats may become hypothyroid, despite normal serum T3 levels. In both experiments we confirmed previous data, showing that the pituitary and liver of iodine-deficient rats with very low plasma T4 levels are hypothyroid as compared to those of animals receiving the same diet supplemented with KI, though not as markedly as animals which had undetectable circulating levels of both T4 and T3 as a consequence of chronic ingestion of KC1O-4, or of surgical thyroidectomy. We have further found that the nuclear T3 content was decreased in the brain of iodine-deficient rats, as compared with the animals on the iodine-supplemented diet. The nuclear to plasma ratios of labeled T3 showed that the uptake of this hormone into liver and brain nuclei is not decreased in the iodine-deficient rats as compared with those on the iodine-supplemented diet. This finding indicates that the decreased liver and brain nuclear T3 contents of iodine-deficient rats are likely to be a consequence of the marked reduction of their T4 pool, leading to decreased amounts of intracellularly generated T3. The number of spines on shafts of pyramidal neurons from the visual cortex of iodine-deficient rats was lower than that of rats fed the same diet supplemented with KI. Their distributions along the shaft were also not the same. Such changes might well be an index of cerebral hypothyroidism, as they are similar to those found after thyroidectomy of adult rats. It is concluded from the present findings that normal circulating T3 levels may not be sufficient to maintain brain euthyroidism in rats fed a diet iodine deficient enough to result in very low circulating T4 levels.

Animals↗