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Biomedical subjects

A Feria-Velasco

Publications and source records attributed to A Feria-Velasco.

At least 19 recordsLinked to original sources

Prenatal-through-postnatal exposure to moderate levels of ethanol leads to damage on the hippocampal CA1 field of juvenile rats: a stereology and Golgi study.

Experimental paradigms conducted to assess the neurotoxic effects of ethanol exposure on hippocampus development have yielded controversial findings. Hippocampal CA1 population and some cytoarchitectural parameters of pyramidal cells were studied after exposure to ethanol during early development, in rats. Examination of 30-day-old offspring of rats exposed to moderate levels of ethanol during gestation through lactation showed an increased volume of the hippocampal CA1 field compared to untreated or pair-fed control pups, as well as a reduced number of pyramidal neurons. In addition, the number of spines from surviving CA1 pyramidal neurons was reduced. Furthermore, stubby and wide spines were proportionally increased, while the proportion of mushroom and ramified spines was reduced; no variation in the proportion of thin spines was observed. Because alcoholic women usually drink alcohol before, during, and after pregnancy, a broad-range experimental model of alcohol exposure was used in this study. The present findings show that experimental exposure to moderate levels of ethanol, resembling the human situation in alcoholic mothers, leads to loss of hippocampal CA1 pyramidal neurons, along with several pathological and plastic events in the dendritic arborization of these neurons. Some ethanol-induced excitotoxicity-related mechanisms, which may be underlying these effects, are discussed.

Animals↗

Ultrastructural analysis of guided nerve regeneration using progesterone- and pregnenolone-loaded chitosan prostheses.

Recently, numerous guide chambers for the treatment of injured nerves made up of different biomaterials have been designed, capable of hosting living cells or carrying neurotrophic or neuroactive substances to be directly released to the injured tissue. In this study, chitosan prostheses containing neurosteroids (progesterone and pregnenolone) were used for bridging a 10-mm gap in the rabbit facial nerve. Gas chromatography was used to quantify neurosteroid content in the prostheses prior to and after subcutaneous implantation at different periods of up to 60 days. The regeneration of the nerve fibers were evaluated at 15 and 45 days after axotomy by means of ultrastructural morphometric analysis. Different nerve fibers regenerative patterns were seen depending the groups studied and the analyzed stages. At 15 days after axotomy, the newly regenerating tissue revealed Schwann cells holding nonmyelinated nerve fiber bundles in an incipient and organized regenerative pattern. At 45 days, the regenerating tissue showed myelinated nerve fibers of different sizes, shapes, and myelin sheath thickness. Although the regeneration of the nerve fibers under neurosteroid treatment showed statistically significant differences in comparison with vehicle regenerated tissue, progesterone-loaded chitosan prostheses produced the best guided nerve regeneration response. These findings indicate that chitosan prostheses allowed regeneration of nerve fibers in their lumen, and when containing neurosteroids produced a faster guided nerve regeneration acting as a long-lasting release delivery vehicle.

Animals↗

Neurogenesis in the subventricular zone following transcranial magnetic field stimulation and nigrostriatal lesions.

Neurogenesis continues at least in two regions of the mammalian adult brain, the subventricular zone (SVZ) and the subgranular zone in hippocampal dentate gyrus. Neurogenesis in these regions is subjected to physiological regulation and can be modified by pharmacological and pathological events. Here we report the induction of neurogenesis in the SVZ and the differentiation after nigrostriatal pathway lesion along with transcranial magnetic field stimulation (TMFS) in adult rats. Significant numbers of proliferating cells demonstrated by bromodeoxyuridine-positive reaction colocalized with the neuronal marker NeuN were detected bilaterally in the SVZ, and several of these cells also expressed tyrosine hydroxylase. Transplanted chromaffin cells into lesioned animals also induced bilateral appearance of subependymal cells. These results show for the first time that unilateral lesion, transplant, and/or TMFS induce neurogenesis in the SVZ of rats and also that TMFS prevents the motor alterations induced by the lesion.

Animals↗

NMDA and AMPA receptor expression and cortical neuronal death are associated with p38 in glutamate-induced excitotoxicity in vivo.

Early overstimulation of ionotropic glutamate receptors (iGluRs), such as the N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors, produces excitotoxicity in several brain regions. The molecular composition of those receptors and their regulation by intracellular signaling systems could be determinants in the development of progressive neurodegenerative mechanisms in the central nervous system (CNS). Studies of p38 mitogen-activated protein kinase (MAPK) activation, morphologic changes including cell number, and the expression of the NR1 and GluR2 subunits, by reverse transcriptase-PCR were evaluated at early postnatal ages (postnatal day [PD]8-14) in cerebral cortex of rats treated with monosodium glutamate (MSG; 4 mg/g body weight) administered subcutaneously on PD1, 3, 5, and 7. An important increase in p38 activity at PD8 and loss of cortical cell number were observed from PD8-14 in animals treated with MSG, together with significant morphologic changes characterized by cell shrinkage, nuclear hyperchromatism, and cytoplasmic vacuolation. These morphologic changes were prevented by SB203580, an inhibitor of p38 signaling, at PD8-14. No change in cerebral cortex thickness was observed among experimental or control rats. A significant increase in NR1 subunit expression was observed in response to MSG from PD8-14. GluR2 expression increased from PD8-12, but at PD14, its expression was reduced to 54% with respect to controls. SB203580 prevented alone the decreased in GluR2 expression induced by MSG. These results suggest that initial neuronal death (at PD8 and 10) in cerebral cortex may be due to an excessive Ca2+ influx through NMDA receptors, whereas the further damage process could be mediated by AMPA receptors through p38 signaling. This could represent a determinant mechanism to decide whether nerve cells survive or die.

Activating Transcription Factor 2↗

Scanning electron microscopy of the superficial pineal gland of the 15-day-old rat (Rattus norvegicus).

The presence of a cortex and medulla in the superficial pineal gland has been a controversial point in the morphology of this structure in mammals. The published reports indicate contradictory data especially in rodents. In this study the pineal gland of 15-day-old male rats (Rattus norvegicus) were studied, using scanning electron microscopy, in an attempt to determine whether or not a cortex and medulla are apparent in the pineal gland of young rats. The superficial pineal gland of the 15-day-old rat exhibited both a cortex and a medulla; these areas exhibited different structural organizations. The cortex had a thickness of 40-80 microm and the cells did not show a particular arrangement. The center of the gland was composed of a medulla, which had a width of 1000-1200 microm, and consisted of cells arranged in cords; its morphology was distinctly different from that of the cortex.

Animals↗

Second female case of Myhre syndrome.

Myhre syndrome is a rare disorder characterized by low birthweight, short stature, mental retardation, facial dysmorphism (blepharophimosis, midfacial hypoplasia, prognathism), heart anomalies, muscle hypertrophy, decreased joint mobility and deafness. To date 11 male cases and only one female case have been reported. This paper describes the second female case and compares the clinical and radiological findings between female and male patients.

Abnormalities, Multiple↗

Facial nerve regeneration through progesterone-loaded chitosan prosthesis. A preliminary report.

Biodegradable nerve guides have represented new treatment alternatives for nerve repairing. They are gradually biodegradable, exert biological effects directly to the injured nerve, and act as drug- or cell-delivery devices. Furthermore, progesterone (PROG) has been demonstrated to promote injured peripheral nerve regeneration. In this study, it was hypothesized that PROG delivered from chitosan prostheses provides better facial nerve regenerative response than chitosan prostheses with no PROG. As there are no reports on the use of the former as nerve-guide material in the regeneration of injured nerves, this is the main objective of the present work. Chitosan prostheses containing PROG were used to bridge 10-mm gaps in rabbit facial nerves. The regenerated nerves were evaluated 45 days after implantation in animals with the use of light microscopy and morphometric analysis. Gas chromatography was used in order to quantify PROG content in prosthesis prior to and after implantation in subcutaneous tissue at different periods of up to 60 days. In addition, the prosthesis walls were evaluated with histological techniques in order to assess their integrity and the surrounding tissue reaction. Chitosan prostheses allowed PROG release during the time needed for nerve regeneration. At 45 days myelinated nerve fibers were observed in both the proximal and distal stumps. This parameter and the N ratio were higher in the progesterone-treated group when compared to that of the vehicle control. Findings indicate that chitosan prostheses were useful in nerve regeneration, acting as a long-lasting PROG delivery device a faster nerve regeneration.

Animals↗

Changes in NMDA-receptor gene expression are associated with neurotoxicity induced neonatally by glutamate in the rat brain.

The N-methyl-D-aspartate receptor (NMDA-R) is fully functional in the rat early in embryogenesis, and diverse neuronal plasticity events are regulated through its activation later in postnatal development. On the other hand, systemic administration of glutamate (Glu) to rats at birth induces neuronal degeneration in glutamatergic central nervous system regions via Glu receptor activation. However, it is not known whether an increase in neonatal Glu levels modifies the gene expression of NMDA-R subunits, or if these putative changes are related to gamma-aminobutyric acid-mediated (GABAergic) neurotransmission. We measured, by means of semi-quantitative reverse transcriptase polymerase chain reaction, changes in gene expression of the NMDA-R subunits: NMDA-R1, NMDA-R 2A and NMDA-R 2B in cerebral cortex (CC), striatum (ST) and hippocampus (HP) in the brains of rats treated neonatally with monosodium L-glutamate (MSG). These studies were supported by histological and quantitative analysis of the glia. Our results showed histological evidence of neuronal damage, and increased glial cell number and activity were detected. This was seen mainly in the ST and HP of MSG-treated animals. Significant increases in NMDA-R1, 2A and 2B subunits gene expression was also observed in ST and HP but not in CC, where only NMDA-R 2B was increased in MSG-treated rats. Our data suggest that increases in Glu levels and activation of Glu-receptors after neonatal administration of MSG induce an increase in glial cell reactivity and important changes in NMDA-R molecular composition, with signs of neuronal damage.

Animals↗

Protein- and tryptophan-restricted diets induce changes in rat gonadal hormone levels.

The release of gonadotrophic hormones starts at puberty and, along with the subsequent estral cyclicity, is subject to hormonal feedback systems and to the action of diverse neuroactive substances such as gamma amino butyric acid and catecholamines. This study shows the effect of the administration during 40 days of protein-restricted and corn-based (tryptophan- and lysine-deficient) diets on the serotonin concentration in medial hypothalamic fragments as well as in follicle-stimulating luteinizing hormones, 17-beta-estradiol and progesterone serum levels, and estral cyclicity in 60- and 100-day-old rats (young, mature, and in gestation). In young rats, a delay in vaginal aperture development, and a lengthening of the estral cycle to a continuous anestral state was observed, mainly in the group fed corn. This group showed a 25% decrease in the serotonin concentration compared with the protein-restricted group, which exhibited an increase of 9% over the control group. Luteinizing hormone levels decreased in 16% and 13%, whereas follicle-stimulating hormone increased in 13% and 5% in the young animals of restricted groups, respectively, compared with the control group. Serum progesterone levels decreased only in young restricted versus control animals, and no differences were seen among adult and gestational rats. Serum levels of 17-beta-estradiol in restricted animals showed different concentration patterns, mainly in the corn group, which was higher at the 20th gestational day, falling drastically postpartum. The results obtained in this study show serotonin to be a very important factor in the release of gonadotrophic hormones and the start of puberty.

Journal Article↗

Parathion, a cholinesterase-inhibiting plaguicide induces changes in tertiary villi of placenta of women exposed: a scanning electron microscopy study.

The objective of this work was to describe the anatomy of placentas from women who were at risk of exposure to parathion during their pregnancy, when examined with the light and scanning electron microscopes. Twenty term placentas were analyzed; 10 from women living in an agricultural area, who were at risk of exposure to parathion during their pregnancy, and 10 from women living in an urban area, not expressly exposed to pesticides. Each sample was examined with both light and scanning electron microscopes. Cholinesterase activity was significantly reduced in blood from women of the exposed group. In some placentas of women exposed to parathion, recent microinfarctions, microcalcifications and increased deposition of fibrinoid material were seen, along with a larger proportion of atypical characteristics of villi, such as bullous and balloon-like formations with nonhomogeneous surface, and other areas devoid of microvilli. These observations suggest that in chronic exposure to pesticides, the rate of atypical characteristics of placental villi increases, which could be related to changes in the fetus biology. In this study, one newborn from the exposed group showed intrauterine growth retardation and another one, some signs of hypoxia.

Adult↗

Different patterns in the histology and autofluorescence of the Harderian glands of the Syrian Hamster, rat, mouse, Mongolian gerbil and guinea pig.

The purpose of this study was to compare the natural fluorescence in the Harderian glands of the Syrian hamster, rat, mouse, Mongolian gerbil and guinea pig (both sexes). For each species, 10 animals (five males and five females) were used. Histological autofluorescence studies were performed using a fluorescence microscope (450-490 nm filter). Two different types of fluorescent cells were observed in both hamster (type AFI high intensity and type AFII, low fluorescence) and rat (type AFI, low fluorescence and type AFII, high fluorescence) Harderian glands. The fluorescence was basally located in all mice cells, whereas it was observed near the epithelial cell nuclei in the Mongolian gerbil (occupying two-thirds and one-third of the cells in males and females, respectively). A high intensity of fluorescence was present throughout the acinar cells in the guinea pig. The patterns of fluorescence identified exhibited a sexual dimorphism in all species studied. These results demonstrate that the Harderian glands of the animal species examined exhibit a variety of histological autofluorescence patterns.

Animals↗

Semen quality of workers occupationally exposed to hydrocarbons.

OBJECTIVE: To determine whether occupational exposure of men to hydrocarbons has adverse effects on the quality of their semen. DESIGN: Comparative study. SETTING: The rubber industry in Mexico City. PATIENT(S): Forty-eight workers who were exposed to hydrocarbons for 2-24 years and 42 unexposed workers. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Environmental hydrocarbon concentrations were determined by continuous air monitoring in all areas of the factory. Analyses of semen samples were performed in accordance with World Health Organization criteria. RESULT(S): Hydrocarbon concentrations were as follows: ethylbenzene, 220.7-234 mg/m3; benzene, 31.9-47.8 mg/m3; toluene, 189.7-212.5 mg/m3; and xylene, 47-56.4 mg/m3. The number of subjects with ejaculates that had normal characteristics was greater in the unexposed group (76%) than in the exposed group (17%). More abnormal characteristics were found in the semen of exposed workers than unexposed workers, including alterations in viscosity, liquefaction capacity, sperm count, sperm motility, and the proportion of sperm with normal morphology. Some abnormal characteristics correlated with the number of years of exposure to the hydrocarbons. CONCLUSION(S): Damage to the spermatogenic process resulting from hydrocarbon exposure was demonstrated by an increased rate of abnormalities in the semen of exposed workers compared with unexposed workers. This information may be useful for conducting future analyses of reproductive risks related to exposure to high concentrations of hydrocarbons.

Adult↗

Prefrontocortical serotonin depletion results in plastic changes of prefrontocortical pyramidal neurons, underlying a greater efficiency of short-term memory.

The prefrontal cortex activity is involved in organizing the short-term memory. Although the involvement of serotonin for an appropriate performance in learning and memory tests is well known, its role is still unclear; as is the cellular basis of short-term memory behavioral performance. Sprague-Dawley rats were stereotactically injected with 1 microg/microl of 5, 7-dihydroxitryptamine to cause a lesion to the dorsal raphe nucleus. Sham-operated or intact rats were also studied as control groups. Before surgery and 20 days post-operatively, each animal was placed in the Biel maze for five consecutive trials. In the pre-treatment test, all three groups decreased significantly the number of errors beginning with the fourth trial. The same occurred in the post-treatment test, except for the experimental group, whose animals committed less errors beginning with the second trial. After behavioral testing, the dorsomedial prefrontal cerebral cortex was dissected out, and the Golgi study of the third-layer pyramidal neurons revealed that the length of both the apical and the basilar dendrites was smaller than that of controls, and that the apical and oblique dendrites had a greater spine density. A major proportion of thin spines was also seen on the basilar and oblique dendrites, and more stubby spines were seen on the apical dendrite. Serotonin depletion in the prefrontal cerebral cortex resulted in cytoarchitectural alterations of the prefrontocortical pyramidal neurons, which may be underlying partially the greater efficiency observed in the short-term memory behavioral performance.

Animals↗

Increased expression of gamma-aminobutyric acid transporter-1 in the forebrain of infant rats with corticotropin-releasing hormone-induced seizures but not in those with hyperthermia-induced seizures.

High affinity, gamma-aminobutyric acid (GABA) plasma membrane transporters (GATs) influence the availability of GABA, the main inhibitory neurotransmitter in the brain. Recent studies suggest a crucial role for GATs in maintaining levels of synaptic GABA in normal as well as abnormal (i.e., epileptic) adult brain. However, the role of GATs during development and specifically changes in their expression in response to developmental seizures are unknown. The present study examined GAT-1-immunolabeling in infant rats with two types of developmental seizures, one induced by corticotropin-releasing hormone (CRH) lasting about 2 h and the other by hyperthermia (a model of febrile seizures) lasting only 20 min. The number of GAT-1-immunoreactive (ir) neurons was increased in several forebrain regions 24 h after induction of seizures by CRH as compared to the control group. Increased numbers of detectable GAT-1-ir cell bodies were found in the hippocampal formation including the dentate gyrus and CA1, and in the neocortex, piriform cortex and amygdala. In contrast, hyperthermia-induced seizures did not cause significant changes in the number of detectable GAT-1-ir somata. The increase in GAT-1-ir somata in the CRH model and not in the hyperthermia model may reflect the difference in the duration of seizures. The brain regions where this increase occurs correlate with the occurrence of argyrophyllic neurons in the CRH model.

Animals↗

Effects of melatonin on the Harderian gland of lipopolysaccharide-treated rats: morphological observations.

Melatonin is a free radical scavenger and antioxidant. This indol is reported to efficiently scavenge both hydroxyl and peroxyl radicals and it also reduces both in vitro and in vivo tissue damage due to oxidants which generate oxygen toxic radicals. Lipopolysaccharide (LPS) administration induces oxidative damage in various tissues mainly due to its ability to increase reactive oxygen species. In the present work, we studied the morphological changes and lipid peroxidation in the Harderian gland after LPS administration and the effects of melatonin in preventing the induced changes. Hyperchromasia, vesicular degeneration, necrosis and infiltration with macrophages, monocytes and neutrophils were observed in the LPS-treated group (10 mg/kg, intraperitonally [i.p.]). Also, a typical structure of the glandular acini of the gland exhibited diffuse damage. In the LPS rats treated with melatonin (10 mg/kg, i.p.), a diminished number of infiltrative cells was seen, and cloudy swelling was reduced, as was nuclear hyperchromasia. Neither necrosis nor vesicular degeneration were noted in the melatonin-treated rats, and in general, glandular structure was preserved. Lipid peroxidation products increased significantly within six hours after LPS administration, and melatonin treatment decreased the LPS-dependent lipid peroxidation products. These data together suggest that melatonin protects the Harderian gland against LPS toxicity in terms of morphological damage.

Animals↗

Neuronal differentiation of chromaffin cells in vitro, induced by extremely low frequency magnetic fields or nerve growth factor: a histological and ultrastructural comparative study.

The application of nerve growth factor (NGF) to primary adrenal medulla chromaffin cell cultures induces phenotypic changes characterized mainly by the presence of neurites. A similar effect has been seen when these cells are stimulated by extremely low frequency magnetic fields (ELFMF). In this study, newborn rat chromaffin cells were cultured and subjected to NGF or ELFMF in order to compare their histological and ultrastructural characteristics. Cells cultured in the presence of NGF developed cytoplasmic projections and their distal ends showed growth cones as well as filopodia. With scanning and transmission electron microscopy, an increased submembranous electron density was observed in the nuclei of cells as well as irregular, wavy neuritic projections with a moderate number of varicosities, as well as the prevalence of intermediate filaments among the cytoskeleton components. Cells stimulated with ELFMF presented straighter neuritic extensions with a greater number of varicosities. With the transmission electron microscope, numerous neurotubules were observed, both in the cell soma and in their neuritic extensions. In both groups, growth cones were clearly identified by their ultrastructural characteristics. The differences seen in the cytoskeleton of cells stimulated with NGF or ELFMF suggest differential stimulation mechanisms possibly determining the biochemical, electrophysiological, and morphological characteristics in both types of cell cultures.

Adrenal Medulla↗

Spontaneous long-term remyelination after traumatic spinal cord injury in rats.

The capability of the central nervous system to remyelinate axons after a lesion has been well documented, even though it had been described as an abortive and incomplete process. At present there are no long-term morphometric studies to assess the spinal cord (S.C.) remyelinative capability. With the purpose to understand this phenomenon better, the S.C. of seven lesionless rats and the S.C. of 21 rats subjected to a severe weight-drop contusion injury were evaluated at 1, 2, 4, 6, and 12 months after injury. The axonal diameter and the myelination index (MI = axolemmal perimeter divided by myelinated fiber perimeter) were registered in the outer rim of the cord at T9 SC level using a transmission electron microscope and a digitizing computer system. The average myelinated fiber loss was 95.1%. One month after the SC, 64% of the surviving fibers were demyelinated while 12 months later, only 30% of the fibers had no myelin sheath. The MI in the control group was 0.72 +/- 0.07 (X +/- S.D.). In the experimental groups, the greatest demyelination was observed two months after the lesion (MI = 0.90 +/- 0.03), while the greatest myelination was observed 12 months after the injury (MI = 0.83 +/- 0.02). There was a statistical difference (p < 0.02) in MI between 2 and 12 months which means that remyelination had taken place. Remyelination was mainly achieved because of Schwann cells. The proportion of small fibers (diameter = 0.5 micron or less) considered as axon collaterals, increased from 18.45% at 1 month to 27.66% a year after the contusion. Results suggest that remyelination is not an abortive phenomenon but in fact a slow process occurring parallel to other tissue plastic phenomena, such as the emission of axon collaterals.

Animals↗

Effect of tryptophan restriction on short-term memory.

Several brain regions are involved in the learning process that is integrated from sensorial inputs. It is thereafter consolidated in short- (STM) or long-term memory. Serotonin is strongly related to both types of memory, and particularly, to STM, however, its regulatory role is still unclear. In this study, the effects of tryptophan (TRY) restriction on learning and STM were evaluated. Ten Sprague-Dawley female rats were fed with a TRY-restricted diet (0.15g/100g) starting from postnatal Day 21. At 21, 40, and 60 days of age, 5 trials per animal were carried out in a "hard-floor"-Biel maze, after 24 h of water abstinence. The number of errors per trial were registered before reaching the goal. At both 40 and 60 days, experimental rats committed less errors than controls. Likewise, the TRY-restricted group learned the task from the second trial on, whereas controls did not solve it until the third trial. TRY restriction, and therefore brain serotonin reduction, could impair normal cholinergic activity in some areas such as the hippocampus and the cerebral cortex, where involvement in learning and memory is well documented. Morphological and neurochemical plastic events could also be related to the more efficient performance of the task by the TRY-restricted rats.

Aging↗