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Biomédica (Bogotá) ; 34(2): 207-217, abr.-jun. 2014. ilus, graf
Article in English | LILACS | ID: lil-712403


Introduction: Cerebral ischemia is the third leading cause of death and the primary cause of permanent disability worldwide. Atorvastatin is a promising drug with neuroprotective effects that may be useful for the treatment of stroke. However, the effects of atorvastatin on specific neuronal populations within the nigrostriatal system following cerebral ischemia are unknown. Objective: To evaluate the effects of atorvastatin on dopaminergic and GABAergic neuronal populations in exofocal brain regions in a model of transient occlusion of the middle cerebral artery. Materials and methods: Twenty-eight male eight-week-old Wistar rats were used in this study. Both sham and ischemic rats were treated with atorvastatin (10 mg/kg) or carboxymethylcellulose (placebo) by gavage at 6, 24, 48 and 72 hours post-reperfusion. We analyzed the immunoreactivity of glutamic acid decarboxylase and tyrosine hydroxylase in the globus pallidus, caudate putamen and substantia nigra. Results: We observed neurological damage and cell loss in the caudate putamen following ischemia. We also found an increase in tyrosine hydroxylase immunoreactivity in the medial globus pallidus and substantia nigra reticulata, as well as a decrease in glutamic acid decarboxylase immunoreactivity in the lateral globus pallidus in ischemic animals treated with a placebo. However, atorvastatin treatment was able to reverse these effects, significantly decreasing tyrosine hydroxylase levels in the medial globus pallidus and substantia nigra reticulata and significantly increasing glutamic acid decarboxylase levels in the lateral globus pallidus. Conclusion: Our data suggest that post-ischemia treatment with atorvastatin can have neuro-protective effects in exofocal regions far from the ischemic core by modulating the GABAergic and dopaminergic neuronal populations in the nigrostriatal system, which could be useful for preventing neurological disorders.

Introducción. La isquemia cerebral es la tercera causa de muerte y la primera de discapacidad permanente en el mundo. La atorvastatina es un fármaco neuroprotector prometedor para el tratamiento de la apoplejía; sin embargo, su acción sobre las poblaciones neuronales del sistema nigroestriatal después de la isquemia aún se desconoce. Objetivo. Evaluar el efecto de la atorvastatina sobre poblaciones gabérgicas y dopaminérgicas en regiones exofocales en un modelo de oclusión transitoria de la arteria cerebral media. Materiales y métodos. Se utilizaron 28 ratas Wistar macho de ocho semanas de edad. Los ejemplares con isquemia simulada y los ejemplares sometidos a isquemia fueron tratados con atorvastatina (10 mg/kg) y carboximetilcelulosa (placebo) administrados por medio de sonda a las 6, 24, 48 y 72 horas después de la reperfusión. Se analizó la inmunorreacción de la descarboxilasa del ácido glutámico y de la tirosina hidroxilasa en el globo pálido, el putamen caudado y la sustancia negra. Resultados. Los datos confirmaron el daño neurológico y la pérdida celular en el putamen caudado. Se incrementó la inmunorreacción de la tirosina hidroxilasa en el globo pálido medial y la sustancia negra pars reticulata , disminuyendo la inmunorreacción de la descarboxilasa del ácido glutámico en el globo pálido lateral de los animales isquémicos tratados con placebo; sin embargo, el tratamiento con atorvastatina pudo revertirla, lo que logró una disminución significativa de la tirosina hidroxilasa en el globo pálido medial y la sustancia negra pars reticulata y aumentando los niveles de descarboxilasa del ácido glutámico en el globo pálido lateral. Conclusión. Nuestros datos sugieren que la atorvastatina en el tratamiento posterior a la isquemia ejerce neuroprotección en las zonas exofocales, modulando las poblaciones neuronales gabérgicas y dopaminérgicas del sistema nigroestriatal, lo que podría prevenir trastornos neurológicos.

Animals , Male , Rats , Corpus Striatum/drug effects , Dopaminergic Neurons/drug effects , GABAergic Neurons/drug effects , Heptanoic Acids/therapeutic use , Infarction, Middle Cerebral Artery/drug therapy , Ischemic Attack, Transient/drug therapy , Neuroprotective Agents/therapeutic use , Pyrroles/therapeutic use , Substantia Nigra/drug effects , Behavior, Animal , Corpus Striatum/blood supply , Corpus Striatum/pathology , Drug Evaluation, Preclinical , Dopaminergic Neurons/enzymology , Dopaminergic Neurons/pathology , Enzyme Induction/drug effects , GABAergic Neurons/enzymology , GABAergic Neurons/pathology , Glutamate Decarboxylase/biosynthesis , Glutamate Decarboxylase/genetics , Heptanoic Acids/pharmacology , Infarction, Middle Cerebral Artery/pathology , Ischemic Attack, Transient/pathology , Movement Disorders/etiology , Movement Disorders/prevention & control , Nerve Tissue Proteins/biosynthesis , Nerve Tissue Proteins/genetics , Neuroprotective Agents/pharmacology , Pyrroles/pharmacology , Rats, Wistar , Recovery of Function , Specific Pathogen-Free Organisms , Sensation Disorders/etiology , Sensation Disorders/prevention & control , Substantia Nigra/blood supply , Substantia Nigra/pathology , /biosynthesis , /genetics
Biol. Res ; 44(4): 311-321, 2011. ilus, tab
Article in English | LILACS | ID: lil-626729


The origin of axoplasmic proteins is central for the biology of axons. For over fifty years axons have been considered unable to synthesize proteins and that cell bodies supply them with proteins by a slow transport mechanism. To allow for prolonged transport times, proteins were assumed to be stable, i.e., not degraded in axons. These are now textbook notions that configure the slow transport model (STM). The aim of this article is to cast doubts on the validity of STM, as a step toward gaining more understanding about the supply of axoplasmic proteins. First, the stability of axonal proteins claimed by STM has been disproved by experimental evidence. Moreover, the evidence for protein synthesis in axons indicates that the repertoire is extensive and the amount sizeable, which disproves the notion that axons are unable to synthesize proteins and that cell bodies supply most axonal proteins. In turn, axoplasmic protein synthesis gives rise to the metabolic model (MM). We point out a few inconsistencies in STM that MM redresses. Although both models address the supply of proteins to axons, so far they have had no crosstalk. Since proteins underlie every conceivable cellular function, it is necessary to re-evaluate in-depth the origin of axonal proteins. We hope this will shape a novel understanding of the biology of axons, with impact on development and maintenance of axons, nerve repair, axonopathies and plasticity, to mention a few fields.

Animals , Mice , Axonal Transport/physiology , Nerve Tissue Proteins/biosynthesis , Models, Neurological , Nerve Tissue Proteins/physiology , Schwann Cells/physiology
Article in English | WPRIM | ID: wpr-205427


Even though there is no direct evidence to prove the cellular and molecular changes induced by radiofrequency (RF) radiation itself, we cannot completely exclude the possibility of any biological effect of mobile phone frequency radiation. We established a carousel-type exposure chamber for 849 MHz or 1763 MHz of mobile phone RF radiation to expose RF to the heads of C57BL mice. In this chamber, animals were irradiated intermittently at 7.8 W/kg for a maximum of 12 months. During this period, the body weights of 3 groups-sham, 849 MHz RF, and 1763 MHz RF-did not show any differences between groups. The brain tissues were obtained from 3 groups at 6 months and 12 months to examine the differences in histology and cell proliferation between control and RF exposure groups, but we could not find any change upon RF radiation. Likewise, we could not find changes in the expression and distribution of NeuN and GFAP in hippocampus and cerebellum, or in cell death by TUNEL assay in RF exposure groups. From these data, we conclude that the chronic exposure to 849 MHz and 1763 MHz RF radiation at a 7.8 W/kg specific absorption rate (SAR) could not induce cellular alterations such as proliferation, death, and reactive gliosis.

Animals , Apoptosis/radiation effects , Body Weight/radiation effects , Brain/pathology , Cell Proliferation/radiation effects , Cell Phone , Dose-Response Relationship, Radiation , Gliosis/etiology , In Situ Nick-End Labeling , Mice , Mice, Inbred C57BL , Nerve Tissue Proteins/biosynthesis , Proliferating Cell Nuclear Antigen/biosynthesis , Radio Waves/adverse effects
Article in English | WPRIM | ID: wpr-184697


The expression of nitric oxide synthase (NOS) isoforms in the ovaries of pigs was examined to study the involvement of nitric oxide, a product of NOS activity, in the function of the ovary. Western blot analysis detected three types of NOS in the ovary, including constitutive neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS); eNOS immunoreactivity was more intense compared with that of iNOS or nNOS. Immunohistochemical studies demonstrated the presence of nNOS and eNOS in the surface epithelium, stroma, oocytes, thecal cells, and endothelial cells of blood vessels. Positive immunoreactions for nNOS and iNOS were detected in the granulosa cells from multilaminar and antral follicles, but not in those of unilaminar follicles. iNOS was detected in the surface epithelium, oocytes, and theca of multilaminar and antral follicles. Taking all of the findings into consideration, the observed differential expression of the three NOS isoforms in the ovary suggests a role for nitric oxide in modulating reproduction in pigs.

Animals , Blotting, Western/veterinary , Female , Immunohistochemistry/veterinary , Nerve Tissue Proteins/biosynthesis , Nitric Oxide/metabolism , Nitric Oxide Synthase/biosynthesis , Nitric Oxide Synthase Type I , Nitric Oxide Synthase Type II , Nitric Oxide Synthase Type III , Ovarian Follicle/enzymology , Swine/physiology
Article in English | WPRIM | ID: wpr-37856


Apoptosis, the cell's intrinsic death program, plays a crucial role in the regulation of tissue homeostasis, and abnormal inhibition of apoptosis is an indicator of cancer and autoimmune diseases, whereas excessive cell death is implicated in neurodegenerative disorders such as Alzheimer's disease (AD). Using cDNA subtraction analysis, we compared p60TRP (p60 transcription regulator protein) expressing cells with control cells during the process of apoptosis and we identified the new zinc-finger protein p48ZnF that is predominantly located in the cytoplasm of the cell. Additionally, we demonstrate here that p48ZnF is up-regulated in rat neuronal PC12 cells upon stimulation with the neurotrophic factor NGF (50 ng/ml). These findings point to a possible pivotal role of p48ZnF in the control of neuronal survival.

Alzheimer Disease/genetics , Animals , Apoptosis , Autoimmune Diseases/genetics , Base Sequence , Biomarkers , CHO Cells , Cell Survival/drug effects , Cloning, Molecular , Cytoplasm/metabolism , DNA-Binding Proteins/biosynthesis , Gene Expression Profiling , Gene Expression Regulation/drug effects , Cricetinae , Molecular Sequence Data , Neoplasms/metabolism , Nerve Growth Factor/pharmacology , Nerve Tissue Proteins/biosynthesis , PC12 Cells , RNA, Messenger/biosynthesis , Rats , Transcription Factors/biosynthesis , Transfection , Zinc Fingers/genetics