Does dexamethasone act in neuropeptides SP and CGRP in neurogenic inflammation of the skin? An experimental study

PURPOSE: To investigate the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) after subcutaneous injection of dexamethasone prior to skin incision in rats.METHODS:Twenty seven Wistar-EPM-1 rats were randomly divided into three groups. The sham group (SG) of rats was injected with 0.9 % saline. The second group (Dexa) was injected with 1.0 mg/kg dexamethasone, and the third group (Dexa+) was injected with 10.0 mg/kg dexamethasone. In all groups, the three subcutaneous injections were performed 30 minutes prior to the surgical skin incision and tissue collection. SP and CGRP (15 kDa pro-CGRP and 5 kDa CGRP) were quantified by Western Blotting.RESULTS: No statistically significant differences (p>0.05) were found in pro-CGRP, CGRP and SP values in all three groups.CONCLUSION:The anti-inflammatory effect of dexamethasone did not occur when the substance P and calcitonin gene-related peptide levels were altered during the neurogenic inflammation process of skin wound healing in rats.

Clinical aspects of patients with sarcoglycanopathies under steroids therapy / Aspectos clínicos de pacientes com sarcoglicanopatias sob efeito de corticoterapia

Patients with sarcoglycanopathies, which comprise four subtypes of autosomal recessive limb-girdle muscular dystrophies, usually present with progressive weakness leading to early loss of ambulation and premature death, and no effective treatment is currently available. Objective To present clinical aspects and outcomes of six children with sarcoglycanopathies treated with steroids for at least one year. Method Patient files were retrospectively analyzed for steroid use. Results Stabilization of muscle strength was noted in one patient, a slight improvement in two, and a slight worsening in three. In addition, variable responses of forced vital capacity and cardiac function were observed. Conclusions No overt clinical improvement was observed in patients with sarcoglycanopathies under steroid therapy. Prospective controlled studies including a larger number of patients are necessary to determine the effects of steroids for sarcoglycanopathies. .

Pacientes com sarcoglicanopatias, que compreendem quatro subtipos de distrofias musculares de cinturas autossômicas recessivas, geralmente apresentam fraqueza progressiva, levando à perda precoce da deambulação e morte prematura, e não há tratamento eficaz disponível até o momento. Objetivo Descrever os aspectos clínicos e a evolução de seis crianças com sarcoglicanopatias tratados com corticosteróides por pelo menos um ano. Método Prontuários dos pacientes foram analisados retrospectivamente. Resultados Estabilização da força muscular foi observada em um paciente, uma ligeira melhora em dois, e um ligeiro agravamento em três. Além disso, foram observadas respostas variáveis de capacidade vital forçada e da função cardíaca. Conclusões Não houve melhora clínica evidente em pacientes com sarcoglicanopatias sob terapia com corticosteróides. Estudos prospectivos controlados incluindo maior número de pacientes são necessários para determinar os efeitos dos corticosteróides para sarcoglicanopatias. .

Effects of subcutaneous carbon dioxide on calcitonin gene related peptide and substance P secretion in rat skin

To investigate the subcutaneous injection of carbon dioxide (CO2) on neuropeptides Calcitonin Gene-Related Peptide (CGRP) and Substance P (SP) secretion in rat skin. Fifty-six Wistar-EPM rats were distributed in two groups: one for CGRP analysis, the other for SP analysis. Each group was subdivided into four subgroups: control (Cont), control with needle (ContNd), CO2 injection (CO2Inj) and atmospheric air injection (AirInj) - with seven animals each. Sample analyses of partial skin were conducted by Western Blotting (WB). RESULTS: In SP group, there was a decrease in the amount of neuropeptides in subgroups CO2Inj and AirInj. Similarly, in CGRP group, there was a decrease in the amount of pro-CGRP neuropeptides (15 kDa) in subgroups CO2Inj and AirInj; Nevertheless, there was no decrease in the amount of CGRP (5 kDa) in any subgroups. Subcutaneous injection of CO2 and atmospheric air decreased the amount of Substance P and pro-Calcitonin Gene-Related Peptide (15 kDa) neuropeptides in rat skin.

A estimulação elétrica funcional (FES) e a plasticidade do sistema nervoso central: revisão histórica / Functional electrical stimulation (FES) and neuronal plasticity: a historical review

Estudos têm revelado modificações plásticas neuronais concomitantes a melhora clínica de pacientes portadores de lesões neurológicas e submetidos às terapias de estimulação, sugerindo que as respostas plásticas observadas no tecido neuronal podem refletir a recuperação funcional encontrada e ser dependentes, pelo menos em parte, da estimulação externa. A literatura já indica também que as terapias de reabilitação mais promissoras são aquelas que interagem com as características plásticas naturais do SNC, encontrando no potencial endógeno de recuperação do tecido lesado o substrato anatômico necessário para a sua atuação. A interpretação desses resultados permanece ambígua, já que há uma grande variabilidade nas respostas neurofisiológicas e comportamentais para as técnicas de estimulaçãoestudadas. Nesse sentido, uma nova área de atuação surge como perspectiva futura promissora no entendimento dos mecanismos que regulam a recuperação funcional após lesões neurológicas: o uso terapêutico da estimulação da plasticidade do SNC. Por exemplo com o uso de terapias de estimulação sensitiva, terapias baseadas na robótica e na realidade virtual e as terapias de neuromodulação baseadas na estimulação cortical direta, na estimulação com o TMS e na estimulação elétrica funcional periférica (FES). Objetivo: Este estudo tem por objetivo realizar uma revisão histórica da literatura para pontuar os principais marcos no estudo da estimulação elétrica periférica e de seus possíveis efeitos no SNC, sobretudo em relação a FES. Método: Foi utilizada a base de dados PUBMED e foram selecionados 169 artigos de melhor rigor metodológico, maior relevância histórica e maior contribuição na construção dos paradigmas que norteiam o estudo dos efeitos da FES na plasticidade do sistema nervoso central. Resultados: A FES pode ser encarada como uma técnica promissora na recuperação motora de doentes com sequela de alterações neurológicas de origem central tanto pela sua capacidade de levar a um treino funcional e melhora clínica sensitivomotora, aspectos já consagrados na literatura, quanto pela sua capacidade de interagir com a plasticidade do SNC, um aspecto que ainda precisa ser estudado.

Neurophysiological imaging studies have revealed changes in the pattern of cortical structures and clinical functionality during recovery after brain lesion, thus suggesting a correlation between clinical functional improvements and the plastic changes of the neuronal tissue. However, the interpretation of these results remains equivocal. Importantly, therapeutic neuronal stimulation leading to neurorehabilitation gains and is able to trigger endogenous nervous system changes that may interact with normal learning. In this way, stimulation of the endogenous CNS neuroplasticity as an anatomical substrate for neuronal functional recovery has emerged as a promising area in the search for understanding the mechanisms that regulate functional recovery after brain lesion. Objective: This study aims to review historical literature to score major milestones in the study of peripheral electrical stimulation and their possible effects on the CNS, particularly in relation to functional electrical stimulation. Method: This review was drawn from an examination of the historical literature articles researched at MEDLINE®, the National Library of Medicine?s database. We selected 169 studies based on historical relevance, importance, and accuracy. Results: FES has the ability to interact with the CNS. The extent to which compensatory plasticity occurs after stroke after FES use and the extent to which that contributes to functional recovery are as yet unclear. Nevertheless, further investigations are warranted for evaluating the effect of FES on cortical structural modifications.

Spinal cord injury as a trigger to develop periodic leg movements during sleep: an evolutionary perspective / Lesão medular como gatilho para desenvolver movimentos periódicos das pernas durante o sono: uma perspectiva evolutiva

The primary trigger to periodic limb movement (PLM) during sleep is still unknown. Its association with the restless legs syndrome (RLS) is established in humans and was reported in spinal cord injury (SCI) patients classified by the American Spinal Injury Association (ASIA) as A. Its pathogenesis has not been completely unraveled, though recent advances might enhance our knowledge about those malfunctions. PLM association with central pattern generator (CPG) is one of the possible pathologic mechanisms involved. This article reviewed the advances in PLM and RLS genetics, the evolution of CPG functioning, and the neurotransmitters involved in CPG, PLM and RLS. We have proposed that SCI might be a trigger to develop PLM.

O gatilho principal para o desenvolvimento de movimentos periódicos dos membros (MPM) durante o sono ainda é desconhecido. A associação entre o MPM e a síndrome das pernas inquietas (SPI) em seres humanos já foi previamente estabelecida e relatada em pacientes com lesão medular (LM), classificados pela American Spinal Injury Association (ASIA) como A. A patogênese do MPM não foi completamente desvendada, apesar de avanços recentes poderem ampliar o conhecimento sobre essas disfunções. Um dos possíveis mecanismos patológicos envolvidos é o gerador de padrão central (GPC). Este artigo revisou os avanços na genética do MPM e da SPI, a evolução do funcionamento do GPC e os neurotransmissores relacionados ao GPC, ao MPM e à SPI. Foi proposta a hipótese de que a LM poderia ser um gatilho para deflagrar os MPM.

The review of the methods to obtain non-neuronal cells to study glial influence on Amyotrophic Lateral Sclerosis pathophysiology at molecular level in vitro / Revisão dos métodos de obtenção de células não neuronais para o estudo da fisiopatologia da Esclerose Lateral Amiotrófica ao nível molecular in vitro

PURPOSE: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that displays a rapid evolution. Current treatments have failed to revert clinical symptoms because the mechanisms involved in the death of motoneuron are still unknown. Recent publications have put non-neuronal cells, particularly, astrocyte and microglia, in the scenario of pathophisiology of the disease. Animal models for ALS, particularly transgenic mice expressing the human SOD1 gene with a G93A mutation (hSOD1), are available and display the phenotype of the disease at cellular and clinical levels. However, it is a lack of detailed information regarding the methods to study the disease in vitro to better understand the contribution of non-neuronal cells in the onset and progression of the pathology. METHODS: Colonies of Swiss mice and transgenic mice expressing hSOD1 mutation as well as non-transgenic controls (wild-type) were amplified after a genotyping evaluation. Disease progression was followed behaviorally and mortality was registered. Highly purified primary cultures of astrocytes and microglia from mouse spinal cord were obtained. Cells were identified by means of GFAP and CD11B immunocytochemistry. The purity of astroglial and microglial cell cultures was also accompanied by means of Western blot and RT-PCR analyses employing a number of markers. RESULTS: The disease onset was about 105 days and the majority of transgenic mice displayed the disease symptoms by 125 days of age and reached the endpoint 20 days later. A substantial motor weakens was registered in the transgenic mice compared to wild-type at the end point. Immunocytochemical, biochemical and RT-PCR analyses demonstrated a highly purified primary cultures of spinal cord astrocytes and microglia. CONCLUSION: It is possible to achieve highly purified primary cultures of spinal cord astrocytes and microglia to be employed in cellular and molecular analyses of the influence of such non-neuronal cells in the pathophysiology of ALS.

OBJETIVO: A esclerose lateral amiotrófica (ELA) é uma doença neurodegenerativa fatal com evolução rápida. Os tratamentos atualmente disponíveis falham em reverter os sintomas porque os mecanismos envolvidos na morte do neurônio motor ainda não são conhecidos. Publicações recentes colocam as células não neuronais, particularmente o astrócito e a microglia, no cenário da fisiopatologia da doença. Modelos animais para a ELA, particularmente os camundongos transgênicos que expressam o gene da SOD1 humana (hSOD1) mutante estão disponíveis e mostram o fenótipo da doença ao nível celular e clínico. Entretanto, informações detalhadas são escassas sobre os métodos de estudo da doença in vitro para a melhor compreensão da participação das células não neuronais no início e na progressão da patologia. MÉTODOS: Colônias de camundongos Swiss e camundongos transgênicos que expressam a hSOD1 mutante assim como os controles não transgênicos (selvagem) foram amplificadas após avaliação genotípica. A progressão da doença foi acompanhada pelo comportamento e a mortalidade foi registrada. Culturas primárias altamente purificadas de astrócitos e microglia da medula espinal dos camundongos foram obtidas. As células foram identificadas pela immunocitoquímica da GFAP e CD11B. A pureza das culturas de astrócitos e microglia foi acompanhada pelas análises do Western blot e RT-PCR empregando-se marcadores específicos. RESULTADOS: Os primeiros sinais da doença ocorreram por volta dos 105 dias de vida e a maioria dos camundongos transgênicos já estava com a doença manifestada aos 125 dias de idade e alcançaram o estágio terminal aproximadamente 20 dias depois. Fraqueza substancial da força muscular foi registrada nos animais transgênicos comparados com os animais selvagens. Análises imuncitoquímica, bioquímica e pelo RT-PCR demonstraram culturas primárias altamente purificadas de astrócito e microglia da medula espinal dos camundongos. CONCLUSÃO: É possível obter culturas purificadas de astrócitos e microglia da medula espinal do camundongo a ser empregadas em análises celulares e moleculares da influência destas células não neuronais na fisiopatologia da ELA.

S100ß and fibroblast growth factor-2 are present in cultured Schwann cells and may exert paracrine actions on the peripheral nerve injury / S100ß e fator de crescimento de fibroblasto-2 estão presentes nas células de Schwann cultivadas e exercem ações parácrinas na lesão do nervo

PURPOSE: The neurotrophic factor fibroblast growth factor-2 (FGF-2, bFGF) and Ca++ binding protein S100ß are expressed by the Schwann cells of the peripheral nerves and by the satellite cells of the dorsal root ganglia (DRG). Recent studies have pointed out the importance of the molecules in the paracrine mechanisms related to neuronal maintenance and plasticity of lesioned motor and sensory peripheral neurons. Moreover, cultured Schwann cells have been employed experimentally in the treatment of central nervous system lesions, in special the spinal cord injury, a procedure that triggers an enhanced sensorymotor function. Those cells have been proposed to repair long gap nerve injury. METHODS: Here we used double labeling immunohistochemistry and Western blot to better characterize in vitro and in vivo the presence of the proteins in the Schwann cells and in the satellite cells of the DRG as well as their regulation in those cells after a crush of the rat sciatic nerve. RESULTS: FGF-2 and S100ß are present in the Schwann cells of the sciatic nerve and in the satellite cells of the DRG. S100ß positive satellite cells showed increased size of the axotomized DRG and possessed elevated amount of FGF-2 immunoreactivity. Reactive satellite cells with increased FGF-2 labeling formed a ring-like structure surrounding DRG neuronal cell bodies.Reactive S100ß positive Schwann cells of proximal stump of axotomized sciatic nerve also expressed higher amounts of FGF-2. CONCLUSION: Reactive peripheral glial cells synthesizing FGF-2 and S100ß may be important in wound repair and restorative events in the lesioned peripheral nerves.

OBJETIVO: O fator neurotrófico fator de crescimento de fibroblastos-2 (FGF-2, bFGF) e a proteína ligante de Ca++ S100ß são expressos pelas células de Schwann dos nervos e por células satélites do gânglio da raiz dorsal (GRD). Estudos recentes indicam a importância das moléculas nos mecanismos parácrinos relacionados à manutenção neuronal e à plasticidade de neurônios periféricos motores e sensoriais. Além disso, células de Schwann cultivadas têm sido empregadas experimentalmente no tratamento de lesões no sistema nervo central, especialmente na lesão da medula espinal, a qual mostrou uma melhora da função sensoriomotora. Estas células são ainda propostas no reparo do nervo lesado com perda de tecido. MÉTODOS: Usamos a dupla marcação imunohistoquímica e o Western blot para caracterizar melhor in vitro e in vivo a presença das proteínas nas células de Schwann e nas células satélites do GRD assim como sua regulação nessas células após a compressão do nervo ciático de ratos. RESULTADOS: FGF-2 e S100ß estão presentes nas células de Schwann do nervo ciático e nas células satélites do GRD. Células satélites do GRD axotomizado positivas para S100ß possuíam quantidade aumentada de imurreatividade da FGF-2. Células satélites reativas apresentando maior quantidade de FGF-2 formaram um anel ao redor dos corpos neuronais do GRD. Células de Schwann do coto proximal à axotomia do nervo ciático e positivas para S100ß também expressaram quantidades aumentadas de FGF-2. CONCLUSÃO: As células gliais periféricas ao sintetizar FGF-2 e S100ß podem ser importantes no reparo de cicatrização e em eventos restaurativos nas lesões do nervo.

Differential astroglial responses in the spinal cord of rats submitted to a sciatic nerve double crush treated with local injection of cultured Schwann cell suspension or lesioned spinal cord extract: implications on cell therapy for nerve repair

PURPOSE: Reactive astrocytes are implicated in several mechanisms after central or peripheral nervous system lesion, including neuroprotection, neuronal sprouting, neurotransmission and neuropathic pain. Schwann cells (SC), a peripheral glia, also react after nerve lesion favoring wound/repair, fiber outgrowth and neuronal regeneration. We investigated herein whether cell therapy for repair of lesioned sciatic nerve may change the pattern of astroglial activation in the spinal cord ventral or dorsal horn of the rat. METHODS: Injections of a cultured SC suspension or a lesioned spinal cord homogenized extract were made in a reservoir promoted by a contiguous double crush of the rat sciatic nerve. Local injection of phosphate buffered saline (PBS) served as control. One week later, rats were euthanized and spinal cord astrocytes were labeled by immunohistochemistry and quantified by means of quantitative image analysis. RESULTS: In the ipsilateral ventral horn, slight astroglial activations were seen after PBS or SC injections, however, a substantial activation was achieved after cord extract injection in the sciatic nerve reservoir. Moreover, SC suspension and cord extract injections were able to promote astroglial reaction in the spinal cord dorsal horn bilaterally. Conclusion: Spinal cord astrocytes react according to repair processes of axotomized nerve, which may influence the functional outcome. The event should be considered during the neurosurgery strategies.

OBJETIVO: Astrócitos reativos participam de vários mecanismos após lesões do sistema nervoso central e periférico, os quais incluem neuroproteção, brotamento neuronal, neurotransmissão e dor neuropática. As células de Schwann (CS), um tipo de glia periférica, também reagem com a lesão do nervo, podendo interferir com o reparo e cicatrização, crescimento de fibras e regeneração neuronais. Investigamos aqui a possibilidade da terapia celular para o reparo do nervo ciático poder alterar o padrão da ativação astrocitária nos cornos anterior e posterior da medula espinal do rato. MÉTODOS: Suspensão de CS cultivadas ou extrato homogeneizado de medula espinal lesada de rato foram inoculados num reservatório feito a partir de dois esmagamentos aplicados no nervo ciático do rato distantes 0,5mm entre si. Injeção local de salina tamponada serviu como controle. Os ratos foram mortos uma semana após e os astrócitos da medula espinal marcados por método imunohistoquímico e quantificados por análise de imagem. RESULTADOS: No corno anterior da medula, ipsilateral à lesão, ativação astrocitária leve foi vista após as injeções de tampão ou CS, entretanto, ativação celular intensa foi observada nesta região com a inoculação neural do extrato homogeneizado de tecido medular lesado. Adicionalmente, as inoculações de CS e de extrato homogeneizado de tecido medular promoveram forte reação astrocitária no corno dorsal da medula espinal, bilateralmente. CONCLUSÕES: Os astrócitos da medula espinal reagem em função do processo de reparo do nervo lesado, o que pode influenciar o resultado funcional esperado, algo que deve ser considerado durante o planejamento da estratégia neurocirúrgica.

Striatal injection of 6-hydroxydopamine induces retrograde degeneration and glial activation in the nigrostriatal pathway

PURPOSE: The effect of a highly selective 6-hydroxydopamine (6-OHDA)-induced lesion of the nigrostriatal system on the astroglial and microglial activation was analysed in adult Wistar rats after an unilateral striatal injection of the neurotoxin. METHODS: Male rats received an unilateral stereotaxical injection of the 6-OHDA in the left side of the neostriatum and were sacrificed 22 days later. Control animals received the injection of the solvent. The rotational behaviour was registered by a rotometer just before the sacrifice. Immunohistochemistry was employed for visualization of the tyrosine hydroxylase (TH) positive dopamine cells, glial fibrillary acidic protein (GFAP) immunolabeled astrocytes and OX42 immunoreactive microglia. Stereological method employing the optical disector was used to estimate the degree of the changes. RESULTS: The striatal injection of the 6-OHDA induced a massive disappearance (32 percent of control) of the TH immunoreactive terminals in a defined area within the striatum surrounding the injection site. A disappearance (54 percent of control) of dopamine cell bodies was observed in a small region of the ipsilateral pars compacta of the substantia nigra (SNc). The GFAP and OX42immunohistochemistry revealed astroglial and microglial reactions (increases in the number and size of the cells) in the ipsilateral neostriatum and SNc of the 6-OHDA injected rats. CONCLUSIONS: The striatal injection of 6-OHDA leads to retrograde degeneration as well as astroglial and microglial activation in the nigrostriatal dopamine pathway. Modulation of activated glial cells may be related to wound repair and to the trophic paracrine response in the lesioned nigrostriatal dopamine system.

Distant microglial and astroglial activation secondary to experimental spinal cord lesion

This paper analysed whether glial responses following a spinal cord lesion is restricted to a scar formation close to the wound or they might be also related to widespread paracrine trophic events in the entire cord. Spinal cord hemitransection was performed in adult rats at the thoracic level. Seven days and three months later the spinal cords were removed and submitted to immunohistochemistry of glial fibrillary acidic protein (GFAP) and OX42, markers for astrocytes and microglia, as well as of basic fibroblast growth factor (bFGF), an astroglial neurotrophic factor. Computer assisted image analysis was employed in the quantification of the immunoreactivity changes. At the lesion site an increased number of GFAP positive astrocytes and OX42 positive phagocytic cells characterized a dense scar formation by seven days, which was further augmented after three months. Morphometric analysis of the area and microdensitometric analysis of the intensity of the GFAP and OX42 immunoreactivities showed reactive astrocytes and microglia in the entire spinal cord white and gray matters 7 days and 3 months after surgery. Double immunofluorescence demonstrated increased bFGF immunostaining in reactive astrocytes. The results indicated that glial reaction close to an injury site of the spinal cord is related to wounding and repair events. Although gliosis constitutes a barrier to axonal regeneration, glial activation far from the lesion may contribute to neuronal trophism and plasticity in the lesioned spinal cord favoring neuronal maintenance and fiber outgrowth

Glial reaction in the hippocampus after global cardiogenic ischemia

Many experimental surgerical procedures have been perfomed in the analyse of the phenomenon of brain trophism and plasticity, however undesirable intercorrence can occour leading to specific changes in the results that should be taken into attention. To study this issue we have promoted a transient cardiogenic interruption of the blood flow together with a transient occlusion of the bilateral common carotid arteries (2VO) in rats and analysed the state of activation of astrocyte and microglia by means of the glial fibrillary acidic protein (GFAP) and OX42 immunohistochemistry, respectively. Rats were submitted to incomplete global cerebral ischemia (IGCI) by occlusion of the bilateral carotid arteries for 30 minutes. During the IGCI surgical, some rats received a higher dose of the chloral hydrate anaesthesia which promoted a cardiogenic interruption of the blood flow (CIBF) for a period of 10 minutes followed by and prompt reperfusion. During that period, animals were submited to a cardiac massage and ventilated. Sham operation were made in control animals. Rats were killed and their brains processed 14 days after the surgery. The animals that have received a IGCI showed a slight astroglial and microglial reaction in all subfields of the hippocampal formation, however the animal submitted to CIBF showed a massive infiltration of the reactive astrocyte and microglia in CA1 subfield. This results demonstrated that a transient occlusion of the bilateral common carotid arteries leads to activation of glial cells in the hippocampus, however this response can be remarkable changed in animal developing a transient systemic hypoperfusion during surgery. Thus, an accurated monitoration of the hemodinamic condition of the animal has to be done in experimental models of brain ischemia and the results have to be analysed in view of this aspect.

O alcoolismo na gravidez e os efeitos na prole / The alcoholism in pregnancy

Os efeitos do consumo de álcool etílico durante a gravidez são discutidos nesta atualização, principalmente em relação aos aspectos clínicos, diagnósticos e experimentais da Síndrome Alcoólica Fetal (SAF), decorrente da teratogenia do etanol. São enfocados ainda os dados históricos, epidemiológicos, dos fatores predisponentes e fisiopatológicos da SAF, os relacionados com os resultados da pesquisa experimental, assim como as diferentes tentativas de prevenção e terapêuticas.

Experimental microneurosurgery of the central and peripheral nervous system in the study of the neuronal and glial trophism and plasticity

Trauma and neurodegenerative diseases commit the nervous system. After an axotomy or nerve injury in the peripheral nervous system the regeneration of the nerve fibers and reinervation of the target are seen. In central nervous system these events are restrictive, however their occurrence are related to the state of glial reaction and the synthesis of neurotrophic factors. Basic fibroblast growth factor (bFGF) has been considered an important trophic factor for neurons and astrocytes of many central nervous system regions. In this study rats were submitted to one of following neurosurgery procedures: callosotomy, pyramidectomy or complete transection of hypoglossal nerve (XII). Sham operations were made in control animals. Seven days later animals were sacrificed and their braims processed for immunohistochemistry. Coronal sections were taken from the central nervous system and incubated with antisera against the glial fibrillary acidic protein (GFAP) or neurofilament (NF), markers for astrocyte and neuronal cell body and fibers, respectively, as well as with the antiserum against the bFGF. The degree of the labelling was quatified with computer assisted stereological methods. The analysis of the NF immunoreactivity revealed a disappearance of fibers in the white matter distal to the pyramidectomy and callosotomy, however no disapperance of NF immunoreactive neurons was found in the XII nucleus following axotomy. These changes was accompanied by a massive astrocytic reaction. The reactive astrocytes synthesized increased amounts of bFGF. These findings suggest that glial reaction synthesizing neurotrophic factors may influence the wound and repair after mechanical lesions of central nervous and subsequent neuronal trophism and plasticity which may be relevant to the regenerative process of the nervous tissue.

Número e espessura de fibras mielínicas do nervo frênico de rato albino jovem e senil / Number and thickness of myelinic fibres of phrenic nerve of young and aged rats

Neste trabalho, säo comparados o número de fibras, a espessura do axônio e da bainha de mielina do nervo frênico em rato albino jovem e senil. Os nervos frênicos foram retirados de três ratos jovens e três senís. Näo observamos diferenças significantes entre os dois grupos quanto aos aspectos estudados