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1.
Pesqui. vet. bras ; 40(7): 501-513, July 2020. tab, ilus
Article in English | LILACS, VETINDEX | ID: biblio-1135655

ABSTRACT

Poisoning by Prosopis juliflora (mesquite) leads to neurological signs, cachexia and death, mainly in cattle and goats. Although the uncontrolled spread of mesquite in the Caatinga biome (biological invasion), which alters the epidemiological conditions of intoxication by this plant, has been proved for approximately 20 years, strategies for its control and prophylaxis still remain out of date. These new epidemiological conditions have allowed the uncontrolled consumption of large amounts of in natura mesquite pods by ruminants for long periods in invaded pastures, thus resulting in increased history of poisoning. This study aimed to describe the new epidemiological aspects of P. juliflora poisoning in cattle and goats, 78 years after the introduction of this plant in the country, with emphasis on its degree of invasion, and to update the control and prophylaxis measures of this intoxication and the mapping of areas of outbreak occurrence in the semiarid region of the state of Bahia, Brazil. Seven outbreaks of natural mesquite poisoning, two in goats (OB 1 and OB 2) and five in cattle (OB 3, OB 4, OB 5, OB 6, and OB 7), were studied in loco in the municipalities of Juazeiro, Iaçu, Tucano, Santa Teresinha, Barra do Mendes, Barra and Tabocas do Brejo Velho. In the studied outbreaks, clinical-epidemiological (OB 1 to OB 7) and histopathological (OB 1, OB 2, OB 3, and OB 5) findings were compatible with mesquite poisoning, and this was the first anatomopathological proof of poisoning by this plant in this state. In addition, in the state of Bahia, disease occurs in an area approximately three times larger than previously known. On the farms investigated, mesquite introduction occurred between 1980 and 2005, through the single planting of an average of 33 seedlings. Since then, propagation of this plant has occurred progressively, with gradual invasion of native pastures, which enabled the evaluation of plant spread (biological invasion) on these farms 15 (OB 2), 25 (OB 7), 30 (OB 5 and OB 6), 35 (OB 3) and 40 (OB 1 and OB 4) years after its introduction. Historical information on the introduction and spread of mesquite in the state of Bahia had never been analyzed. In 2020, a degree of mesquite invasion an average 59.57% was verified in the pastures of the seven farms where the outbreaks occurred. The great biological invasion capacity of this plant drew attention, especially in OB 5. The high degree of mesquite invasion observed (new epidemiological conditions) justifies the increased number of cases of poisoning observed in this study. Processing of P. juliflora pods (grinding) was not carried out on any farm (OB 1 to OB 7), and ruminants uncontrollably consumed large amounts of pods in natura for long periods in invaded pastures, which allowed massive dispersal of seeds through feces over decades. The main factors responsible for the gradual invasion of pastures by mesquite over time were absence of crop management plans (silvicultural treatments) and lack of knowledge by producers on disease etiology. Given the new epidemiological conditions, restriction of animal access to in natura pods in pastures and supply of mesquite bran are crucial for the control and prophylaxis of this poisoning, as consumption of in natura pods had a strong correlation with the high degree of invasion in the pastures where the seven outbreaks occurred. Additionally, although the commercialization of pods and exploitation of wood of mesquite trees can provide livestock farmers with extra income - being the correct management for areas invaded by this plant, such practice is either not yet known or not carried out technically or satisfactorily by farmers. In addition to being a threat to the Caatinga's biodiversity, the increasing invasion of semiarid areas by mesquite 78 years after its introduction in the Northeast region of Brazil, is a risk for herds, since the occurrence of poisoning outbreaks may become more frequent. Therefore, it is highly advisable that effective measures be adopted to control P. juliflora propagation.(AU)


A intoxicação por Prosopis juliflora (algaroba) cursa com sinais neurológicos, caquexia e morte, principalmente em bovinos e caprinos. Embora a disseminação descontrolada da algaroba na Caatinga (invasão biológica) tenha sido comprovada há cerca de 20 anos, o que altera as condições epidemiológicas dessa intoxicação, as estratégias de controle e profilaxia permanecem desatualizadas. Essas novas condições epidemiológicas permitem o consumo descontrolado de grande quantidade de vagens in natura de algaroba, por longos períodos, nas pastagens invadidas, o que tem resultado em aumento dos históricos de intoxicação. Objetivou-se com esse estudo descrever os novos aspectos epidemiológicos da intoxicação por P. juliflora em bovinos e caprinos, 78 anos após a introdução da planta no país, com ênfase no grau de invasão da planta, bem como atualizar as medidas de controle e profilaxia dessa intoxicação e das áreas de ocorrência dos surtos no semiárido baiano. Foram estudados in loco sete surtos (S1 a S7) de intoxicação natural por algaroba, sendo dois em caprinos (S1 e S2) e cinco em bovinos (S3, S4, S5, S6 e S7) no semiárido baiano (Juazeiro, Iaçu, Tucano, Santa Teresinha, Barra do Mendes, Barra e Tabocas do Brejo Velho). Nos surtos estudados, os achados clínico-epidemiológicos (S1 a S7) e histopatológicos (S1, S2, S3 e S5) foram compatíveis com intoxicação por algaroba, sendo essa intoxicação comprovada, pela primeira vez, com exames anatomopatológicos na Bahia. Ademais, na Bahia a doença ocorre em uma área cerca de três vezes maior do que a, até então, conhecida. Nas fazendas estudadas a introdução da algaroba ocorreu entre 1980 e 2005, através do plantio único de, em média, 33 mudas. Desde então, a disseminação da planta ocorreu de forma progressiva, invadindo gradativamente as pastagens nativas, o que permitiu avaliar a disseminação da planta (invasão biológica) nessas fazendas cerca de 15 (S2), 25 (S7), 30 (S5 e S6), 35 (S3) e 40 (S1 e S4) anos, após sua introdução. Informações históricas acerca da introdução da algaroba e sua disseminação na Bahia nunca haviam sido estudadas. Em 2020, verificou-se que nas pastagens das sete fazendas onde os surtos ocorreram, o grau de invasão por algaroba alcançou, em média, 59,57%. Chamou a atenção a grande capacidade de invasão biológica da planta, sobretudo, no S5. O alto grau de invasão da algaroba observado (novas condições epidemiológicas) justificou o aumento dos casos de intoxicação verificados nesse estudo. O beneficiamento das vagens (moagem) não era realizado em nenhuma fazenda (S1 a S7) e os ruminantes consumiam de forma descontrolada (livre) grande quantidade de vagens in natura, por longos períodos, nas pastagens invadidas, o que possibilitou a dispersão massiva das sementes da planta pelas fezes ao longo das décadas. O que aliado à inexistência de um plano de manejo do cultivo (tratamentos silviculturais) e ao desconhecimento da etiologia da doença pelos produtores foram os principais fatores responsáveis pela invasão gradativa da planta nas pastagens, ao longo dos anos, o que justifica o aumento dos casos de intoxicação observados na Bahia. Frente às novas condições epidemiológicas, a restrição do acesso dos animais as vagens in natura nas pastagens e o fornecimento do farelo de algaroba são cruciais para o controle e profilaxia dessa intoxicação, pois o consumo das vagens in natura teve forte correlação com o alto grau de invasão das pastagens onde os sete surtos ocorreram. Adicionalmente, embora a comercialização das vagens e a exploração da madeira da algaroba possam proporcionar renda extra aos pecuaristas e serem boas formas de manejo de áreas invadidas por algaroba, tais práticas ainda não são conhecidas ou não são realizadas de forma técnica ou a contento. A crescente invasão da algaroba no semiárido, 78 anos após a sua introdução no Nordeste, além de ser uma ameaça à biodiversidade da Caatinga é um risco para os rebanhos, visto que, a ocorrência de surtos de intoxicação podem se tornar mais frequentes. Desta maneira alerta-se para adoção de medidas efetivas de controle da propagação descontrolada da algaroba.(AU)


Subject(s)
Plant Poisoning/etiology , Plant Poisoning/epidemiology , Prosopis/poisoning , Plants, Toxic/poisoning , Ruminants , Cattle Diseases/etiology
2.
Motriz (Online) ; 25(3): e101957, 2019. tab, graf
Article in English | LILACS | ID: biblio-1040652

ABSTRACT

Aim: The preventive and therapeutic role of physical exercise in Parkinson's disease (PD) has been the target of study of many scientific groups, and the research often is done in experimental models, especially rodents. Thus, the aim of this review was to analyze a database, elucidating the main benefits that the systematized practice of physical activity/ exercises can contribute to PD in animal models. Method: Based on this question, a search on PubMed and Medline database containing the terms: "Parkinson's disease" AND "animal model" AND "physical exercise" was performed. The most pertinent studies were selected by the criteria year of publication (2009- 2018) and the original article. It was used papers involving animal models and physical exercises, as well as other studies, which allowed an introductory explanation in PD, covering its pathophysiology, and the neurochemical responses of physical exercise in rodents. Results: The results showed that there was a decrease in the levels of nigrostriatal neurodegeneration and an increase in the neuroprotective effect related to the training program. Conclusion: It was concluded that physical exercise has been pointed as an important neuroprotective strategy in animal models of Parkinson's disease, especially those applied at moderate intensities, which were effective in reducing the inflammatory profile, elevating the expression of genes and proteins related to neuronal restoration, mitochondrial biogenesis, repair of the dopaminergic system, besides other events also capable of reflecting improvements in motor and cognitive behavior of animals.(AU)


Subject(s)
Animals , Rats , Parkinson Disease/therapy , Exercise Therapy/instrumentation , Dopamine/therapeutic use , Models, Animal
3.
Braz. j. otorhinolaryngol. (Impr.) ; 83(6): 691-696, Nov.-Dec. 2017. tab, graf
Article in English | LILACS | ID: biblio-889319

ABSTRACT

Abstract Introduction: The use of mobile phones has become widespread in recent years. Although beneficial from the communication viewpoint, the electromagnetic fields generated by mobile phones may cause unwanted biological changes in the human body. Objective: In this study, we aimed to evaluate the effects of 2100 MHz Global System for Mobile communication (GSM-like) electromagnetic field, generated by an electromagnetic fields generator, on the auditory system of rats by using electrophysiological, histopathologic and immunohistochemical methods. Methods: Fourteen adult Wistar albino rats were included in the study. The rats were divided randomly into two groups of seven rats each. The study group was exposed continuously for 30 days to a 2100 MHz electromagnetic fields with a signal level (power) of 5.4 dBm (3.47 mW) to simulate the talk mode on a mobile phone. The control group was not exposed to the aforementioned electromagnetic fields. After 30 days, the Auditory Brainstem Responses of both groups were recorded and the rats were sacrificed. The cochlear nuclei were evaluated by histopathologic and immunohistochemical methods. Results: The Auditory Brainstem Responses records of the two groups did not differ significantly. The histopathologic analysis showed increased degeneration signs in the study group (p = 0.007). In addition, immunohistochemical analysis revealed increased apoptotic index in the study group compared to that in the control group (p = 0.002). Conclusion: The results support that long-term exposure to a GSM-like 2100 MHz electromagnetic fields causes an increase in neuronal degeneration and apoptosis in the auditory system.


Resumo Introdução: O uso de telefones celulares tornou-se generalizado nos últimos anos. Embora benéfico do ponto de vista da comunicação, os campos eletromagnéticos gerados por celulares pode causar alterações biológicas indesejáveis no corpo humano. Objetivo: Nesse estudo, o objetivo foi avaliar os efeitos do campo eletromagnético na frequência de 2.100 MHz, similar à modulação do Sistema Global para Comunicações Móveis, produzido por um gerador de campo eletromagnético, sobre o sistema auditivo de ratos usando os métodos eletrofisiológico, histopatológico e imunohistoquímico. Método: Foram incluídos no estudo catorze adultos ratos albinos Wistar. Os ratos foram divididos aleatoriamente em dois grupos de sete animais cada. O grupo de estudo foi exposto continuamente por 30 dias a um campo eletromagnético em 2100 MHz com um nível de sinal (potência) de 5,4 dBm (3,47 miliwatts) para simular o modo de conversação em um celular. O grupo controle não foi exposto ao campo eletromagnético acima mencionado. Após 30 dias, o potencial evocado auditivo de tronco encefálico de ambos os grupos foi gravado e os ratos foram sacrificados. Os núcleos cocleares foram avaliados pelos métodos histopatológico e imunohistoquímico. Resultados: Os registros do potencial evocado auditivo de tronco encefálico dos dois grupos não diferiram significativamente. A análise histopatológica mostrou aumento dos sinais de degeneração no grupo de estudo (p = 0,007). Além disso, a análise imuno-histoquímica revelou aumento do índice de apoptose no grupo de estudo em comparação com o grupo controle (p = 0,002). Conclusão: Os resultados confirmam que a exposição a longo prazo a um campo eletromagnético em 2100 MHz similar à modulação do sistema global para comunicações móveis causa um aumento na degeneração neuronal e apoptose no sistema auditivo.


Subject(s)
Animals , Male , Radio Waves/adverse effects , Cochlear Nucleus/radiation effects , Radiation Exposure/adverse effects , Cell Phone , Electromagnetic Fields/adverse effects , Hearing/radiation effects , Reference Values , Time Factors , Immunohistochemistry , Risk Factors , Evoked Potentials, Auditory, Brain Stem/radiation effects , Rats, Wistar , Apoptosis/radiation effects , Cochlear Nucleus/pathology , Nerve Degeneration/etiology
4.
Arq. bras. med. vet. zootec. (Online) ; 69(5): 1181-1185, set.-out. 2017. ilus
Article in Portuguese | LILACS, VETINDEX | ID: biblio-877359

ABSTRACT

Um caso de abiotrofia cerebelar em um gato com 45 dias de idade foi diagnosticado no Laboratório de Patologia Animal, Hospital Veterinário da Universidade Federal de Campina Grande. O animal apresentava, havia 15 dias, apatia, anorexia, desidratação, ataxia, hipermetria, espasticidade dos membros torácicos e pélvicos, tremores de intenção, nistagmo, opistótono, déficit proprioceptivo e ausência de resposta de ameaça. Clinicamente, havia a suspeita de hipoplasia cerebelar, e, devido ao prognóstico desfavorável, o animal foi eutanasiado. Na necropsia, não foram observadas alterações macroscópicas. Microscopicamente, as lesões estavam restritas ao cerebelo e caracterizavam-se por alterações neurodegenerativas e necróticas, com desaparecimento segmentar dos neurônios de Purkinje. Nessas áreas, também se verificaram espaços em branco, denominado aspecto de cesto vazio, resultantes da perda dos neurônios de Purkinje, além de raros esferoides axonais e proliferação dos astrócitos de Bergmann. Em algumas áreas, a camada granular estava hipocelular e havia moderada gliose multifocal na camada molecular. O diagnóstico de abiotrofia cerebelar foi realizado com base nos dados epidemiológicos, clínicos e, principalmente, pelas alterações histopatológicas dos neurônios de Purkinje características da doença.(AU)


The aim of this report was to describe a case of cerebellar abiotrophy in cat with 45-year-old diagnosed at the Animal Pathology Laboratory, Veterinary Hospital of the Federal University of Campina Grande. The animal had presented 15-day apathy, anorexia, dehydration and neurological signs, characterized by ataxia, hypermetria, spasticity of fore and hindlimbs, intention tremor, nystagmus, opisthotonos, proprioceptive deficits, and absence of threat response. Clinically, cerebellar hypoplasia was suspected and the animal was euthanized due to poor prognosis. During necropsy, gross lesions were not observed. Microscopically the lesions were restricted to the cerebellum and were characterized by neurodegenerative and necrotic damage with segmental disappearance of the Purkinje cells. In these areas, there were also empty spaces, called the empty basket aspect, resulting from the loss of Purkinje cells, as well as rare axonal spheroids and proliferation of Bergmann's astrocytes. In some areas, the granular layer was hypocellular and there was moderate multifocal gliosis in the molecular layer. The diagnosis of cerebellar abiotrophy was based on epidemiological, clinical and mainly on histopathological changes in neurons of Purkinje disease characteristics.(AU)


Subject(s)
Animals , Cats , Abiotrophia , Cerebellar Diseases/veterinary , Nerve Degeneration/veterinary , Purkinje Cells/pathology
5.
Journal of Veterinary Science ; : 137-144, 2016.
Article in English | WPRIM | ID: wpr-121459

ABSTRACT

Hippocalcin participates in the maintenance of neuronal calcium homeostasis. In the present study, we examined the time-course changes of neuronal degeneration and hippocalcin protein level in the mouse hippocampus following pilocarpine-induced status epilepticus (SE). Marked neuronal degeneration was observed in the hippocampus after SE in a time-dependent manner, although neuronal degeneration differed according to the hippocampal subregions. Almost no hippocalcin immunoreactivity was detected in the pyramidal neurons of the cornu ammonis 1 (CA1) region from 6 h after SE. However, many pyramidal neurons in the CA2 region showed hippocalcin immunoreactivity until 24 h after SE. In the CA3 region, only a few hippocalcin immunoreactive cells were observed at 12 h after SE, and almost no hippocalcin immunoreactivity was observed in the pyramidal neurons from 24 h after SE. Hippocalcin immunoreactivity in the polymorphic cells of the dentate gyrus was markedly decreased from 6 h after SE. In addition, hippocalcin protein level in the hippocampus began to decrease from 6 h after SE, and was significantly decreased at 24 h and 48 h after pilocarpine-induced SE. These results indicate that marked reduction of hippocalcin level may be closely related to neuronal degeneration in the hippocampus following pilocarpine-induced SE.


Subject(s)
Animals , Mice , Calcium , Dentate Gyrus , Hippocalcin , Hippocampus , Homeostasis , Neurons , Pyramidal Cells , Status Epilepticus
6.
Gut and Liver ; : 411-416, 2013.
Article in English | WPRIM | ID: wpr-163966

ABSTRACT

BACKGROUND/AIMS: The primary pathophysiologic abnormality in achalasia is known to be a loss of inhibitory myenteric ganglion cells, which may result from an immune-mediated response or neuronal degeneration. The aim of this study was to identify proteins suggestive of an immune-mediated response or neuronal degeneration in the serum of achalasia patients using a proteomic analysis. METHODS: Blood samples were collected from five symptomatic achalasia patients and five sex- and age-matched healthy controls. Serum proteomic analysis was conducted, and the protein spots were identified using matrix-assisted laser desorption ionization/time-of-flight and a proteomics analyzer. The serum level of C3 was measured by enzyme-linked immunosorbent assay in nine patients with achalasia and 18 sex- and age-matched healthy controls. RESULTS: Of the 658 matched protein spots, 28 spots were up-regulated over 2-fold in the serum from achalasia patients compared with that from controls. The up-regulated proteins included complement C4B5, complement C3, cyclin-dependent kinase 5, transthyretin, and alpha 2 macroglobulin. The serum levels of C3 in achalasia patients were significantly higher than those of controls. CONCLUSIONS: The serum proteomic analysis of achalasia patients suggests an immune-mediated response or neuronal degeneration. Further validation studies in larger samples and the esophageal tissue of achalasia patients are required.


Subject(s)
Humans , alpha-Macroglobulins , Complement C3 , Complement System Proteins , Cyclin-Dependent Kinase 5 , Enzyme-Linked Immunosorbent Assay , Esophageal Achalasia , Ganglion Cysts , Neurons , Prealbumin , Proteins , Proteomics
7.
Pesqui. vet. bras ; 29(3): 233-240, mar. 2009. ilus, tab
Article in Portuguese | LILACS | ID: lil-513296

ABSTRACT

Descrevem-se três surtos de intoxicação por vagens de Prosopis juliflora no Sertão e Agreste de Pernambuco, na região semi-árida, em animais pastejando áreas invadidas pela planta ou que ingeriram as vagens como alimento concentrado. Em duas fazendas nas que a doença ocorria esporadicamente foram observados casos individuais. Em outra, o surto afetou um rebanho de 1206 bovinos, dos quais adoeceram 112 (9,28 por cento) e morreram 84 (6,96 por cento), enquanto os demais 28 (2,32 por cento) recuperaram-se e ganharam peso após a retirada das vagens da alimentação. Clinicamente observou-se, principalmente, perda de peso progressiva, atrofia da musculatura da face e masseter, mandíbula pendulosa, protrusão de língua, dificuldade de apreensão e mastigação dos alimentos, torção da cabeça para mastigar ou ruminar, salivação excessiva, disfagia e hipotonia lingual. Nos exames laboratoriais constatou-se anemia e hipoproteinemia. Na necropsia havia caquexia e diminuição de volume e coloração acinzentada dos músculos masseteres. Na histologia observou-se degeneração de neurônios do núcleo motor do trigêmeo, degeneração Walleriana do nervo trigêmeo e atrofia muscular por denervação do músculo masseter com substituição por tecido fibroso. Recomendam-se medidas para a profilaxia da intoxicação e discute-se a necessidade de desenvolver pesquisas para determinar a viabilidade econômica e sustentabilidade da utilização da algaroba como alimento animal ou humano e para produção de carvão, lenha ou madeira.


Three outbreaks of poisoning by Prosopis juliflora pods are reported in the semiarid region of the state of Pernambuco, Northeastern Brazil, in cattle grazing in fields invaded by the plant or ingesting mesquite beans as a concentrate food. In two farms the disease occurred sporadically. In another, 112 (9.28 percent) cattle out of 1206 were affected, 84 (6.96 percent) died due to emaciation, and 28 (2.32 percent) gained weight after the pods had been withdrawn from the feed. Main clinical signs were progressive weight loss, atrophy of the masseter muscles, dropped jaw, tongue protrusion, difficulties in prehending food, tilting the head during mastigation or rumination, salivation, impaired swallowing, and decreased tone of the tongue. The hematology reveals hypoproteinemia and anemia. Gross lesions were emaciation and reduction in size of the masseter muscles, which appear thinner than normal and grayish due muscular atrophy. Degeneration of neurons of the trigeminal motor nuclei, Wallerian degeneration of the trigeminal nerve roots, and muscular atrophy of the masseter muscles with substitution by fibrous tissue were observed on histologic examination. For the prevention of the poisoning is necessary to limit the amount of mesquite beans in animal nutrition. It is also necessary to develop research to determine the economic and sustainability of the use of Prosopis juliflora for animal food, human food or other uses such as charcoal, wood and fuel wood.


Subject(s)
Animals , Cattle , Disease Outbreaks , Nerve Degeneration/chemically induced , Cranial Nerves/pathology , Prosopis/adverse effects , Prosopis/toxicity
8.
Chinese Pharmacological Bulletin ; (12)2003.
Article in Chinese | WPRIM | ID: wpr-679351

ABSTRACT

Bone marrow stromal cells(MSCs) have been shown to be extremely versatile.Recently,it is demonstrated that MSCs differentiate into neurons.Moreover,under the appropriate conditions,MSCs differentiate into special phynotype of neurons,such as 5-hydroxytryptamine-sensitive neurons,and dopaminergic neurons.The mechanism remains to be elucidated,and an overexpression of neuronal specific genes(such as Sox,Pax,Notch gene) may play an important role,especially RB/PBO gene.However,RB triggers cholinergic differentiation.Extrinsic factor such as concentration of cAMP plays certain role in differentiation.MSCs have also been shown to have certain therapeutic effect on neuronal degeneration disease.These cells have great potential because it is easy to isolate,culture,amplify,and no ethics neither immunologic rejection problem was concerned.

9.
Journal of Korean Neurosurgical Society ; : 29-39, 1997.
Article in Korean | WPRIM | ID: wpr-228727

ABSTRACT

The neurotoxic effects of excitatory amino acids(EAAs) in the brain are well documented, but their toxicity in the spinal cord has not been thoroughly studied. Intraspinal microinjections of quisqualic acid(QA) were done to evaluate its neurotoxic effects on neurons in the adult rat spinal cord. Animals were divided into four groups based on times of post-QA injections, ranging from 7-49 days. Total volume injected in each group ranged from 0.3 to 2.0microL of QA and normal saline(vehicle) were injected in lower thoracic and upper lumbar spinal cord. Kinematic analysis of recovery process was performed using a computerized motion analysis system after intraspinal injection of QA and saline. Our results showed that unilateral injections of QA produced either unilateral or bilateral neuronal degenerations during the survival period. This was accompanied by an inflammatory reaction and initiation of pathological process leading to spinal cavitation in 23 of 25 animals. Segments affected by QA injections showed darkly stained, hypertrophied neuronal profiles, and an increased expression of glial fibrillary acidic protein(GFAP). Immunostaining for GFAP was especially intense in the areas of neuronal degeneration and around the border of spinal cavities. The kinematic analysis of locomotion in the right hindlimb showed a decrease in gait height(pre-injection level: 2.07+/-0.12cm) at post QA injection 1 week(1.53+/-0.09cm), but returned to pre-injection level at 5 weeks(1.83+/-0.15cm). There was no statistical difference in the gait distance before and after QA injections. Results of this study have shown that the intraspinal injection of QA may be a suitable model to study cellular events of EAA-induced neurotoxicity on spinal neurons and the pathological process of spinal cavitation following neuronal degeneration. Computerized motion analysis system was useful for detection of the neurological deficits from minor spinal cord injury.


Subject(s)
Adult , Animals , Humans , Rats , Brain , Gait , Hindlimb , Injections, Spinal , Locomotion , Microinjections , Neurons , Spinal Cord Injuries , Spinal Cord , Syringomyelia
10.
Acta Anatomica Sinica ; (6)1957.
Article in Chinese | WPRIM | ID: wpr-573876

ABSTRACT

Objective To test experimentally Fluoro-Jade B(FJB) stain method for detecting degeneration of neurons in the basal ganglia. Methods Kainic acid(KA)-lesion model by stereotaxical injection of KA into striatum of rats,MPTP-lesion model by injection of MPTP into intraperitoneal cavity of mice,as well as KA-lesion model of cultured striatal cells were firstly prepared.FJB stain dye was then used to visualize degeneration of neurons in above KA-or MPTP-lesion models. Results KA-or MPTP-induced degenerative neurons including cell bodies and processes could be clearly visualized by FJB stain dye.In the brain sections,FJB-positive stained degenerative neurons were numerously observed in the striatum of KA-lesion rats and the substantia nigra pars compacta of MPTP-treated mice,but not detected in the control animals.Moreover,degenerative neurons were also detected with FJB stain in cultured striatal neurons.Semi-quantitative analysis on percentage(?s) of FJB-positive neurons constituting total cultured striatal neurons in unit area showed that degenerative neurons of KA-lesion group (8.42?1.09)% was evidently more than that of controls (3.42?0.45)%,P

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