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1.
Arq. neuropsiquiatr ; 75(7): 477-483, July 2017. graf
Artigo em Inglês | LILACS | ID: biblio-888290

RESUMO

ABSTRACT In this study, we proposed that administration of hippocampal growth hormone in ageing animals with growth hormone deficiency can compensate long-term potentiation and synaptic plasticity in nucleus basalis magnocellularis (NBM)-lesioned rats. Aged male Wistar rats were randomly divided into six groups (seven in each) of sham-operated healthy rats (Cont); NBM-lesioned rats (L); NBM-lesioned rats and intrahippocampal injection of growth hormone vehicle (L + Veh); NBM-lesioned and intrahippocampal injection of growth hormone (10, 20 and 40 µg.2 µl-1) (L + GH). In vivo electrophysiological recording techniques were used to characterize maintenance of long-term potentiation at distinct times (1, 2, 3, 24 and 48 hours) after high-frequency stimulation. The population spike was enhanced significantly for about 48 hours following tetanic stimulation in rats treated with a dose-dependent growth hormone compared to the vehicle group (p < 0.05), possibly through neuronal plasticity and neurogenesis in affected areas.


RESUMO Neste estudo, propusemos que a administração de hormônio hipocampal do crescimento em animais envelhecidos com deficiência de hormônio do crescimento pode compensar a potencialização em longo prazo e a plasticidade sináptica em ratos lesados do núcleo basalis magnocellularis (NBM). Ratos machos Wistar foram divididos aleatoriamente em seis grupos (sete ratos em cada grupo) de ratos falso-operados saudáveis (Cont); ratos lesados do NBM (L); ratos lesados do NBM e injeção intrahipocampal de veículo de hormônio do crescimento (L + Veh); ratos lesados do NBM e injeção de hormônio do crescimento (10, 20 e 40 μg.2 μl-1) (L + GH). Técnicas de registro eletrofisiológico in vivo foram utilizadas para caracterizar a manutenção da potencialização em longo prazo em momentos distintos (1, 2, 3, 24 e 48 horas) após estimulação de alta frequência. O pico populacional aumentou significativamente cerca de 48 horas após a estimulação tetânica em ratos tratados com um hormônio do crescimento dose-dependente, em comparação com o grupo veículo (p <0,05), possivelmente através da plasticidade neuronal e da neogênese nas áreas afetadas.


Assuntos
Animais , Masculino , Hormônio do Crescimento/farmacologia , Núcleo Basal de Meynert/efeitos dos fármacos , Hipocampo/efeitos dos fármacos , Plasticidade Neuronal/efeitos dos fármacos , Fatores de Tempo , Ratos Wistar , Núcleo Basal de Meynert/fisiologia , Modelos Animais , Hipocampo/fisiologia , Plasticidade Neuronal/fisiologia
2.
Arq. bras. oftalmol ; 76(2): 85-89, mar.-abr. 2013. ilus, tab
Artigo em Inglês | LILACS | ID: lil-678172

RESUMO

BACKGROUND: Visual processing deficits have been reported for patients with schizophrenia. Previous studies demonstrated differences in early-stage processing of schizophrenics, although the nature, extent, and localization of the disturbance are unknown. The magnocellular and parvocellular visual pathways are associated with transient and sustained channels, but their respective contributions to schizophrenia-related visual deficits remains controversial. PURPOSE: The aim of this study was to evaluate magnocellular dysfunction in schizophrenia using frequency doubling technology. METHODS: Thirty-one patients with schizophrenia and 34 healthy volunteers were examined. Frequency doubling technology testing was performed in one session, consisting of a 15-minute screening strategy followed by the C-20 program for frequency doubling technology. RESULTS: Schizophrenic patients showed lower global mean sensitivity (30,97 ± 2,25 dB) compared with controls (32,17 ± 3,08 dB), p<0.009. Although there was no difference in the delta sensitivity of hemispheres, there was a difference in sensitivity analysis of the fibers crossing the optic chiasm, with lower mean sensitivity in the patient group (28,80 dB) versus controls (30,66 dB). The difference was higher in fibers that do not cross the optic chiasm, with lower mean sensitivity in patients (27,61 dB) versus controls (30,26 dB), p<0.005. CONCLUSIONS: Our results suggest that there are differences between global sensitivity and fiber sensitivity measured by frequency doubling technology. The different sensitivity of fibers that do not cross the optic chiasm is consistent with most current etiological hypotheses for schizophrenia. The decreased sensitivity responses in the optic radiations may significantly contribute to research assessing early-stage visual processing deficits for patients with schizophrenia.


HISTÓRICO: Déficits de processamento visual foram relatados em pacientes com esquizofrenia. Estudos anteriores demonstraram diferenças no estágio inicial de processamento de esquizofrênicos, embora a natureza, extensão e localização do distúrbio são desconhecidas. As vias magnocelulares e parvocelular visuais são associados com canais transitórios e sustentado, mas suas respectivas contribuições para a esquizofrenia relacionados com déficits visuais permanece controverso. OBJETIVO: Avaliar a disfunção magnocelular na esquizofrenia usando a tecnologia de frequência dupla. MÉTODOS: Trinta e um pacientes com esquizofrenia e 34 voluntários saudáveis ​​foram examinados. Tecnologia de frequência dupla foi realizada em uma sessão, consistindo de uma estratégia de rastreio de 15 minutos, seguido do programa de C-20 para tecnologia de frequência dupla. RESULTADOS: Os pacientes esquizofrênicos apresentaram sensibilidade média inferior global (30,97 ± 2,25 dB), em comparação com os controles (32,17 ± 3,08 dB), p<0,009. Embora não tenha ocorrido diferença na sensibilidade do delta de hemisférios, houve uma diferença na análise de sensibilidade das fibras que atravessam a quiasma, com menor sensibilidade média no grupo de pacientes (28,80 dB) versus controlos (30,66 dB). A diferença foi maior em fibras que não cruzam o quiasma óptico, com menor sensibilidade média em pacientes (27,61 dB) versus controles (30,26 dB), p<0,005. CONCLUSÕES: Nossos resultados sugerem que há diferenças entre a sensibilidade global e sensibilidade da fibra medida pela tecnologia de frequência dupla. A sensibilidade diferente de fibras que não cruzam o quiasma óptico é compatível com a maioria das atuais hipóteses etiológicas para a esquizofrenia. As respostas diminuição da sensibilidade nas radiações ópticas podem contribuir significativamente para pesquisar a avaliação em estágio inicial déficits de processamento visual em pacientes com esquizofrenia.


Assuntos
Adulto , Feminino , Humanos , Masculino , Corpos Geniculados/fisiopatologia , Esquizofrenia/fisiopatologia , Testes de Campo Visual/métodos , Vias Visuais/fisiopatologia , Percepção Visual/fisiologia , Estudos de Casos e Controles , Sensibilidades de Contraste/fisiologia , Esquizofrenia/complicações
3.
Chinese Journal of Neuroanatomy ; (6): 234-238, 2000.
Artigo em Chinês | WPRIM | ID: wpr-412372

RESUMO

The distribution of TrkA and the postnatal development(PD) of TrkA and ChAT-immunoreactive(-IR) neurons andthe relation between them in the basal nucleus of Meynert of rats were studied with immunohistochemical method. The number,mean profile areas and grey degree of TrkA-IR and ChAT-IR neurons were examined with image analyser. The data revealed thatTrkA-IR neurons were localized in the basal forebrain of rats. TrkA immunostaining was present at PDI, but ChAT was not.ChAT immunostaining was present at PD5. Most densely stained TrkA and ChAT neuronal bodies and fibers were present atPD20, the mean grey degrees of TrkA-IR and ChAT-IR neuronal profiles reached its peak. Both TrkA and ChAT neurons beganto cline at PD30 and maintained a relatively higher level in the adult. However, during aging both TrkA and ChAT-IR neuronsatrophy and became smaller than that in the adult. The number of TrkA-IR and ChAT-IR neurons were decreased by 41.38% and 51.61%; the mean profile areas decreased by 15.7% and 12.8%; and the mean grey degrees by 29.9% and 9.9%, respec-tively. The mean profile areas of TrkA-IR and ChAT-IR neurons from PD5 to aged rats were positively correlated. The resultsindicated that the expression of TrkA was earlier than ChAT. The expression of TrkA and ChAT followed a very similar tempo-ral pattern in the basal nucleus of Meynert from PD5 to aged rats, suggesting that TrkA might participate the regulation ofChAT-IR neuronal development, differentiation, maturation, and ageing. The down-regulation of TrkA and ChAT of aged ratsis associated with neuronal atrophy and loss and may contribute to the pronounced vulnerability of these neurons to degenerationin aging animals and Alzheimer's disease.

4.
Journal of the Korean Neurological Association ; : 736-748, 1995.
Artigo em Coreano | WPRIM | ID: wpr-113584

RESUMO

Thiamine deficiency is generally accepted as the primary etiologic factor for the Wernicke encephalopathy in human and for the similar neurologic symptoms in thiamine depleted experimental animals. Although pyrithiariiineinduced thiamine deficiency has been known to produce histopathologic lesions within many nuclei of the rat brain, the pathogenic mechanisms involved have not been clarified. Furthermore, the effect of thiamine deprivation on the nature and anatomic distribution of neurotransmitter changes has not been fully explored. The present studies were undertaken to investigate - morphological changes of the basal nucleus of Meynert and vestibular nucleus in thiamine deficient rats induced by pyrithiamine and thiamine deficient diet. For this purpose immunohistochemical stain for choline acetyltransferase was performed. Fifty healthy Sprague-Dawley strain rats weighing about 150 gm, were divided into 10 control group and 40 thiamine deficient group. Animals in thiamine deficient group were treated with daily intraperitoneal injection of pyrithiamine( 50 ug/lOOgm of BW/dbLy, Sigma Co.) for 9 days and were continuously given thiamine deficient diet until to be sacrificed. Thiamine deficient rats were subdivided into 3 groups according to different stages of neurologic manifestations ; the early group, the beginning stage of anorexia, hypothermia and weight loss without neurologic manifestations(sacrificed day ; 9th-13th day) the intermediate group, the developing stage of gait ataxia and hypotonia(sacrificed day ; 17th-19th day) the late group, the established stage of tremor, convulsion and back arching(sacrificed day ; 23th-26th day). All animals were anesthetized with sodium pentobarbital(40mg/kg, I.p.) and perfused in vivo through the ascending aorta with 10% neutral buffered formalin or 4% paraformaldehyde-0. 1% glutaraldehyde in PBS, and then brains were removed. Luxol-fast blue and cresyl violet stain was performed according to routine paraffin method for observing morphologic changes in basal nucleus of Meynert and vestibular nucleus. In addition immunohistochemical stains in the same regions were performed by free floating method in cell culture plate. All preparations were observed with a light microscope. The results obtained were as follows ; 1. Sequential changes of the neurologic manifestations in thiamine deficient rats were weight loss, hypothermia and ariorexia on the 9th-10th day, followed by gait ataxia and hypotonia on the 13th-15th day, and then tremor, convulsion and back arching on the 22th-26th day. 2. Glial proliferation was noted in the basal nucleus of the early group but not in the vestibular nucleus. Atrophy and pyknosis of neurons in basal nucleus and vestibular nucleus were shown in the intermediate group and marke neuronal loss and edematous tissue necrosis were noted in the late group. 3. Choline acetyltransferase immurforeactivity in the basal nucleus and vestibular nucleus was markedly positive in the early group as well as control group, moderately positive in the intermediate groupand minimally positive in the late group. It is suggested that the extent of neuronal damage in thiamine deficient rats is proportional to the duration of thiamine depletion. And the data presented here may account for: the regional susceptability and reversibility of certain symptoms in thiamine deficient rats.


Assuntos
Animais , Humanos , Ratos , Anorexia , Aorta , Atrofia , Núcleo Basal de Meynert , Encéfalo , Técnicas de Cultura de Células , Colina O-Acetiltransferase , Colina , Corantes , Dieta , Formaldeído , Marcha Atáxica , Glutaral , Hipotermia , Injeções Intraperitoneais , Hipotonia Muscular , Necrose , Manifestações Neurológicas , Neurônios , Neurotransmissores , Parafina , Piritiamina , Ratos Sprague-Dawley , Convulsões , Sódio , Deficiência de Tiamina , Tiamina , Tremor , Viola , Redução de Peso , Encefalopatia de Wernicke
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