RESUMO
CARIBRO was founded in response to the United Nations declaration that the 1990s be designated the Decade of the Brain. The Program of Action is: 1. Annual meetings; 2. Training courses of the Caribbean School of Neurosciences; 3. Network scientific programs; 4. Fellowship programs; and 5. Dissemination of information on neuroscience. In the same program, a CARIBRO Laboratory was created in one of the Medical Faculties of Havana with the aim to teach students from the Caribbean in neuroscience research. As part of this program, we have been working in lateralized motor functions. Preliminary results in rats show that reaching acquisition allows classification of the animals as right-handed (40%), left-handed (40%), and ambidextrous (20%). Electrolytic lesion of caudate nucleus or amygdala impairs lateralized response. Contralateral lesions increase reaching attempts. Ipsilateral lesions to the preferred forepaw do not affect the reaction. The results remain the same 10, 20, and 90 d after the interference. Pharmacological experiments showed that trihexiphenidil (0.1 mg/kg i.p.) induced handedness reversion in 50% if the animals, whereas haloperidol (1 mg/kg i.p.) produced immobility, tremor, and autonomic symptoms. This effect remained the same in young as well as in old animals. We are also working on mathematical modelation. In this sense, preliminary reports about a model for synaptic modification in the framework of the Fukushima hypothesis is discussed.
Assuntos
Comportamento Animal , Comportamento , Encéfalo/fisiologia , Neurociências , Organizações , Animais , Região do Caribe , Cuba , Bolsas de Estudo , Humanos , Ratos , PesquisaRESUMO
Rats (n=11) with bilateral kainate lesions of the caudate nucleus and subsequen unilateral transplantation of embryonic striatal tissue into the damaged area prefered 4 months later to reach for food with the forepaw contralateral to the graft. No such asymmetry was observed in lesioned, nontransplanted (n=8) or unoperated (n=5) control rats. Good integration of the graft with the host brain was indicated by the fnding that cortical spreading depression did not enter the lesioned caudate nucleus but did penetrate into the lesioned caudate with the graft almos as regulary as in intact rats. Behavioral asymmetry produced by unilateral grafts in bilaterally lesioned animals reveals the effects of transplantation with more sensitivity than the graft-induced compensation of the asymmetries caused by unilateral lesions (AU)
Assuntos
Animais , Corpo Estriado , Transplante , Ratos , Núcleo Caudado , Modelos Animais de DoençasRESUMO
Rats (n=11) with bilateral kainate lesions of the caudate nucleus and subsequen unilateral transplantation of embryonic striatal tissue into the damaged area prefered 4 months later to reach for food with the forepaw contralateral to the graft. No such asymmetry was observed in lesioned, nontransplanted (n=8) or unoperated (n=5) control rats. Good integration of the graft with the host brain was indicated by the fnding that cortical spreading depression did not enter the lesioned caudate nucleus but did penetrate into the lesioned caudate with the graft almos as regulary as in intact rats. Behavioral asymmetry produced by unilateral grafts in bilaterally lesioned animals reveals the effects of transplantation with more sensitivity than the graft-induced compensation of the asymmetries caused by unilateral lesions
Assuntos
Animais , Núcleo Caudado , Corpo Estriado , Ratos , Transplantes , Modelos Animais de DoençasRESUMO
El estudio de los mecanismos de propagación de la crisis epiléptica, es de importancia para el conocimiento del desarrollo de las crisis clínicas y electroencefalográficas desde su inicio, ya en forma explosiva o a punto de partida de las descargas interictales, permitiendo explicar al mismo tiempo la forma en que estos ataques tienen lugar en diferentes pacientes. En el presente trabajo se discuten las distintas posibilidades que se han planteado en relación a estos mecanismos, particularizando en los mecanismos intracorticales de propagación, los que tienen lugar a través de vías extracorticales largas y el papel que juegan un conjunto de estructuras facibilatoras e inhibidoras del sistema nervioso central (SNC) (AU)
Assuntos
Humanos , Epilepsia/fisiopatologia , EletrofisiologiaRESUMO
El estudio de los mecanismos de propagación de la crisis epiléptica, es de importancia para el conocimiento del desarrollo de las crisis clínicas y electroencefalográficas desde su inicio, ya en forma explosiva o a punto de partida de las descargas interictales, permitiendo explicar al mismo tiempo la forma en que estos ataques tienen lugar en diferentes pacientes. En el presente trabajo se discuten las distintas posibilidades que se han planteado en relación a estos mecanismos, particularizando en los mecanismos intracorticales de propagación, los que tienen lugar a través de vías extracorticales largas y el papel que juegan un conjunto de estructuras facibilatoras e inhibidoras del sistema nervioso central (SNC)
Assuntos
Humanos , Epilepsia/fisiopatologia , EletrofisiologiaAssuntos
Animais , Adulto , Ratos , Epilepsia/fisiopatologia , Aprendizagem/fisiologia , Memória/fisiologia , Transtorno da CondutaRESUMO
Se presenta el primer trabajo de una serie de artículos donde se analizan aspectos de la electrofisiología de las crisis epilépticas experimentales. Se efectúa un bosquejo histórico del desarrollo de las concepciones sobre la epilépsia que han tenido lugar desde la antigüedad hasta nuestros días. Por otra parte, se sumarizan los conceptos principales y clasificaciones más empleadas del síndrome epiléptico en la actualidad(AU)