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@#Introduction: Preclinical studies have reported that Murraya koenigii leaves (MKL) could enhance memory. MKL is also known for its antioxidant activity. The current study was to assess the possible neuroprotective potential of MKL methanolic extract in a two vessel occlusion (2VO) rat model of partial global cerebral ischaemia. Methods: Rats were divided into memory and learning groups. Each group was subdivided into sham control, untreated 2VO and MKL-treated 2VO subgroups. The Morris water maze test was implemented to assess the rats’ cognitive function postoperatively. Brain samples were histopathologically examined for viable neurons within the CA1 hippocampal region. Results: Water maze test findings showed that MKL positively improved memory and learning impairments. However, this improvement in memory test for the treated group was still significantly inferior to that of the healthy control group. Additionally, MKL treated group exhibited insignificant difference in the number of viable hippocampal CA1 pyramidal neurons from that of the untreated 2VO group, whereas both MKL treated and untreated 2VO groups showed significantly less viable neurons when compared with the control group. Conclusion: MKL extract modestly improved memory without providing substantial neuroprotective action to the hippocampal neurons in rats with chronic partial global cerebral ischaemia.
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Abstract Previous studies suggested that mastication activity can affect learning and memory function. However, most were focused on mastication impaired models by providing long-term soft diet. The effects of chewing food with various hardness, especially during the growth period, remain unknown. Objective: To analyze the difference of hippocampus function and morphology, as characterized by pyramidal cell count and BDNF expression in different mastication activities. Materials and Methods: 28-day old, post-weaned, male-Wistar rats were randomly divided into three groups (n=7); the first (K0) was fed a standard diet using pellets as the control, the second (K1) was fed soft food and the third (K2) was fed hard food. After eight weeks, the rats were decapitated, their brains were removed and placed on histological plates made to count the pyramid cells and quantify BDNF expression in the hippocampus. Data collected were compared using one-way ANOVA. Results: Results confirmed the pyramid cell count (K0=169.14±27.25; K1=130.14±29.32; K2=128.14±39.02) and BDNF expression (K0=85.27±19.78; K1=49.57±20.90; K2=36.86±28.97) of the K0 group to be significantly higher than that of K1 and K2 groups (p<0.05); no significant difference in the pyramidal cell count and BNDF expression was found between K1 and K2 groups (p>0.05). Conclusion: A standard diet leads to the optimum effect on hippocampus morphology. Food consistency must be appropriately suited to each development stage, in this case, hippocampus development in post-weaned period.
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Animales , Masculino , Células Piramidales/fisiología , Factor Neurotrófico Derivado del Encéfalo/análisis , Alimentos , Hipocampo/fisiología , Masticación/fisiología , Valores de Referencia , Factores de Tiempo , Distribución Aleatoria , Recuento de Células , Ratas Wistar , Dureza/fisiologíaRESUMEN
Numerous studies have implicated the hippocampus in the encoding and storage of declarative and spatial memories. Several models have considered the hippocampus and its distinct subfields to contain homogeneous pyramidal cell populations. Yet, recent studies have led to a consensus that the dorso-ventral and proximo-distal axes have different connectivities and physiologies. The remaining deep-superficial axis of the pyramidal layer, however, remains relatively unexplored due to a lack of techniques that can record from neurons simultaneously at different depths. Recent advances in transgenic mice, two-photon imaging and dense multisite recording have revealed extensive disparities between the pyramidal cells located in the deep and the superficial layers. Here, we summarize differences between the two populations in terms of gene expression and connectivity with other intra-hippocampal subregions and local interneurons that underlie distinct learning processes and spatial representations. A unified picture will emerge to describe how such local segregations can increase the capacity of the hippocampus to compute and process numerous tasks in parallel.
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Animales , Ratones , Consenso , Expresión Génica , Hipocampo , Interneuronas , Aprendizaje , Memoria , Ratones Transgénicos , Neuronas , Células Piramidales , Memoria EspacialRESUMEN
Hypoxia-ischemia (HI) is a major cause of brain damage in the newborn. Several studies elicited the neuroprotective effects of progesterone in adult rats but there is very little literature available on neonatal rats. Therefore the present study is undertaken to see the effect of progesterone in hypoxic ischemic brain injury in neonatal rats, using an established neonatal HI rat pup model. Seven-day-old rat pups were subjected to right common carotid artery ligation and then 60 minutes hypoxia. The first dose of progesterone to treatment group was administered by peritoneal injection (4 mg/kg), after 10 minutes of exposure and subsequent doses were given by subcutaneous injection at 6 h, 24 h and 48 h intervals. Control group was also exposed to HI and was given only the vehicle (peanut oil) through the same route and intervals as that of treatment group. After 96 h, the pups were perfused with 10% formalin and brains were sampled and stained with toluidine blue. Cells density and number of pyramidal cells of the hippocampal Cornu Ammonis (CA) regions were examined by stereological methods. The histomorphometric assessment of the effects of progesterone showed minimal but no significant protective value in the volume, cells density and total number of pyramidal cells of hippocampal CA region of the treatment and control groups (p>0.05) after HI. Our results concluded that 4 mg/kg of PROG had no significant neuroprotective effect in HI model of the neonatal rat's hippocampus.
La hipoxia-isquémica (HI) es una causa importante de daño cerebral en el recién nacido. Varios estudios indican los efectos neuroprotectores de la progesterona en ratas adultas, sin embargo existe poca literatura disponible en ratas recién nacidas. Por tanto, el presente estudio se llevó a cabo para ver el efecto de la progesterona en la lesión cerebral HI en ratas recién nacidas, utilizando un modelo de cría de rata neonata HI establecido. A los siete días de nacidas, las crías de ratas fueron sometidas a la ligadura de la arteria carótida común derecha y luego 60 minutos de hipoxia. La primera dosis de progesterona fue administrada al grupo de tratamiento mediante inyección peritoneal (4 mg/kg), después de 10 minutos de exposición y las dosis posteriores fueron administradas por inyecciones subcutáneas en intervalos de 6 h, 24 h y 48 h. El grupo control también fue expuesto a HI y se le administró solamente aceite de cacahuete a través de la misma ruta y con los intervalos que recibió el grupo de tratamiento. Después de 96 h, las crias fueron perfundidas con formalina al 10% y se tomaron muestras de los cerebros, los que se tiñeron con azul de toluidina. La densidad celular y el número de células piramidales de las regiones del hipocampo Cornu Ammonis (CA) fueron examinadas por métodos estereológicos. La evaluación histomorfométrica de los efectos de la progesterona mostró un valor protector mínimo, pero no significativo en el volumen, densidad de las células y el número total de células piramidales de la región de CA del hipocampo de los grupos de tratamiento y control (p>0,05) después de HI. En conclusión, nuestros resultados indican que 4 mg/kg de progesterona no tuvo efecto neuroprotector significativo en el modelo de HI del hipocampo de ratas neonatas.
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Animales , Masculino , Ratas , Hipocampo/efectos de los fármacos , Hipoxia-Isquemia Encefálica/patología , Progesterona/farmacología , Animales Recién Nacidos , Hipocampo/citología , Hipocampo/patología , Fármacos Neuroprotectores , Células Piramidales/efectos de los fármacos , Células Piramidales/patología , Ratas Sprague-DawleyRESUMEN
Objective To explore the pathogenesis of autism by observation of changes of brain-derived neurotrophic factor(BDNF) positive neurons and the morphology of pyramidal cells in hippocampal CA1 region,and provide theoretical evidence for the therapeutic schedule.Methods Animal model of autism was obtained by Schneider method.Using the immunohistochemistry methods and image analysis,the number of BDNF positive neurons was examined in hippocampal CA1 region of the autism model rats and the normal rats,and the changes of pyramidal cell were observed in hippocampal CA1 region after HE staining.Results The numbers of BDNF positive neurons in the hippocampal CA1 region of the autism model rats were more than those of the normal rats (5.00 ±1.60 vs 3.00 ± 1.04,t =3.63,P =0.0015).The morphology of pyramidal cells showed that the pyramidal cells of the autism model rats in hippocampal CA1 region had apoptosis.Conclusion The occurrence of autism may be related to the changes of BDNF and the morphology of pyramidal cells in hippocampal CA1 region.
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The pyramidal cell density of CA1 hippocampal subfield following STZ-induced diabetes in young rats were studied. 12 male albino 6-week Wistar rats were allocated equally in groups of normal and diabetic. Hyperglycemia induced by Streptozotocin (80 mg/kg) in animals of diabetic group. After 5 weeks of study, all the rats were sacrificed and coronal sections were taken from dorsal hippocampal formation of the right cerebral hemispheres and stained with crysel violet. The area densities of the CA1 pyramidal cells were measured and compared among two groups. No significant difference between the densities of two experimental groups was found. The results can arise from the short period of diabetes and also the possible regenerative processes in developing brain of the young diabetic rats which compensated significant diabetes-induced neuronal loss.
La densidad de las células piramidales del subcampo CA1 hipocampal resultantes de diabetes inducida por STZ en ratas jóvenes fue estudiada. 12 ratas albinas Wistar macho, de 6 semanas fueron asignadas equitativamente en grupos normal y diabético. La hiperglicemia fue inducida por Streptozotocin (80 mg/kg) en los animales del grupo de diabéticos. Después de 5 semanas de estudio, todas las ratas se sacrificaron y se tomaron secciones coronales de la formación del hipocampo dorsal de los hemisferios cerebrales derecho y se tiñeron con violeta crisol. Las áreas de densidad de las células piramidales CA1 fueron medidas y comparadas entre los dos grupos. No se encontraron diferencias significativas entre las densidades de los dos grupos experimentales. Los resultados pueden explicarse debido al corto periodo de diabetes y también por la posibilidad de procesos regenerativos del cerebro en desarrollo de las ratas jóvenes diabéticas los cuales compensan significativamente la pérdida neuronal en la diabetes inducida.
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Masculino , Animales , Ratas , Células Piramidales/ultraestructura , Diabetes Mellitus Experimental/patología , Intolerancia a la Glucosa , Hipocampo , Ratas Wistar , Factores de TiempoRESUMEN
@#Objective To study the effect of hyperbaric oxygen(HBO)therapy on abilities of learning and memory and hippocampal pyramidal cell in vascular dementia rats.MethodsThe vascular dementia model was reproduced and divided into control,sham and treatment groups.After 30 d of HBO therapy,the rats were assessed with the Morris water maze,and their hippocampal pyramidal cells were observed after HE staining.ResultsCompared with the control group,the ability of learning and memory of rats in treatment group increased,as well as the hippocampal pyramidal cells did.ConclusionHyperbaric oxygen therapy can be used to treat vascular dementia.
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Objective To detect the change of discharge phase of guinea pig hippocampal CA1 pyramidal cells during visual discriminative task with an effective and convenient program we designed. Methods Five guinea pigs were performed by extracellular single unit recording in vivo when they were performing visual discriminative task. Discharge signals of individual pyramidal cells were extracted from different frequency signals by wavelet transform (WT), which made it feasible to calculate discharge phase of pyramidal cells in terms of time correlation between discharge and ? rhythm. Results The discharge phase of CA1 pyramidal cells in the 1 to 5s interval before visual discriminative task (172??1.8?) was obviously earlier than that in the 6 to 10s interval after visual discriminative task (189??3.7?) ( P0.01). Conclusion The program we designed is capable of detecting discharge phase of pyramidal cells. Regular shift of discharge phase of hippocampal CA1 pyramidal cells emerges before and after performing visual discriminative task.
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OBJECTIVE: A previous study indicated that acute treatment of clozapine increased the neural activity of prefrontal cortical neurons of anesthetized rats. This study was to investigate the effect of clozapine on prefrontal cortical neurons in behaving rats. METHODS: Neural activities of prefrontal cortical neurons of behaving rats were measured before and after clozapine administration using single unit recording. RESULTS: Sixty nine single units (N=69) in the medial prefrontal cortex were isolated in forty three Sprague-Dawley rats. Although clozapine did not change the overall average firing rate of prefrontal cortical neurons, there was a tendency to increase in the neural activity of neurons with low firing rate that were considered to be putative pyramidal cells (N=40). In contrast, neurons with high firing rate assumed to be putative interneurons (N=29) tended to decrease in neural activity by clozapine treatment. CONCLUSION: This result suggests that clozapine treatment enhances the neural activity of pyramidal cells and to inhibit interneurons in the prefrontal cortex. It is speculated that the enhancement of neural activity of pyramidal cells in the prefrontal cortex by clozapine treatment may contribute to its therapeutic effect.
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Animales , Ratas , Clozapina , Incendios , Interneuronas , Neuronas , Corteza Prefrontal , Células Piramidales , Ratas Sprague-Dawley , EsquizofreniaRESUMEN
In order to study damages on brain cells upon occlusion and reperfusion, brain infarction was induced by insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. After occlusion of 1 hr and reperfusion for variable duration, brain slices were used to observe changes in the brain morphology and in the pyramidal neurons of the himppocampal formation. In this study we found following results. 1) The operation took 20~30 min and about 30% of the operated animals were suitable for studying neurological aspects. 2) The TTC stain showed that about 23.9% of the total brain area was damaged in the 72 hr-reperfusioned sample. 3) The degree of brain edema was larger in the left hemisphere (damaged side) than in the right one (contralateral undamaged side). 4) Pyramidal cells of the damaged hippocampal formation showed features of necrosis such as shrinkage, large vacuole, swelling, and cell debris. 5) The numbers of survived cells per mm2 of the hippocampal formation were 93 in the undamaged animal, and 23 and 3 in the 3 and 7 days after reperfusion, respectively.
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Animales , Encéfalo , Edema Encefálico , Infarto Encefálico , Arteria Carótida Interna , Hipocampo , Isquemia , Arteria Cerebral Media , Necrosis , Neuronas , Nylons , Células Piramidales , Reperfusión , VacuolasRESUMEN
Objective To study the ultrastructure changes of hippocampus pyramidal cells and capillaries in genetically diabetic mice C57BL/KsJ (db/db).Methods We chose 5 obese C57BL/KsJ db/db mice of 6 weeks old with fast blood glucose (FBG) higher than 11 1mmol/L as diabetic group and 5 normal weight C57BL/KsJ (?/+) mice with FBG lower than 6 0mmol/L as normal group. Mice were killed at 30 weeks and hippocampus samples were embedded in Epon 812. Thin sections were cut with ultrathin microtome and observed with electron microscopes. Results Pyramidal cells of hippocampus in diabetic mice had significant retrograde changes. The basement membrane of capillaries thickened significantly and endothelial cells and pericytes degenerated.Conclusion The significant pathological changes in hippocampus pyramidal cells and capillaries of diabetic mice may related to dysfunction of cognition.
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Objective To investigate the inhibitory effects of fentanyl on GABAA receptors in hippocampal pyramidal neurons of rat.Methods Pyramidal neurons were acutely isolated from 3-10 day old SD rats of either sex by enzymatic-mechanic method. GABAA receptor mediated currents ( IGABA) were recorded using voltage clamped whole cell patch clamp technique in gap-free mode at the holding potential (VH) of - 50 mV. Current-voltage relationship of IGABA was obtained in ramp protocol ranging from + 30 mV to - 110 mV and lasting for 1 600 ms. Data were collected by using a system consisting of Axopatch 200B patch-clamp amplifier, Pentium Ⅲ computer and Digidata 1200 interface. All experiments were performed at room temperature (22-25℃). Five to twelve neurons were used for each fentanyl concentration. The effects of fentanyl from 1.0 ? 10-5 ?mol?L-1 to 10. 0 ?mol?L-1 were evaluated by the inhibition rate of the peak amplitude of IGABA, the desensitization time constant (?des) of IGABA and the reversal potential (Ecl- ) of IGABA. A ?-opioid receptor selective antagonist CTAP 1 ?mol?L-1 was applied and its effects on fentanyl were recorded. Results (1) GAB A 1-1 000 ?mol?L-1 induced inward currents (IGABA) dose-dependently with an EC50 of 23.73 ?mol?L-1.IGABA induced by GABA 30 ?mol?L-1 was blocked by bicuculline 1 ?mol?L-1. (2) Fentanyl depressed IGABA dose-dependently with EC50 of 0.011 ?mol?L-1 and shortened the rdes of IGABA.(3) The inhibitory effects of fentanyl on IGABA were antagonized by CTAP. (4) Fentanyl 0.01 ?mol?L-1 and CTAP did not influence the reversal potential of IGABA (Ecl- -3.0 mV) .Conclusion Fentanyl inhibits the function of GABAA receptors through ?-opioid receptors in hippocampal pyramidal neurons. Hippocampus may play a role in the neuroexcitatory effects of opioids.