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SUMMARY: Currently many people with epilepsy do not have seizure control even with the best available medications. Moreover various antiepileptics have adverse cognitive impact with other side effect. Thus, need for new antiepileptic drugs still remains challenge. However, many of the natural components have antiepileptic action and this fact remains scientifically unexplored. This study was designed to check the behavioral and neuro-pathological outcome of 1-Triacontanol cerotate (1TAC), isolated from Marsilea quadrifolia Linn. (MQ) on chronic Pentylenetetrazol (PTZ) kindling model of epilepsy in rats. Two-month-old adult male Wistar rats (n=60) were randomly divided into six groups; Group I (Cage Control), II (Vehicle Control), III (Positive Control), IV (Standard drug treated), V (1TAC: 40 mg/kg) & VI (1TAC: 80 mg/kg). To induce kindling a 35 mg/kg dose of PTZ was injected i.p. in every 48 hrs for 30 days in Group III to VI. Spatial memory performance was tested using Morris water maze, following which brains were further processed for histopathological investigations. Interestingly, 1TAC was able to minimize the loss of pyramidal cells in hippocampal CA3 region. These cellular changes were behaviorally responded as improved special learning and memory, a better spatial navigation and object place configuration. The current study strongly implicates that 1TAC from MQ has potent neuroprotective role and augments special memory deficit in chronic epileptic rats. The isolated component which attenuates spatial memory performance could be beneficial outcome to retain cognitive blunting in chronic epilepsy.
RESUMEN: Actualmente, muchas personas con epilepsia no cuentan con un control adecuado de las convulsiones, incluso con los mejores medicamentos disponibles. Además, varios antiepilépticos tienen un impacto cognitivo adverso además de efectos secundarios. Por lo tanto, la necesidad de nuevos fármacos antiepilépticos sigue siendo un desafío. Sin embargo, muchos de los componentes naturales tienen acción antiepiléptica y este hecho permanece científicamente inexplorado. Este estudio se diseñó para verificar el resultado conductual y neuro-patológico del cerotato de 1-triacontanol (1TAC), aislado de Marsilea quadrifolia Linn. (MQ) en el modelo de epilepsia en ratas del pentilenetetrazol (PTZ) crónico (PTZ). Ratas Wistar adultas de dos meses de edad (n = 60) se dividieron aleatoriamente en seis grupos; Grupo I (Control de jaula), II (Control de vehículo), III (Control positivo), IV (Medicamento estándar de tratamiento), V (1TAC: 40 mg / kg) y VI (1TAC: 80 mg / kg). Para inducir la inflamación se inyectó una dosis de 35 mg / kg de PTZ i.p. en cada 48 horas durante 30 días en los grupos III a VI. El rendimiento de la memoria espacial se probó utilizando el laberinto de agua de Morris, después de lo cual se procesaron los cerebros para investigaciones histopatológicas. Curiosamente, 1TAC pudo minimizar la pérdida de células piramidales en la región CA3 del hipocampo. Estos cambios celulares respondieron de manera conductual como una mejora del aprendizaje especial y la memoria, una mejor navegación espacial y la configuración del lugar del objeto. El estudio actual implica fuertemente que 1TAC de MQ tiene un potente papel neuroprotector y mejora el déficit de memoria especial en ratas epilépticas crónicas. El componente aislado que atenúa el rendimiento de la memoria espacial podría ser un resultado beneficioso para retener la reducción cognitiva en la epilepsia crónica.
Subject(s)
Animals , Male , Rats , Marsileaceae/chemistry , Epilepsy/drug therapy , Fatty Alcohols/administration & dosage , CA3 Region, Hippocampal/drug effects , Spatial Memory/drug effects , Pentylenetetrazole/adverse effects , Chronic Disease , Rats, Wistar , Pyramidal Cells , Epilepsy/chemically induced , Fatty Acids , Fatty Alcohols/isolation & purification , Morris Water Maze Test , Hippocampus/drug effectsABSTRACT
Resumen Introducción. El grupo de investigación del Laboratorio de Neurofisiología Comportamental de la Universidad Nacional de Colombia ha descrito modificaciones estructurales y electrofisiológicas en neuronas piramidales de la corteza motora producidas por la lesión del nervio facial contralateral en ratas. Sin embargo, poco se sabe sobre la posibilidad de que dichos cambios neuronales se acompañen también de modificaciones en las células gliales circundantes. Objetivo. Caracterizar el efecto de la lesión unilateral del nervio facial sobre la activación y proliferación de las células de la microglía en la corteza motora primaria contralateral en ratas. Materiales y métodos. Se hicieron pruebas de inmunohistoquímica para detectar las células de la microglía en el tejido cerebral de ratas sometidas a lesión del nervio facial, las cuales se sacrificaron en distintos momentos después de la intervención. Se infligieron dos tipos de lesiones: reversible (por compresión, lo cual permite la recuperación de la función) e irreversible (por corte, lo cual provoca parálisis permanente). Los tejidos cerebrales de los animales sin lesión (grupo de control absoluto) y de aquellos sometidos a falsa cirugía se compararon con los de los animales lesionados sacrificados 1, 2, 7, 21 y 35 días después de la lesión. Resultados. Las células de la microglía en la corteza motora de los animales lesionados irreversiblemente mostraron signos de proliferación y activación entre el tercero y séptimo días después de la lesión. La proliferación de las células de la microglía en animales con lesión reversible fue significativa solo a los tres días de infligida la lesión. Conclusiones. La lesión del nervio facial produce modificaciones en las células de la microglía de la corteza motora primaria. Estas modificaciones podrían estar involucradas en los cambios morfológicos y electrofisiológicos descritos en las neuronas piramidales de la corteza motora que comandan los movimientos faciales.
Abstract Introduction: Our research group has described both morphological and electrophysiological changes in motor cortex pyramidal neurons associated with contralateral facial nerve injury in rats. However, little is known about those neural changes, which occur together with changes in surrounding glial cells. Objective: To characterize the effect of the unilateral facial nerve injury on microglial proliferation and activation in the primary motor cortex. Materials and methods: We performed immunohistochemical experiments in order to detect microglial cells in brain tissue of rats with unilateral facial nerve lesion sacrificed at different times after the injury. We caused two types of lesions: reversible (by crushing, which allows functional recovery), and irreversible (by section, which produces permanent paralysis). We compared the brain tissues of control animals (without surgical intervention) and sham-operated animals with animals with lesions sacrificed at 1, 3, 7, 21 or 35 days after the injury. Results: In primary motor cortex, the microglial cells of irreversibly injured animals showed proliferation and activation between three and seven days post-lesion. The proliferation of microglial cells in reversibly injured animals was significant only three days after the lesion. Conclusions: Facial nerve injury causes changes in microglial cells in the primary motor cortex. These modifications could be involved in the generation of morphological and electrophysiological changes previously described in the pyramidal neurons of primary motor cortex that command facial movements.
Subject(s)
Animals , Male , Rats , Microglia/pathology , Facial Nerve Injuries/pathology , Facial Paralysis/physiopathology , Motor Cortex/pathology , Time Factors , Random Allocation , Afferent Pathways , Cell Division , Rats, Wistar , Pyramidal Cells/physiology , Pyramidal Cells/pathology , Axotomy , Facial Nerve Injuries/complications , Facial Nerve Injuries/physiopathology , Facial Muscles/innervation , Facial Paralysis/etiology , Facial Paralysis/pathology , Nerve Crush , Nerve RegenerationABSTRACT
The emergence of research about the biological effects of electromagnetic field (EMF) have growing concern among researchers. The aim of this study was to investigate the effects on the brain of rats periodically exposed to 0.1 mT EMF. Total 24 adult male Sprague Dawley rats were subdivided randomly to 4 groups: 2 control groups (C1 6 hours: 6 h/ day for 5 days; C2 20 hours: 20 h/day for 5 days) and 2 treatment groups which exposed to 0.1 mT EMF (T1 6 hours: 6 h/day for 5 days; T2 20 hours: 20 h/day for 5 days). A significant decrease in the pyramidal cell number was higher as the exposure duration to EMF was extended (T1, p<0.05; T2, p<0.001). The total numbers of pyramidal cells for T1 was 15.18 % lower than of the total found in C1; and in concurring to the pattern, the number of pyramidal cells in T2 was 33.54 % lower than the total in C2. Similarly, there was a significant decrease of the Purkinje cell number as the duration exposure to EMF, extended (T1, p<0.05; T2, p<0.001). The total numbers of Purkinje cells for T1 was 11.20 % lower than C1, in T2 was 16.19 % lower than in C2. There were significant differences between the thickness of granular layer and molecular layer in the control groups and treatment groups. We also report a significant difference in the levels of norepinephrine in T2, 10.71 % higher than C2. Cumulatively, these results suggested that exposure to EMF can exert negative effect on rats brains.
Subject(s)
Electromagnetic FieldsABSTRACT
Introduction: Lead, a heavy metal is well known for its toxic effects on the central nervous system. Clinically, overall effects of lead on different organ system are called plumbism. Diverse writing can be seen on the subject, but rarely there has been a comparison in any of these writings on different parts within the brain of the changes happening as the result of lead exposure. This study was taken up to draw a comparison and correlation of damaging effects on different parts of brain at microscopic level as a result of lead toxicity so that the affected elements in the tissue can be further connected to the histopathological and clinical outcomes of the lead toxicity. Materials and Methods: To conduct the study albino rats of Charles Foster strain were administered orally with 4% lead acetate in drinking water. The behavioral and clinical changes during the period of lead administration were closely observed that extended from irritability, agitation and aggressive behavior in the beginning to drastic fall in activity, indifference towards varieties of stimulus and severe motor deficit. At the end of an average of 17 days the rats were sacrificed for both gross and microscopic examination of brain for changes in the cerebral cortex, hippocampus, cerebellum, pons & medulla. The elements of the tissue observable as per the selected staining were the neurons, fibers, glia & the vessels. Results: The changes showed up with similarities between different parts as the shrinkage of neurons, damaged fibers, stunting of cell processes and increased glial cell population, whereas there were dissimilarities with regards to the extent of shrinkage of neuron and distribution of perineuronal spaces, vacuoles & the glial cells. Discussion and Conclusion: The comparative picture of the changes as a result of lead exposure showed widespread damage to nearly all the elements of the nervous tissue with reactive changes e.g. gliosis, and variations in the extend of changes in the selected brain parts. As a result these changes observed can be of used to correlate in the overall outcome of plumbism in relation to the functions of different parts of the brain.
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Objective To study the therapeutic effects and related mechanism of Tongmai Yizhi granules on vascular dementia in rats. Methods Bilateral carotid artery ligation was used to establish rat model of vascular dementia (VD). The rats were randomly divided into 6 groups: sham operated,the model control,piracetam (0. 375 g·kg-1 ·d-1 ) as positive con-trol,low dose (2. 5 g·kg-1 ·d-1 ),middle dose(5. 0 g·kg-1 ·d-1 ),and high dose (10. 0 g·kg-1 ·d-1 ) of Tongmai Yizhi granules. Each group was intragastrically administered with 10 mL·kg-1 of corresponding medications for 31 days after the VD model was established. The sham group was given with 0. 9% NaCl solution. Y-electric maze was used to test the learning and memory function of rats at the second and fourth weeks. On the day 32,hippocampal tissues were collected for pathological analy-sis by microscope. The activities of SOD and content of MDA in serum and tissue homogenate were tested. Results Compared with model control group,each dose of Tongmai Yizhi granules obviously shortened the incubation period of VD rats in electric maze test,and accuracy of learning and memory was improved (P<0. 05 or P<0. 01). The activity of SOD was decreased,and the content of MDA was increased after treatment with Tongmai Yizhi granules (P < 0. 01). Hippocampal neuronal cells were disar-ranged,and the number of cone cells was decreased significantly in the model control group. In contrast,the necrosis and degener-ation of hippocampal neurons were alleviated in all Tongmai Yizhi treatment groups. Conclusion Tongmai Yizhi granule can apparently improve learning and memory function of VD rats. It can also improve the activity of SOD and reduce the content of MDA in serum and hippocampus,effectively remove free radicals,and alleviate the injury of hippocampal pyramidal cells.
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Objective To survey the effects of repetitive transcranial magnetic stimulation (rTMS) on learning,memory and the dendrite morphology of neurons in the CA1 area of the hippocampus in rats with vascular dementia.Methods Thirty-six male SD rats were divided into a control group,a model group and a rTMS group randomly,12 rats in each group.A model of vascular dementia (VaD) was established using the two vessel occlusion method.The rats in the rTMS group were given rTMS treatment.The rats in the other two groups had no therapy.The Morris water maze (MWM) test was used to evaluate the rats' learning and memory abilities on the 30th day after the operation.After the MWM test the dendrite morphology of the pyramidal cells in the CA1 area of the hippocampus was detected after Golgi-Cox staining using light microscopy and the expression of brain-derived neurotrophic factor (BDNF) was detected using immunohistochemistry methods.Results The average MWM escape latency in the rTMS group was shorter than in the model group on the 1 st,2nd,3rd and 4th day.The number of crossings of the platform quadrant in the rTMS group was significantly more than in the model group.The number of branch segments,their total length and the dendritic spine density of pyramidal cell dendrites in the CA1 area of the hippocampus were all significantly lower in the model group than in the control group,but in the rTMS group all these indicators were significantly improvedcompared with the model group.The expression of BDNF in the CA1 area in rTMS group was significantly higher than in the model group.Conclusions rTMS can improve learning and memory in VaD,at least in rats.The mechanism may be associated with rTMS promoting the expression of BDNF in the hippocampus and so improving the dendrite morphology of pyramidal cells.
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Dementia is one of the most important problems nowadays. Aging is associated with learning and memory impairments. Diet rich in cholesterol has been shown to be detrimental to cognitive performance. This work was carried out to compare the effect of high cholesterol diet on the hippocampus of adult and aged male albino rats. Twenty adult and twenty aged male rats were used in this study. According to age, the rats were randomly subdivided into balanced and high cholesterol diet fed groups. The diet was 15 g/rat/day for adult rats and 20 g/rat/day for aged rats for eight weeks. Serial coronal sections of hippocampus and blood samples were taken from each rat. For diet effect evaluation, Clinical, biochemical, histological, immunohistochemical, and morphometric assessments were done. In compare to a balanced diet fed rat, examination of Cornu Ammonis 1 (CA 1) area in the hippocampus of the high cholesterol diet adult rats showed degeneration, a significant decrease of the pyramidal cells, attenuation and/or thickening of small blood vessels, apparent increase of astrocytes and apparent decrease of Nissl's granules content. Moreover, the high cholesterol diet aged rats showed aggravation of senility changes of the hippocampus together with Alzheimer like pathological changes. In conclusion, the high cholesterol diet has a significant detrimental effect on the hippocampus and aging might pronounce this effect. So, we should direct our attention to limit cholesterol intake in our food to maintain a healthy life style for a successful aging.
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Adult , Animals , Humans , Male , Rats , Aging , Astrocytes , Blood Vessels , Cholesterol , Dementia , Diet , Hippocampus , Learning , Life Style , Memory , Pyramidal CellsABSTRACT
Dementia is one of the most important problems nowadays. Aging is associated with learning and memory impairments. Diet rich in cholesterol has been shown to be detrimental to cognitive performance. This work was carried out to compare the effect of high cholesterol diet on the hippocampus of adult and aged male albino rats. Twenty adult and twenty aged male rats were used in this study. According to age, the rats were randomly subdivided into balanced and high cholesterol diet fed groups. The diet was 15 g/rat/day for adult rats and 20 g/rat/day for aged rats for eight weeks. Serial coronal sections of hippocampus and blood samples were taken from each rat. For diet effect evaluation, Clinical, biochemical, histological, immunohistochemical, and morphometric assessments were done. In compare to a balanced diet fed rat, examination of Cornu Ammonis 1 (CA 1) area in the hippocampus of the high cholesterol diet adult rats showed degeneration, a significant decrease of the pyramidal cells, attenuation and/or thickening of small blood vessels, apparent increase of astrocytes and apparent decrease of Nissl's granules content. Moreover, the high cholesterol diet aged rats showed aggravation of senility changes of the hippocampus together with Alzheimer like pathological changes. In conclusion, the high cholesterol diet has a significant detrimental effect on the hippocampus and aging might pronounce this effect. So, we should direct our attention to limit cholesterol intake in our food to maintain a healthy life style for a successful aging.
Subject(s)
Adult , Animals , Humans , Male , Rats , Aging , Astrocytes , Blood Vessels , Cholesterol , Dementia , Diet , Hippocampus , Learning , Life Style , Memory , Pyramidal CellsABSTRACT
Objective To investigate the effects of hyperbaric oxygen on learning and memory ability in rats with a model of VPA autism and on the pyramidal cells in the CA1 region of the hippocampus.Methods An animal model of autism was established in the offspring of Wistar rats which had received a single intraperitoneal injection of sodium valproate at the 12.5th day of pregnancy.A total of 48 male VPA autism model rats were randomly divided into the hyperbaric oxygen group,a high pressure air group,a normal pressure high oxygen group and a normal pressure air group (each group with 12 rats).A normal control group was obtained by injecting physiological saline.The autism model rats of the hyperbaric oxygen group were treated with high pressure oxygen in an animal experiment cabin which was cleaned with pure oxygen for 10 min,pressurized for 15 min,held at 2.0 atmospheres absolute (ATA) for 45 min and then had the pressure relieved over 15 min.For the high pressure air group the cabin was pressurized with air for 15 min,held at 2.0 ATA for 45 min and the pressure was relieved over 15 min.For the normal pressure,high oxygen group the cabin was cleaned for 10 min with pure oxygen,then pure oxygen was supplied for 1 hour with the cabin door open.The normal pressure air group rats were placed in the open cabin with no pressure or additional oxygen.The testing lasted 7 days for 1 hour per day.The normal control group rats were placed in ordinary cages.Learning and memory were evaluated using the Y electric maze test before and after the interventions.Any changes in the pyramidal cells in the CA1 region of the hippocampus were observed after hematoxylin and eosin (HE) staining.Results The average number of tries of the hyperbaric oxygen group after treatment was significantly less than before treatment and memory retention times were increased.The number was also less in the normobaric hyperoxia group and memory retention times again improved.The number of apoptotic cells was reduced and the number of normal form cells in the CA1 region increased after the hyperbaric oxygen intervention.Conclusions The learning and memory abilities of the autistic rats improved after the hyperbaric oxygen intervention.Pyramidal cells in the CA1 region proliferated and the number of apoptotic cell decreased.This may be the mechanism by which hyperbaric oxygen intervention treats autism.
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Cognitive dysfunction is reportedly associated with poorly-managed diabetes mellitus. In this study, we report the effect of oral treatment with combined leaf extract (CLE) of neem and bitter leaf on the prefrontal cortex of diabetic Wistar rats. Adult male Wistar rats were randomized to one of the following groups: control, diabetic (STZ-induced), STZ + CLE, STZ + metformin and CLE only. At euthanasia, paraffin sections of the prefrontal cortex were stained with cresyl fast violet; while malondialdehyde (MDA) and glutathione peroxidase (GPx) were assayed in prefrontal homogenates. Oral CLE produced normoglycemia in the treated hyperglycaemic rats. Besides, Nissl-stained prefrontal sections showed no morphologic deficits in all the groups except the untreated diabetic rats. In the latter, there was weak Nissl staining, while prefrontal MDA was significantly high at euthanasia, compared with the control and CLE-treated rats (P<0.05). This study showed that untreated diabetes mellitus is associated with prefrontal Nissl body deficit and oxidative stress in Wistar rats. The absence of these deficits in CLE-treated rats suggests a neuroprotective effect of the extract in streptozotocin-induced diabetic rats. This may improve the cognitive function of the prefrontal cortex in diabetes mellitus.
La disfunción cognitiva es presuntamente asociada con un mal manejo de la diabetes mellitus. En este estudio, se presenta el efecto del tratamiento oral combinado con extracto de hoja (CLE) de hoja de neem amarga sobre la corteza prefrontal de ratas Wistar con diabetes. Las ratas Wistar adultas fueron asignadas al azar a uno de los siguientes grupos: control, diabetes (STZ inducida), STZ + CLE, STZ + metformina y CLE. Después de la eutanasia, los cortes de parafina de la corteza prefrontal se tiñeron con violeta de cresil rápido, mientras que el malondialdehído (MDA) y la glutatión peroxidasa (GPx) fueron analizadas en homogenizados prefrontales. El CLE produce normoglucemia en las ratas hiperglucémicas tratadas. Además, las secciones prefrontales teñidas para Nissl no muestran ningún déficit morfológico en todos los grupos excepto en las ratas diabéticas sin tratamiento. En este último caso, hubo una tinción de Nissl débil, mientras que la MDA prefrontal fue significativamente más alta en comparación con los grupos de ratas control y las tratadas con CLE (p <0,05). Este estudio mostró que la diabetes mellitus no tratada se asocia con déficit prefrontal de cuerpos de Nissl y estrés oxidativo en ratas Wistar. La ausencia de estos déficits en las ratas tratadas CLE, sugiere un efecto neuroprotector del extracto en ratas diabéticas inducidas por estreptozotocina. Esto puede mejorar la función cognitiva de la corteza prefrontal en la diabetes mellitus.
Subject(s)
Rats , Azadirachta , Azadirachta/ultrastructure , Diabetes Mellitus, Experimental/blood , Diabetes Mellitus, Experimental/therapy , Retrograde Degeneration , Streptozocin/adverse effects , Streptozocin/toxicity , Nigeria , Rats, Wistar/physiology , Rats, Wistar/bloodABSTRACT
Objective This study aimed at the effect of glutamate(Glu) on rat cortical pyramidal cells in cultured brain slices treated by threohydroxyaspartate(THA),an inhibitor of glutamate transporter.Methods The brain slice cultures were prepared using 1-day-old rat.Various concentrations of THA(50,100 and(500 ?mol/L))were added into the culture medium respectively.Cortical pyramidal cells' survival was evaluated by immunohistochemistry staining monoclonal antibody SMI-32,a nonphosphorylated neurofilament marker,Glu level in the culture medium was also measured.Ultrastructural picture of neuropathology were examined by EM microscopy. Results The brain slices in the control group maintain excellent organization and a stable population of pyramidal cells.THA caused a slow dose-dependent loss of cortical pyramidal cells and an increase of Glu level in the culture medium.THA of 100 ?mol/L resulted in a significant decrease in cortical pyramidal cells after culturing for 5 weeks.Pyramidal cells appeared vacuolar degeneration.Conclu-(sions Extra-cellular) Glu caused chronic excitotoxicity to cortical pyramidal cells.
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AIM: To observe pathomorphological changes in cerebral cortex and hippocampus in the mouse with synthetic vascular dementia. METHODS: The synthetic vascular dementia model was produced in the mouse. Animals were killed 7 d, 15 d, and 30 d after the operation, brain tissues were removed and embedded in paraffin. Section of 8?m thickness were stained with hematoxylin-eosin(HE) and Nissl methods, and observed with light microscope. RESULTS: The cerebral cortex in the mouse became thinner on the seventh day, karyopyknosis in partial nervous cells was formed, the number of local neurons was reduced, sieve structure was observed, and glial cells proliferated, with the similar results 15 d and 30 d after operation. Model mouses hippocampal cells in CA 1 area were reduced and almost disappeared 30 d after operation. At the same time, glial cells were abundantly proliferated, tubercles were formed. Cells in CA 2, CA 3 area were also reduced and hippocampal sclerosis occurred. CONCLUSION: Delayed necrosis of hippocampal pyramidal cells may be the pathological basis of ischemia cerebral vascular dementia.
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Objective To investigate the effect of glucocorticoid on ischemia-induced neuronal damage in gerbil hippocampus with forebrain ischemia model.Methods Twenty-one gerbils were randomly assigned to 3 groups (7 animals each). The animal was anesthetized and both common carotid arteries were exposed and separated. Silk threads were looped around these arteries. In group A and group B ,10 ?l saline was given and in group C dexamethasone-water soluble ( 3?g dissolved in 10 ?l saline ) was administered intracerebroventricularly. After a stabilization period of 60 min, transient forebrain ishcmia for 2.5 min was induced in group B and group C by pulling the arteries with 8g weights under the brain temperature of 37.5℃?0.2℃. Seven days after the ischemia, the brains were taken out and fixed with 10% buffered formalin. Brain slices, 5 ?m thick, were stained with hematoxylin and eosin. The numbers of preserved pyramidal cells in the hippocampal CA1 field per 1 mm length of stratum pyramidal were counted.Results (1) Compared with those in group A, the preserved pyramidal cells in hippocampal CA1 field were reduced in group B and group C (P
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In the present study, 10 healthy adult dogs were used,8 for the experimental group and 2 for the normal group. We observed the histochemical and ultrastrac- tural changes of the enzymes in the pyramidal cells in the cerebral cortex under the condition of acute ischemia. The result demonstrated that the activity of LDH, AcP and AchE was increased, while the activity of SDH, MAO, ATP ase was decreased. The ultrastructural chnges showed that in the acute ischemia gromp, there were enlargement perinucleus spaces of neurone, brisement, disappearance and vasicularization of the mitochondrial crista. This indicated that acute ischemia had an obvious effect on the histochcmistry of enzymes and the ultra- structure of the neurone in the cerebral cortex.
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Objective To investigate the characteristics of spontaneous discharges of hippocampal pyramidal cells (PC) in rats in age and memory groups with the help of nonlinear theory. Methods Rats were randomly divided into age group and memory group. Age group included aged group (16-19 months) and young group (3-4 months) whereas memory group included good memory and poor memory groups in adult. Extracellular single cell recording was performed in vivo . Results No characteristics of the rhythm of spontaneous discharges of hippocampal pyramidal cells in distribution figure of interspike interval(ISI) were found, but the loss of complexity(C) and low percentage of favored patterns(PF) were found in age and poor memory groups. Conclusion The ISI complexity and the PF of the hippocampal pyramidal cells are correlated to age and memory, suggesting that the analysis of the complexity and favored patterns may be helpful for the discovery of the characteristics of the information coding in spontaneous discharges of hippocampal pyramidal cells.
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This article presents a brief introduction of the gap junctions on CA_1 pyramidal cells of guinea pig hippocampus observed by freeze replica technique. In freeze replicas of the hippocampus of guinea pig, gap junctions were observed on the E-face of the CA_1 pyramidal cells and the apical dendrites, the intramembranous particles aggregated as a large or a small area and arranged regularly or irregularly.