Effects of glossy privet fruit on neural cell apoptosis in the cortical parietal lobe and hippocampal CA1 region of vascular dementia rats**☆

BACKGROUND： Glossy privet fruit inhibits neural cell apoptosis following the onset of vascular dementia. OBJECTIVE： To confirm glossy privet fruit effects on neural cell apoptosis in the cortical parietal lobe and hippocampal CAI region of rat models of vascular dementia using molecular biology techniques. DESIGN, TIME AND SETTING： The neural cell morphology experiment was performed at the Laboratory of Flow Cells and Biochemistry, Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, and the Basic Room of Pathology, Academy of Chinese Medicine from December 2006 to May 2008. MATERIALS： A total of 60 Wistar rats were used to establish vascular dementia models using a photochemical reaction method. Glossy privet fruit was purchased from Fujian, China. Hydergine was co-produced by Sandoz, Switzerland and Huajin, China. METHODS： The 60 Wistar rats were randomly divided into 6 equal sized groups （n = 10）, i.e. model, blank, high, moderate and low doses of Chinese medicine, and hydergine control groups. Rats in the model group were treated with distilled water （1 mL/100 g） by gavage following model establishment. Rats in the blank group underwent experimental procedures as for the model group, except that rat models were created without illumination. Rats in the high, moderate and low doses of Chinese medicine groups, and the hydergine control group respectively received high, moderate and low doses of glossy privet fruit, and hydergine suspension （1 mL/100 g） by gavage, once a day, for 30 days. MAIN OUTCOME MEASURES： Morphology of neural cells from the rat cortical parietal lobe and hippocampal CA1 region of all groups was observed with an electron microscope. Positive neural cells in the injury site of the rat cortical parietal lobe and hippocampal CA1 region were investigated using the Fas immunohistochemieal method. Absorbance of Fas-positive neurons was detected by the MPIAS-500 multimedia color imaging analysis system. RESULTS： Neural cells were normal, and     

皮质发育障碍大鼠小脑回形态学和海马苔藓纤维发芽的研究

目的 探讨液氮损伤诱导局灶性皮质发育障碍大鼠海马形态学及苔藓纤维发芽的情况。方法 实验随机分为正常对照组、假手术组和液氮损伤组，建立局灶性皮质发育障碍动物模型，察看其行为改变；采用常规HE染色、Nissl染色和Timm’s硫化银组织化学方法染色，肉眼和光镜下观察大鼠脑皮质形态变化，光镜下评估海马苔藓纤维发芽情况，各组数据取苔藓纤维发芽评分，采用非参数秩和Kruskal—Wallis H检验，组间两两比较用Nemenyi法。结果 液氮损伤组大鼠行为轻微改变，鼠脑嘴尾方向形成了一小的脑回，同侧海马CA3区有苔藓纤维发芽．而正常对照组和假手术组却没有。结论 幼鼠早期液氮损伤可导致小脑回形成及海马CA3区苔藓纤维发芽。小脑回周围异常兴奋性突触环路和海马CA3区苔藓纤维发芽形成推测是局灶性皮质发育障碍导致癫痫发生的重要机制。     

脑瘫丸对神经细胞损伤修复及缺氧缺血幼鼠认知功能障碍的影响

BACKGROUND： Hypoxia and ischemia induce neuronal damage, decreased neuronal numbers and synaptophysin levels, and deficits in learning and memory functions. Previous studies have shown that lycium barbarum polysaccharide, the most effective component of barbary wolfberry fruit, has protective effects on neural cells in hypoxia-ischemia. OBJECTIVE： To investigate the effects of Naotan Pill on glutamate-treated neural cells and on cognitive function in juvenile rats following hypoxia-ischemia. DESIGN, TIME AND SETTING： The randomized, controlled, in vivo study was performed at the Cell Laboratory of Lanzhou University, Lanzhou Institute of Modern Physics of Chinese Academy of Sciences, and Department of Traditional Chinese Medicine of Gansu Provincial Rehabilitation Center Hospital, China from December 2005 to August 2006. The cellular neurobiology, in vitro experiment was conducted at the Institute of Human Anatomy, Histology, Embryology and Neuroscience, School of Basic Medical Sciences, Lanzhou University, and Department of Traditional Chinese Medicine of Gansu Provincial Rehabilitation Center Hospital, China from March 2007 to January 2008. MATERIALS： Naotan Pill, composed of barbary wolfberry fruit, danshen root, grassleaf sweetflag rhizome, and glossy privet fruit, was prepared by Gansu Provincial Rehabilitation Center, China. Rabbit anti-synaptophysin, choline acetyl transferase polyclonal antibody, streptavidin-biotin complex kit and diaminobenzidine kit （Boster, Wuhan, China）, as well as glutamate （Hualian, Shanghai, China） were used in this study. METHODS： Cortical neural cells were isolated from neonatal Wistar rats. Neural cell damage models were induced using glutamate, and administered Naotan Pill prior to and following damage. A total of 54 juvenile Wistar rats were equally and randomly assigned into model, Naotan Pill, and sham operation groups. The left common carotid artery was ligated, and then rat models of hypoxic-ischemic injury were assigned to the model and Naotan Pill groups. At 2 days following model induction, rats in the Naotan Pill group were administered Naotan Pillsuspension for 21 days. In the model and sham operation groups, rats received an equal volume of saline. MAIN OUTCOME MEASURES： Neural cell morphology was observed using an inverted phase contrast microscope. Survival rate of neural cells was measured by MTT assay. Synaptophysin and choline acetyl transferase expression was observed in the hippocampal CA1 region of juvenile rats using immunohistochemistry. Cognitive function was tested by the Morris water maze. RESULTS： Pathological changes were detected in glutamate-treated neural cells. Neural cell morphology remained normal after Naotan Pill intervention. Absorbance and survival rate of neural cells were significantly greater following Naotan Pill intervention, compared to glutamate-treated neural cells （P 〈 0.05）. Synaptophysin and choline acetyl transferase expression was lowest in the hippocampal CA1 region in the model group and highest in the sham operation group. Significant differences among groups were observed （P 〈 0.05）. Escape latency and swimming distance were significantly longer in the model group compared to the Naotan Pill group （P 〈 0.05）. CONCLUSION： Naotan Pill exhibited protective and repair effects on glutamate-treated neural cells. Naotan Pill upregulated synaptophysin and choline acetyl transferase expression in the hippocampus and improved cognitive function in rats following hypoxia-ischemia.     

Effects of Naotan Pill on repair of neural cells and cognitive disorders in juvenile rats following hypoxia and ischemia

BACKGROUND:Hypoxia and ischemia induce neuronal damage,decreased neuronal numbers and synaptophysin levels,and deficits in learning and memory functions.Previous studies have shown that lycium barbarum polysaccharide,the most effective component of barbary wolfberry fruit,has protective effects on neural cells in hypoxia-ischemia.OBJECTIVE:To investigate the effects of Naotan Pill on glutamate-treated neural cells and on cognitive function in juvenile rats following hypoxia-ischemia.DESIGN,TIME AND SETTING:The randomized,controlled,in vivo study was performed at the Cell Laboratory of Lanzhou University,Lanzhou Institute of Modern Physics of Chinese Academy of Sciences,and Department of Traditional Chinese Medicine of Gansu Provincial Rehabilitation Center Hospital,China from December 2005 to August 2006.The cellular neurobiology,in vitro experiment was conducted at the Institute of Human Anatomy,Histology,Embryology and Neuroscience,School of Basic Medical Sciences,Lanzhou University,and Department of Traditional Chinese Medicine of Gansu Provincial Rehabilitation Center Hospital,China from March 2007 to January 2008.MATERIALS:Naotan Pill,composed of barbary wolfberry fruit,danshen root,grassleaf sweetflag rhizome,and glossy privet fruit,was prepared by Gansu Provincial Rehabilitation Center,China.Rabbit anti-synaptophysin,choline acetyl transferase polyclonal antibody,streptavidin-biotin complex kit and diaminobenzidine kit (Boster,Wuhan,China),as well as glutamate (Hualian,Shanghai,China) were used in this study.METHODS:Cortical neural cells were isolated from neonatal Wistar rats.Neural cell damage models were induced using glutamate,and administered Naotan Pill prior to and following damage.A total of 54 juvenile Wistar rats were equally and randomly assigned into model,Naotan Pill,and sham operation groups.The left common carotid artery was ligated,and then rat models of hypoxic-ischemic injury were assigned to the model and Naotan Pill groups.At 2 days following model induction,rats in the Naotan Pill group were administered Naotan Pill suspension for 21 days.In the model and sham operation groups,rats received an equal volume of saline.MAIN OUTCOME MEASURES:Neural cell morphology was observed using an inverted phase contrast microscope.Survival rate of neural cells was measured by MTT assay.Synaptophysin and choline acetyl transferase expression was observed in the hippocampal CA1 region of juvenile rats using immunohistochemistry.Cognitive function was tested by the Morris water maze.RESULTS:Pathological changes were detected in glutamate-treated neural cells.Neural cell morphology remained normal after Naotan Pill intervention.Absorbance and survival rate of neural cells were significantly greater following Naotan Pill intervention,compared to glutamate-treated neural cells (P<0.05).Synaptophysin and choline acetyl transferase expression was lowest in the hippocampal CA1 region in the model group and highest in the sham operation group.Significant differences among groups were observed (P<0.05).Escape latency and swimming distance were significantly longer in the model group compared to the Naotan Pill group (P<0.05).CONCLUSION:Naotan Pill exhibited protective and repair effects on glutamate-treated neural cells.Naotan Pill upregulated synaptophysin and choline acetyl transferase expression in the hippocampus and improved cognitive function in rats following hypoxia-ischemia.     

Effects of subacute lead exposure on [H]MK-801 binding in hippocampus and cerebral cortex in the adult rat

We used the NMDA receptor non-competitive antagonist, [³H]MK-801, as a ligand for an autoradiographic study to determine the effects of lead on NMDA receptor in the rat brain. Adult male rats were administered lead acetate, 100 mg/kg, or sodium acetate, 36 mg/kg (control), by i.p. for 7 days. High lead levels were detected in blood (41.1 μg/dl) and in brain (16.7–29.4 μg/g). Concentrations of lead in brain regions were not significantly different. The [³H]MK-801 binding was heterogeneously distributed throughout the rat brain with the following order of binding densities: hippocampal formation>cortex>caudate-putamen>thalamus>brainstem. Lead exposure produced a significant decrease in [³H]MK-801 binding to the NMDA receptor in the hippocampal formation including CA2 stratum radiatum, CA3 stratum radiatum, hilus dentate gyrus and presubiculum, and in the cerebral cortex including agranular insular, cingulate, entorhinal, orbital, parietal and perirhinal areas. The hippocampal formation is known as a critical neural structure for learning and memory processes, whereas, cortical and subcortical regions have been demonstrated to be involved in the modulation of complex behavioral processes. The NMDA receptor has been demonstrated to play a key role in synaptic plasticity underlying learning and memory. Lead-induced alterations of NMDA receptors in the hippocampal formation and cortical areas may play a role in lead-induced neurotoxicity.     

Optimal compatible doses and effects of ephedrine and naloxone on neural plasticity in cerebral ischemia/reperfusion rats

BACKGROUND： Ephedrine promotes neural plasticity in rats following cerebral ischemia/reperfusion injury. Ephedrine has been combined with naloxone in some studies, and it has been confirmed that their combination has synergistic effects on increasing neural plasticity following cerebral ischemia/reperfusion injury. OBJECTIVE： To investigate the effects of ephedrine combined with various doses of naloxone on neural plasticity and to find an optimal dose of naloxone in rats after cerebral ischemia/reperfusion injury by analyzing growth associated protein-43 （GAP-43）, synaptophysin and β-endorphin expression in the hippocampal CA3 area. DESIGN, TIME AND SETTING： This immunohistochemical, randomized, controlled, animal experiment was performed at the Chongqing Research Institute of Pediatrics, China from September 2007 to June 2008. MATERIALS： Ephedrine hydrochloride injection and naloxone hydrochloride injection were respectively purchased from Shandong Lvliang Pharmaceutical Factory, China and Sichuan Jingwei Pharmaceutical Co., Ltd., China. A total of 192 healthy adult Sprague Dawley rats were used to establish models of left middle cerebral artery occlusion using the suture occlusion method. METHODS： At 2 hours following cerebral ischemia, the rats were intraperitoneally injected with 1.5 mg/kg/d ephedrine （ephedrine group）, with 0.1, 0.2, or 0.3 mg/kg/d naloxone （low, moderate and high doses of naloxone groups）, with 1.5 mg/kg/d ephedrine ＋ 0.1, 0.2, or 0.3 mg/kg/d naloxone （ephedrine ＋ low, moderate and high doses of naloxone groups）, and with 0.5 mL saline （model group）, respectively. MAIN OUTCOME MEASURES： GAP-43, synaptophysin and β -endorphin expression were detected in the hippocampal CA3 area using immunohistochemistry 1-4 weeks after surgery. Sensorimotor integration in rats was assessed using the beam walking test. RESULTS： GAP-43 and synaptophysin expression was greater in the ephedrine group, and in the ephedrine ＋ moderate and high doses of naloxone groups co     

Tuberous sclerosis complex coexistent with hippocampal sclerosis

Tuberous sclerosis and hippocampal sclerosis are both well-defined entities associated with medically intractable epilepsy. To our knowledge, there has been only one prior case of these two pathologies being co-existent. We report a 7-month-old boy who presented with intractable seizures at 2 months of age. MRI studies showed diffuse volume loss in the brain with bilateral, multiple cortical tubers and subcortical migration abnormalities. Subependymal nodules were noted without subependymal giant cell astrocytoma. Genetic testing revealed TSC2 and PRD gene deletions. Histopathology of the hippocampus showed CA1 sclerosis marked by loss of neurons in the CA1 region. Sections from the temporal, parietal and occipital lobes showed multiple cortical tubers characterized by cortical architectural disorganization, gliosis, calcifications and increased number of large balloon cells. Focal white matter balloon cells and spongiform changes were also present. The patient underwent resection of the right fronto-parietal lobe and a subsequent resection of the right temporal, parietal and occipital lobes. The patient is free of seizures on anti-epileptic medication 69 months after surgery. Although hippocampal sclerosis is well documented to be associated with coexistent focal cortical dysplasia, the specific co-existence of cortical tubers and hippocampal sclerosis appears to be rare.     

Guipi decoction effects on arginine vasopressin protein and gene expression in the hippocampus, ventromedial hypothalamic nucleus, and prefrontal lobe in rats with spleen deficiency

BACKGROUND： Arginine vasopressin has been shown to enhance learning in experimental animal models. OBJECTIVE： To determine whether Guipi decoction enhances memory and learning by increasing arginine vasopressin levels, and to verify the influence of Guipi decoction on arginine vasopressin protein and gene expression in the hippocampal CA1 region, prefrontal lobe cortex, and ventral nucleus of hypothalamus in rats with spleen deficiency. DESIGN, TIME AND SETTING： The randomized, neuropharmacological, control study was performed in the College of Basic Medical Sciences, Beijing University of Chinese Medicine between March 2002 and March 2005. MATERIALS： Sixty, healthy, male, Wistar rats were used to establish spleen deficiency models according to the traditional Chinese medicine principle of bitter drugs for purgation, improper diet, and overstrain. Arginine vasopressin-1 polyclonal anti-rabbit antibody immunohistochemistry kit and arginine vasopressin in situ hybridization kit were provided by Department of Neuroanatomy in Shanghai Second Military Medical University of Chinese PLA. METHODS： Sixty rats were divided into five groups at random： normal control （n = 11）, model （n = 13）, Guipi decoction （n = 12）, recipe control A （n = 12）, and recipe control B groups （n = 12）. Rats in the latter four groups received 7.5 g/kg of the drugs by intragastric administration each morning, which comprised Dahuang, Houpu, and Zhishi, prepared at a ratio of 2： 1 ： 1. The rats were fasted every other day, but were allowed free access to water at all times. The rats were forced to swim in 25℃ water until fatigued. Rats in the Guipi decoction and two recipe control groups were intragastrically administered 7.5 g/kg Guipi decoction, Chaihu Shugan powder, and Tianwang Buxin pellets, respectively, each afternoon. Rats in the normal group were intragastrically administered the same amount of normal saline. All rats were treated for 6 weeks. MAIN OUTCOME MEASURES： At 6 weeks after drug administrati     

Coexistent arteriovenous malformation and hippocampal sclerosis

Cavernous angiomas or cavernomas have been occasionally described in patients presenting with medically intractable epilepsy. Reports of cavernomas associated with a second pathology potentially causative of seizures have rarely been documented; most commonly, the second pathology is focal cortical dysplasia or less frequently, hippocampal sclerosis. To our knowledge, cases of arteriovenous malformation arising in this clinical setting and associated with hippocampal sclerosis have not been previously described. We report a 56-year-old woman who initially presented at age 24 years with staring spells. Imaging studies revealed an arteriovenous malformation in the right parietal lobe. At age 51 years, she represented with signs and symptoms related to a hemorrhage from the malformation. The patient underwent Gamma Knife radiosurgery (Elekta AB, Stockholm, Sweden) of the lesion. She subsequently developed seizures, refractory to medical management. MRI studies showed atrophy in the right hippocampus. She underwent resection of the right parietal lobe and hippocampus. Histopathologic examination of the right parietal lesion revealed an arteriovenous malformation marked by focally prominent vascular sclerosis, calcification and adjacent hemosiderin deposition. The hippocampus was marked by prominent neuronal loss and gliosis in the CA1 region, consistent with CA1 sclerosis or hippocampal sclerosis International League Against Epilepsy type 2.     

Projections from the posterior cortical nucleus of the amygdala to the hippocampal formation and parahippocampal region in rat

The posterior cortical nucleus of the amygdala is involved in the processing of pheromonal information and presumably participates in ingestive, defensive, and reproductive behaviors as a part of the vomeronasal amygdala. Recent studies suggest that the posterior cortical nucleus might also modulate memory processing via its connections to the medial temporal lobe memory system. To investigate the projections from the posterior cortical nucleus to the hippocampal formation and the parahippocampal region, as well as the intra-amygdaloid connectivity in detail, we injected the anterograde tracer phaseolus vulgaris-leucoagglutinin into different rostrocaudal levels of the posterior cortical nucleus. Within the hippocampal formation, the stratum lacunosum-moleculare of the temporal CA1 subfield and the adjacent molecular layer of the proximal temporal subiculum received a moderate projection. Within the parahippocampal region, the ventral intermediate, dorsal intermediate, and medial subfields of the entorhinal cortex received light to moderate projections. Most of the labeled terminals were in layers I, II, and III. In the ventral intermediate subfield, layers V and VI were also moderately innervated. Layers I and II of the parasubiculum received a light projection. There were no projections to the presubiculum or to the perirhinal and postrhinal cortices. The heaviest intranuclear projection was directed to the deep part of layer I and to layer II of the posterior cortical nucleus. There were moderate-to-heavy intra-amygdaloid projections terminating in the bed nucleus of the accessory olfactory tract, the central division of the medial nucleus, and the sulcal division of the periamygdaloid cortex. Our data suggest that via these topographically organized projections, pheromonal information processed within the posterior cortical nucleus can influence memory formation in the hippocampal and parahippocampal areas. Also, these pathways provide routes through which seizure activity can spread from the epileptic amygdala to the surrounding region of the temporal lobe.     

Neural Changes Associated With Relational Learning in Schizophrenia

Relational learning, which is learning the relationship among items, is impaired in schizophrenia but can be improved with training. This study investigated neural changes with functional magnetic resonance imaging before and after training on a relational learning task in schizophrenia and healthy control subjects. Despite their acquiring similar relational learning performance, the groups exhibited different neural activation patterns before and following training. Controls engaged regions within the relational learning network that included frontal, parietal, and medial temporal lobe, before and following training. Controls also exhibited activation reductions in region and spatial extent with relational learning proficiency, a commonly observed phenomenon in successful learning. In contrast, subjects with schizophrenia displayed no positive activations compared with the control condition before training. After training, subjects with schizophrenia displayed bilateral inferior parietal region activation as predicted. Contrary to hypothesis, hippocampal activation was not observed following training in schizophrenia. These findings suggest that the parietal lobe may be receptive to cognitive training interventions and that successful relational learning may be achieved in schizophrenia through the use of alternative extrahippocampal brain regions.     

大鼠脑缺血再灌注后星形胶质细胞反应性变化差异与海马CA1区的迟发性神经元死亡

BACKGROUND： Blood supply to the hippocampus is not provided by the middle cerebral artery. However, previous studies have shown that delayed neuronal death in the hippocampus may occur following focal cerebral ischemia induced by middle cerebral artery occlusion.
OBJECTIVE： To observe the relationship between reactive changes in hippocampal astrocytes and delayed neuronal death in the hippocampal CA1 region following middle cerebral artery occlusion.
DESIGN, TIME AND SETTING： The immunohistochemical, randomized, controlled animal study was performed at the Laboratory of Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, from July to November 2007.
MATERIALS： Rabbit anti-glial fibrillary acidic protein （GFAP） （Neomarkers, USA）, goat anti-rabbit IgG （Sigma, USA） and ApoAlert apoptosis detection kit （Biosciences Clontech, USA） were used in this study. METHODS： A total of 42 healthy adult male Wistar rats, aged 3–5 months, were randomly divided into a sham operation group （n = 6） and a cerebral ischemia/reperfusion group （n = 36）. In the cerebral ischemia/reperfusion group, cerebral ischemia/reperfusion models were created by middle cerebral artery occlusion. In the sham operation group, the thread was only inserted into the initial region of the internal carotid artery, and middle cerebral artery occlusion was not induced. Rats in the cerebral ischemia/reperfusion group were assigned to a delayed neuronal death （＋） subgroup and a delayed neuronal death （–） subgroup, according to the occurrence of delayed neuronal death in the ischemic side of the hippocampal CA1 region following cerebral ischemia.
MAIN OUTCOME MEASURES： Delayed neuronal death in the hippocampal CA1 region was measured by Nissl staining. GFAP expression and delayed neuronal death changes were measured in the rat hippocampal CA1 region at the ischemic hemisphere by double staining for GFAP and TUNEL.
RESULTS： After 3 days of ischemia/reperfusion, astrocytes with abnormal morphology were detected in the rat hippocampal CA1 region in the delayed neuronal death （＋） subgroup. No significant difference in GFAP expression was found in the rat hippocampal CA1 region at the ischemic hemisphere in the sham operation group, delayed neuronal death （＋） subgroup and delayed neuronal death （–） subgroup （P 〉 0.05）. After 7 days of ischemia/reperfusion, many GFAP-positive cells, which possessed a large cell body and an increased number of processes, were activated in the rat hippocampal CA1 region at the ischemic hemisphere. GFAP expression in the hippocampal CA1 region was greater in the delayed neuronal death （＋） subgroup and delayed neuronal death （–） subgroup compared with the sham operation group （P 〈 0.01）. Moreover, GFAP expression was significantly greater in the delayed neuronal death （–） subgroup than in the delayed neuronal death （＋） subgroup （P 〈 0.01）. After 30 days of ischemia/reperfusion, GFAP-positive cells were present in scar-like structures in the rat hippocampal CA1 region at the ischemic hemisphere. GFAP expression was significantly greater in the delayed neuronal death （＋） subgroup and delayed neuronal death （–） subgroup compared with the sham operation group （P 〈 0.05）. GFAP expression was significantly lower in the delayed neuronal death （–） subgroup than in the delayed neuronal death （＋） subgroup （P 〈 0.05）. The delayed neuronal death rates were 42% （5/12）, 33% （4/12） and 33% （4/12） at 3, 7 and 30 days, respectively, followingischemia/reperfusion. No significant differences were detected at various time points （χ2 = 0.341, P 〉 0.05）.
CONCLUSION： The activation of astrocytes was poor in the hippocampal CA1 region during the early stages of ischemia, which is an important reason for delayed neuronal death. Glial scar formation aggravated delayed neuronal death during the advanced ischemic stage.     

Electroacupuncture at Du channel and meridian of foot-Taiyang for hippocampal neurons in rats with depression

BACKGROUND: Long-term anti-depression treatment can promote the regeneration of hippocampal regeneration. Up-regulation of hippocampal regeneration can reverse or prevent against the injury of stress to cerebrum, especially to hippocampal structure and function. Therefore, promoting hippocampal neuronal regeneration may be a new strategy for treating depression and anxiety. OBJECTIVE: To observe the effect of electro-acupuncture at Du channel and meridian of foot-Taiyang on hippocampal neurons from model rats of depression. DESIGN: A randomized controlled animal experiment. SETTING: Department of Acupuncture and Moxibustion, Shenzhen Affiliated Hospital, Guangzhou University of Traditional Chinese Medicine. MATERIALS: Twenty-four Wistar rats, of either gender, aged 2 months old, weighing 200–220 g, were provided by the Animal Experimental Center, Guangzhou University of Traditional Chinese Medicine. METHODS: This experiment was carried out in the Clinical Molecular Biochemical Laboratory, Shenzhen Affiliated Hospital, Guangzhou University of Traditional Chinese Medicine between October 2006 and April 2007. ①The involved rats were randomized into 4 groups according to body mass: blank control group, model group, electroacupuncture A group and electroacupuncture B group, with 6 in each. Rats in the blank control group were free to access to water, and were not given any intervention. Rats in the latter 3 groups were developed into rat depression models by chronic stress combined with feeding alone, and received 21-day unpredictable various stresses. Rats in the model group were euthanized at 14 days after modeling, and their brain tissues were harvested. Rats in the electroacupuncture A group were modeled, then points "Baihui" and "Shenting" were chosen, and given electroacupuncture, once a day, 20 minutes once. Rats in the electroacupuncture B group were modeled, then points "Baihui", "Shenting", "Xinshu"and "Ganshu" were chosen, and frequency and therapeutic time were the same as those of electroacupuncture A group. Rats in the latter 2 groups were also given electroacupuncture, and their brain tissues were harvested 14 days later. ②Index evaluation: Neurons in hippocampal CA1 and CA3 regions as well as dentate gyrus [neuron specific enolase (NSE)-positive cells] were counted by immunofluorescent technique. Each rat was weighted on the day of grouping and before execution at 35 days. MAIN OUTCOME MEASURES: Neuron amount in each hippocampal region and body mass of rats in each group. RESULTS: Twenty-four rats were involved in the final analysis. ①Neuronal amount in each region of hippocampus: Neurons in the hippocampal CA1 and CA3 regions as well as dentate gyrus of rats in the model group were significantly less than those in the blank control group (P < 0.01). Neurons in hippocampal CA1and CA3 regions as well as dentate gyrus of rats in the electroacupuncture A and B groups were more than those in the model group (P < 0.05). ② Change in body mass of rats: Body mass increase of rats in the model group was less than that in the blank control group (P < 0.05), and body mass increase of electroacupuncture A and B groups was significantly more than that in the model group, respectively (P < 0.01). CONCLUSION: Electroacupuncture at Du channel and meridian of foot-Taiyang alleviates hippocampal neuronal injury of rats, and thereby, improves depression and promotes the increase of body mass of rats.     

Medium-intensity acute exhaustive exercise induces neural cell apoptosis in the rat hippocampus

The present study assessed the influence of medium-intensity (treadmill at a speed of 19.3 m/min until exhaustion) and high-intensity (treadmill at a speed of 26.8 m/min until exhaustion) acute exhaustive exercise on rat hippocampal neural cell apoptosis. TUNEL staining showed significantly increased neural cell apoptosis in the hippocampal CA1 region of rats after medium- and high-intensity acute exhaustive exercise, particularly the medium-intensity acute exhaustive exercise, when compared with the control. Immunohistochemistry showed significantly increased expression of the antiapoptotic protein Bcl-2 and the proapoptotic protein Bax in the hippocampal CA1 region of rats after medium- and high-intensity acute exhaustive exercise. Additionally, the ratio of Bax to Bcl-2 increased in both exercise groups. In particular, the medium-intensity acute exhaustive exercise group had significantly higher Bax and Bcl-2 protein expression and a higher Bax/Bcl-2 ratio. These findings indicate that acute exhaustive exercise of different intensities can induce neural cell apoptosis in the hippocampus, and that medium-intensity acute exhaustive exercise results in greater damage when compared with high-intensity exercise.     

重度颈动脉狭窄患者颈动脉粥样硬化斑块的稳定性对脑灌注的影响

目的 对比研究重度颈动脉狭窄患者稳定与易损动脉粥样硬化斑块间的脑灌注情况,探讨斑块性质与脑灌注的关系。方法 利用磁共振成像技术检测颈动脉动脉粥样硬化性病变,并筛选单侧颈内动脉狭窄程度为70％～99％患者30例。对30例患者行动态磁敏感对比增强磁共振成像,测定患侧与健侧大脑半球、额叶、顶叶、半卵圆中心、皮质分水岭前区、皮质分水岭后区的平均通过时间（MTT）、相对脑血流量（rCBF）、相对脑血容量（rCBV）比值。将颈动脉粥样硬化斑块的纤维帽是否完整、斑块表面是否有大片钙化、其内是否有近期出血及是否有较大的脂质中心作为易损斑块诊断标准,分为稳定和易损斑块两组,比较两组患者脑血流动力学参数的差异。结果 与稳定斑块组比较,易损斑块组在皮质分水岭前区和后区的MTT值明显延长(t =1.561,P =0.042和t =1.227,P =0.038),rCBF和rCBV无统计学差异。上述两组在其余部位的血液动力学参数比值无统计学差异。结论 颈动脉粥样硬化斑块的稳定性和相应皮质分水岭供血区域灌注情况有关,易损斑块容易导致同侧皮质分水岭区低灌注,MTT是最敏感的指标。     

18F-FDG PET/CT脑显像评价认知障碍患者中的脑小血管病变对皮层功能的影响

目的 探讨18氟代脱氧葡萄糖（18F-fluorodeoxyglucose,18F-FDG）正电子发射断层成像/计算机断层扫
描（positron emission tomography/computed tomography,PET/CT）脑显像评价认知障碍患者中的脑小血
管病变对皮层功能的影响。
方法 本研究为回顾性研究,纳入2009年1月～2010年12月北京协和医院PET中心行18F-FDG PET/CT
脑显像且颅脑磁共振成像（magnetic resonance imaging,MRI）提示存在小血管病变的认知障碍患者21例,
其中临床诊断血管性痴呆（vascular dementia,VaD）10例,阿尔茨海默病（Alzheimer’s disease,AD）或混
合型痴呆（mixed dementia,MD）11例。首先目测两组患者的18F-FDG PET/CT脑显像皮层及皮层下核团代
谢减低特点,并结合颅脑MRI判断病变血管对脑代谢的影响。使用NeuroQ软件和Scenium软件对18F-FDG
PET/CT脑图像在像素基础上进行定量分析比较两组患者的皮层代谢情况。
结果 通过目测和NeuroQ软件分析发现VaD组患者18F-FDG PET/CT脑显像图像特点为无规律,不对
称皮层或皮层下核团代谢减低,其中额叶皮层代谢减低范围最广,程度最重。结合颅脑MRI改变,考
虑皮层和皮层下核团代谢减低主要为小血管病变引起。AD或MD组患者脑代谢均呈现双侧颞顶叶代谢
减低,其中8例出现皮层代谢减低不对称表现,6例出现基底节丘脑不对称代谢减低表现,与典型AD
的表现不符,结合颅脑MRI表现,考虑为病变血管所致,小血管病变可能导致相应皮层代谢减低。通
过定量分析发现两组患者的SUV比值在左右顶叶、内外颞叶和枕叶差异具有显著性。
结论 18F-FDG PET/CT脑显像作为功能影像可以推断小血管病变与皮层及皮层下核团代谢的关系。     

Anatomical and functional correlates of human hippocampal volume asymmetry

Hemispheric asymmetry of the human hippocampus is well established, but poorly understood. We studied 110 healthy subjects with 3-Tesla MRI to explore the anatomical and functional correlates of the R>L volume asymmetry. We found that the asymmetry is limited to the anterior hippocampus (hemisphere×region interaction: F(1,109)=42.6, p<.001). Anterior hippocampal volume was correlated strongly with the volumes of all four cortical lobes. In contrast, posterior hippocampal volume was correlated strongly only with occipital lobe volume, moderately with the parietal and temporal lobe volumes and not with the frontal lobe volume. The degree of R>L anterior hippocampal volume asymmetry predicted performance on a measure of basic cognitive abilities. This provides evidence for regional specificity and functional implications of the well-known hemispheric asymmetry of hippocampal volume. We suggest that the developmental profile, genetic mechanisms and functional implications of R>L anterior hippocampal volume asymmetry in the human brain deserve further study.     

Guipi decoction effects on brain somatostatin levels and receptor mRNA expression in rats with spleen deficiency*☆

BACKGROUND： Somatostatin is abundant in the hypothalamus, cerebral cortex, limbic system, and mesencephalon. Somatostatin mRNA expression in the brain of rats with spleen deficiency is noticeably reduced, as well as attenuation of cognitive function. OBJECTIVE： To observe the interventional effect of Guipi decoction on somatostatin level and somatostatin receptor 1 （SSTRl） mRNA expression in different encephalic regions of rats with spleen deficiency, and to compare the interventional effects of Guipi decoction, Chaihu Shugan powder, and Tianwang Buxin pellet. DESIGN： A randomized controlled observation.
SETTING： Basic Medical College, Beijing University of Traditional Chinese Medicine.
MATERIALS： Fifty adult Wistar male rats, of clean grade, weighing （160 ± 10） g, were provided by Beijing Weitong Lihua Laboratory Animal Technology Co., Ltd. The protocol was performed in accordance with ethical guidelines for the use and care of animals. Somatostatin 1 polyclonal anti-rabbit antibody and SSTRl in situ hybridization kit were provided by Department of Neuroanatomy, Shanghai Second Military Medical University of Chinese PLA. The drug for developing rat models of spleen deficiency was composed of Dahuang, Houpu and Zhishi, and prepared at 2：1：1. Guipi decoction, Chaihu Shugan powder, and Tianwang Buxin pellet recipes were made according to previous studies. METHODS： This study was performed at the Basic Medical College, Beijing University of Traditional Chinese Medicine from March 2002 to March 2005. The rats were randomly divided into 5 groups, with 10 rats in each group： normal, model, Guipi decoction, Chaihu Shugan powd.er, and Tianwang Buxin pellet groups. Rat models of the latter 4 groups were developed by methods of purgation with bitter and cold nature drugs, improper diet, and overstrain. The rats received 7.5 g/kg of the drugs each morning and were fasted every other day, but were allowed free access to water at all times. The rats were forced to swim in 25 ℃ water until fati     

Regional distribution of fluoro-jade B staining in the hippocampus following traumatic brain injury

Fluoro-Jade B (FJB) is an anionic fluorescein derivative that has been reported to specifically stain degenerating neurons. We were interested in applying FJB staining in a well-characterized model of traumatic brain injury (TBI) in order to estimate the total number of neurons in different regions of the hippocampus that die after a mild or moderate injury. Rats were subjected to a mild or moderate unilateral cortical contusion (1.0- or 1.5-mm displacement from the cortical surface) with a controlled cortical impacting device. Animals were allowed to survive for 1, 2, or 7 days and the total number of FJB-positive neurons in hippocampal areas CA1, CA3, and the dentate gyrus granule layer was estimated using sterological methods. The region that had the highest number of FJP-positive neurons after TBI was the dentate gyrus. In both 1- and 1.5-mm injuries, FJB-positive granule cells were observed throughout the rostro-caudal extent of the dentate. In contrast, labeled pyramidal neurons of area CA3 were most numerous after the 1.5-mm injury. The area that had the fewest number of FJB-labeled cells was area CA1 with only scattered neurons seen in the 1.5-mm group. In both injury groups and in all hippocampal regions, more FJB-positive neurons were seen at the earlier times post injury (1 and 2 days) than at 7 days. FJB appears to be a reliable marker for neuronal vulnerability following TBI.