The effects of ethanol on the hippocampal neural tissue development and kainite receptor expression in young mouse / 中国神经精神疾病杂志

Objectives To investigate the effects of ethanol on neural development and kainate receptor expression in young mice. Methods Fetal alcohol spectrum disorder model was established by administration of 20% ethanol solu?tion to 7-day-old Kunming mice and control animals received physiological saline (The number of treatment and control were 80 and 40, respectively ). Body weight and general biological features were observed every day. Morris water maze was used to test learning and memory ability. Fluoro-Jade B was used to examine neural cells 24 hours after treatment in additional thirty 7-day-old Kunming mice which were further divided into two groups:a treatment group receiving 20%ethanol solution (n=15) and a control group receiving physiological saline (n=15). The development of neural cells and expression levels of kainite receptors were examined by using immunofluorescence staining. Results The body weight was significantly lighter in treatment group than in control group(control:21.13 ± 1.72g,treatment:13.96 ± 2.98g,P<0.05). Morris test showed that model group had longer latency than control group to find hidden platform(control:21.05± 5.31s,treatment:34.15±3.26s,P<0.05). Spatial probe test revealed that the number of passing through the platform were significantly smaller in model group than in control group(control:2.70 ± 1.25 times,treatment:0.93 ± 0.80 times,P<0.05). Astrocyte development anomaly was evident after ethanol treatment for 7 days. The expression levels of kainite re?ceptor GluR-6 and KA2 were up-regulated in the CA region of the hippocampus after ethanol treatment for 7 days. Con?clusion Kainite receptor GluR-6 and KA2 in CA region of the hippocampus may contribute to ethanol-induced hippo?campal neural development anomaly.

La asociación atorvastatina-meloxicam reduce el daño cerebral, atenuando la gliosis reactiva consecuente a embolismo arterial / The association atorvastatin-meloxicam reduces brain damage, attenuating reactive gliosis subsequent to arterial embolism

Introducción: el accidente cerebrovascular es la primera causa de discapacidad y la tercera de muerte en Colombia y en el resto del mundo y está asociado a enfermedades mentales y neurodegenerativas. Objetivo: determinar los efectos de la asociación atorvastatina-meloxicam sobre la gliosis reactiva en un modelo de isquemia cerebral por embolización arterial. Materiales y métodos: se utilizaron 56 ratas Wistar macho adultas, distribuidas en cuatro grupos isquémicos y cuatro controles, además de otras 10 para determinar la distribución y extensión del infarto, induciendo lesión en seis de ellas y simulación (sham) en las cuatro restantes. Los tratamientos fueron: placebo, atorvastatina (ATV), meloxicam (MELOX) y ATV + MELOX en isquémicos y simulados. Veinticuatro horas después de la isquemia se evaluó la actividad enzimática mitocondrial con trifeniltetrazolio (TTC) y a las 120 horas, la reactividad astrocitaria (anti-GFAP), mediante inmunohistoquímica convencional. Resultados: la asociación ATV+MELOX favoreció la modulación en la respuesta de los astrocitos protoplasmáticos y fibrosos del hipocampo y de la zona paraventricular, reduciendo su hiperreactividad. Conclusión: ATV y MELOX, aisladamente o asociados, reducen el daño cerebral atenuando la gliosis reactiva consecuente a la embolización arterial, lo que sugiere nuevos mecanismos de neuroprotección frente a la isquemia cerebral tromboembólica y abre nuevas perspectivas para su tratamiento temprano.

Introduction: Stroke is the leading cause of disability and the third of death in Colombia and in the world and it is associated with neurodegenerative and mental diseases. Objective: To determine the effects of the atorvastatin- meloxicam association on reactive gliosis in a model of cerebral ischemia produced by arterial embolization. Materials and methods: 56 adult male Wistar rats were used, divided into four ischemic and four control groups, plus 10 additional animals to determine the distribution and extent of infarction by injury in six of them and simulation (sham) in the remaining four. The treatments were: placebo, atorvastatin (ATV), meloxicam (MELOX) and ATV + MELOX in ischemic and simulated animals. 24 hours post-ischemia mitochondrial enzymatic activity was evaluated with triphenyl- tetrazolium (TTC), and at 120 hours astrocytic reactivity (anti-GFAP) was analyzed by conventional immunohistochemistry. Results: The association ATV + MELOX favored the modulation of the response of protoplasmatic and fibrous astrocytes in both the hippocampus and the paraventricular zone by reducing their hypereactivity. Conclusion: Atorvastatin and meloxicam, either individually or associated, reduce cerebral damage by lessening the reactive gliosis produced by arterial embolization; this suggests new mechanisms of neuroprotection against thromboembolic cerebral ischemia, and opens new perspectives in its early treatment.

Effects of fluoxetine on special learning and memory and serum S100B level in depressed model rats / 中华行为医学与脑科学杂志

ObjectiveTo explore the effects of fluoxetine on special learning and memory and serum S100B level in depressed model rats.MethodsAdult male SD rats were divided into six groups randomly according random digits table:control group ( A ),depressed model group ( B ),group of depressed model treated with single dose of fluoxetine for one day ( C ),group of depressed model treated with fluoxetine for one week (D),group of depressed model treated with fluoxetine for two weeks (E) and group of depressed model treated with fluoxetine for four weeks (F),ten rats in each group.Except control group,others were subjected to forced-swimming for four weeks,15 min a day.Fluoxetine (10 mg/kg) was given intragastric administration to group C-F before swimming everyday.Morris water maze ( MWM ) was used to measure the spatial learning and memory of rats.ELISA was used to determine the level of serum S100B.ResultsIn the hiding platform test of MWM,there was significant longer of escape latency (EL) in B group than that in A group(P ＜ 0.05 ).And the EL in all groups treated with fluoxetine became shorter with the prolonging of treatment.In the probe test,there were significant longer time in target quadrant in D,E,F than in other quadrant (F =5.162,P ＜ 0.01 ).The levels of serum S100B were lower in E,F groups ( E group ( 0.91 ± 0.23 ) ng/ml,F group ( 0.85 ± 0.21 ) ng/ml) than that in B group (( 1.26 ±0.61 )ng/ml,P＜0.05).ConclusionChronic administration of fluoxetine could improve the impairment of spatial learning and memory and reverse the increase of S100B level in serum of depressed model rats.

Rapid Disruption of Cellular Integrity of Zinc-treated Astroglia Is Regulated by p38 MAPK and Ca(2+)-dependent Mechanisms

Cultured cortical primary astroglia treated with zinc died while rapidly detached from culture plates, a distinct part of zinc-treated astroglia. In the present study, we investigated the mechanism underlying the rapid change in the morphologic integrity of zinc-treated astroglia. Among the early cellular events occurring in zinc-treated astroglia, strong activation of p38 MAPK and JNK was evident. Although inhibitors of p38 (SB203580 and SB202190) or JNK (SP600125) did not protect zinc-insulted astroglia from cell death, the p38 inhibitors, but not the JNK inhibitor, suppressed actin filament and cell morphology disruption. The Ca2+ ionophore, A23187, also suppressed actin filament and cell morphology disruption, but not cell death, of zinc-insulted astroglia. However, A23187 did not inhibit p38 MAPK activation in zinc-treated astroglia. Together these results suggest that zinc influx in astroglia results in rapid loss of the morphologic integrity via mechanisms regulated by p38 kinase and/or Ca2+ signaling.

Chelation of GRP78 with Lead and Its Localization Changes in the Astroglia of Rats Exposed to Lead / 华中科技大学学报（医学）（英德文版）

remarkably increase when it transferred from ER to the cytosol around the nuclei 24 h after treatment with Pb. It is concluded that GRP78 in astroglia could strongly chelate with Pb ions and it might be a target protein of Pb.

Relationship Between Cerebral Ischemia-induced Inflammation and Astroglia (review) / 中国康复理论与实践

@#Astroglia is the first cell type in the central nervous system to encounter insult after brain ischemia. Then ischemia stimulates hypertrophic and proliferative changes in astroglia and induces it produce inflammatory factors involved in the initiation of immunologic cascade. The expression of these cytokines which interact in the central nervous system can both damage and protect the brain tissue. Therefore, it is important to study astroglia and cytokines in order to find a new way to reduce inflammation insults after brain ischemia.

Experimental Study on Buyang Huanwutang in Inhibiting Astroglial Reactivity in Vitro / 中国中医药信息杂志

Objective To study the effect of Buyang Huanwutang in inhibiting the astroglial reactivity induced by injury in vitro. Methods After cultured the spinal astroglia from newborn Wistar rats for fifteen days, cells were divided into two groups, Buyang Huanwutang group and control group without Chinese herb. Nicked the bottom of cultivated cells and a injured strip of astroglia cells of 1 mm width 15 mm length was made. Immunocytochemistry method was used to demonstrate the expression of glial fibrillary acidic protein (GFAP). Results From 2 to 48 hours after the nick, GFAP expression and the astroglial reactivity were apparently inhibited by Buyang Huanwutang. Conclusion Buyang Huanwutang can inhibit the astroglial reactive proliferation induced by injury in vitro.

Regulation of Astroglia on Synaptic Plasticity in the CA1 Region of Rat Hippocampus / 华中科技大学学报（医学）（英德文版）

The regulation of astroglia on synaptic plasticity in the CA1 region of rat hippocampus was examined. Rats were divided into three groups: the newly born (＜24 h), the juvenile (28-30days) and the adult groups (90-100 days), with each group having 20 animals. The CA1 region of rat hippocampus was immunohistochemically and electron-microscopically examined, respectively,for the growth of astroglia and the ultrastructure of synapses. The high performance liquid chromatography was employed to determine the cholesterol content of rat hippocampus. In the newly-born rats, a large number of neurons were noted in the hippocampal CA1 region of the newly-born rats,and few astroglia and no synaptic structure were observed. In the juvenile group, a few astroglias and some immature synapses were found, which were less than those in adult rats (P＜0.01). The cholesterol content was 2.92±0.03 mg/g, 11.20± 3.41 mg/g and 12.91 ± 1.25 mg/g for newly born, the juvenile and the adult groups, respectively, with the differences among them being statistically significant (P＜0.01). Our study suggests that the astrocytes may play an important role in the synaptic formation and functional maturity of hippocampal neurons, which may be related to the secretion of cholesterol from astrocytes.

Reactive Plasticity of Neuroglial Cells on Brain Lesion / 대한해부학회지

Neuroglial cells are actively participate in the pathogenesis or in the recovery procedures following brain lesions. The study was performed to evaluate the plasticity of glial cells following different degree of brain lesions. Neurosurgical operations were made on the rats fixed on the stereotaxic apparatus. Tissue column of 3 mm-diameter was isolated in the caudatoputamen with concomitant severe bleeding in the first group. In the second group, the sensorimotor cortex was suctioned out with moderate bleeding. In the third group, the mammillary body was electrically coagulated with minimal bleeding. Caudatoputamens, as a lesioned tissue or as a target tissue of lesioned area, were studied light and electron microscopically. Observations on reactivities and plasticities of neuroglial cells on the different situations, the following results were obtained : 1. Astrocytes were swollen within an hour following brain lesions. 2. In case of smaller lesion, astroglia alone remove altered structures. 3. Microglia are increased in number, if the lesion is large with severe bleeding. The microglia might come from blood monocyte via transformation to pericyte. 4. In large lesion, astroglia were greatly hypertropied, and microglia might be moving and functioning effeciently within the hypertropied cytoplasm of astroglia. 5. In the stabilizing stage, astroglia produce glial fibers and fix the exhausted microglia. Fixed microglia are proceed into apoptotic process in the cytoplasm of astroglia and removed by them. All these procedures might be controlled by various receptors and secretions of astroglia. It means that astroglia is not only the basic supporting element of nervous tissue, but also an actively functioning element for the most effective homeostatic functioning of the neuropil.

The tolerance of focal cerebral ischemia and astroglial reaction / 临床神经病学杂志

Objective To investigate the protective role of transient focal ischemic precondition(PC) against permanent focal cerebral ischemia, to define the proper time dose for precondition, and to study the reaction of astroglia in cerebral ischemic tolerance. Methods Temporary middle cerebral artery occlusion(10 minutes, 20 minutes, 30 minutes) followed three day reperfusion before permanent middle cerebral artery occlusion(PMCAO) transcranially was used as precondition in Wistar rats. The protective role was evaluated by observing the neurological deficits, analyzing the infarct volume and studying changes of pathohistology. The reaction of astroglia was observed by using anti GFAP immunohistochemistry.Results Compared with the control group, 20 min ischemic precondition, which did not produce neuronal damage obviously, alleviated the neurological deficits and reduced the infarct volume significantly( P

Effects of idazoxan on changes of neuroglia in spinal cords of rats with experimental autoimmune encephalomyelitis / 中国免疫学杂志

Objective:To explore effects of Idazoxan(IDA) on changes of neuroglial cells in spinal cords of rats with experimental autoimmune encephalomyelitis(EAE).Methods:Rat EAE was induced by immunization with spinal cord homogenates of Geania pigs.EAE clinical manifestations were assessed in terms of the scoring standards.Histological investigation and immunohistochemistry were observed for the inflammatory dedmylinative lesion of CNS and morphology of glial cells.Results:Ida could not decrease the incidence of EAE,but alleviate its clinical manifestation and histological changes.On day 15 after immunization,astrocytes in and around the inflammatory dedmylinative lesion of CNS in EAE rats treated with Ida increased in number and size,on the contrary,microglia decreased in number and size.Conclusion:Ida has protective effects on EAE and its functional mechanism may be concerned with modulation of immunological mechanism of CNS.