共查询到20条相似文献,搜索用时 0 毫秒
1.
Eagle Yi-Kung Huang Pi-Fen Tsui Tung-Tai Kuo Jing-Jr. Tsai Yu-Ching Chou Hsin-I Ma Yung-Hsiao Chiang Yuan-Hao Chen 《PloS one》2014,9(1)
Aims
To investigate the role of dopamine in cognitive and motor learning skill deficits after a traumatic brain injury (TBI), we investigated dopamine release and behavioral changes at a series of time points after fluid percussion injury, and explored the potential of amantadine hydrochloride as a chronic treatment to provide behavioral recovery.Materials and Methods
In this study, we sequentially investigated dopamine release at the striatum and behavioral changes at 1, 2, 4, 6, and 8 weeks after fluid percussion injury. Rats subjected to 6-Pa cerebral cortical fluid percussion injury were treated by using subcutaneous infusion pumps filled with either saline (sham group) or amantadine hydrochloride, with a releasing rate of 3.6mg/kg/hour for 8 weeks. The dopamine-releasing conditions and metabolism were analyzed sequentially by fast scan cyclic voltammetry (FSCV) and high-pressure liquid chromatography (HPLC). Novel object recognition (NOR) and fixed-speed rotarod (FSRR) behavioral tests were used to determine treatment effects on cognitive and motor deficits after injury.Results
Sequential dopamine-release deficits were revealed in 6-Pa-fluid-percussion cerebral cortical injured animals. The reuptake rate (tau value) of dopamine in injured animals was prolonged, but the tau value became close to the value for the control group after amantadine therapy. Cognitive and motor learning impairments were shown evidenced by the NOR and FSRR behavioral tests after injury. Chronic amantadine therapy reversed dopamine-release deficits, and behavioral impairment after fluid percussion injuries were ameliorated in the rats treated by using amantadine-pumping infusion.Conclusion
Chronic treatment with amantadine hydrochloride can ameliorate dopamine-release deficits as well as cognitive and motor deficits caused by cerebral fluid-percussion injury. 相似文献2.
María del Mar Romero Fredrik Holmgren-Holm Maria del Mar Grasa Montserrat Esteve Xavier Remesar José Antonio Fernández-López Marià Alemany 《PloS one》2013,8(2)
In the metabolic syndrome, glucocorticoid activity is increased, but circulating levels show little change. Most of blood glucocorticoids are bound to corticosteroid-binding globulin (CBG), which liver expression and circulating levels are higher in females than in males. Since blood hormones are also bound to blood cells, and the size of this compartment is considerable for androgens and estrogens, we analyzed whether sex or eating a cafeteria diet altered the compartmentation of corticosterone in rat blood. The main corticosterone compartment in rat blood is that specifically bound to plasma proteins, with smaller compartments bound to blood cells or free. Cafeteria diet increased the expression of liver CBG gene, binding plasma capacity and the proportion of blood cell-bound corticosterone. There were marked sex differences in blood corticosterone compartmentation in rats, which were unrelated to testosterone. The use of a monoclonal antibody ELISA and a polyclonal Western blot for plasma CBG compared with both specific plasma binding of corticosterone and CBG gene expression suggested the existence of different forms of CBG, with varying affinities for corticosterone in males and females, since ELISA data showed higher plasma CBG for males, but binding and Western blot analyses (plus liver gene expression) and higher physiological effectiveness for females. Good cross- reactivity to the antigen for polyclonal CBG antibody suggests that in all cases we were measuring CBG.The different immunoreactivity and binding affinity may help explain the marked sex-related differences in plasma hormone binding as sex-linked different proportions of CBG forms. 相似文献
3.
Wangshu Xu Xiaopeng Mu Huibin Wang Chengguang Song Wenping Ma Jukka Jolkkonen Chuansheng Zhao 《Molecular neurobiology》2017,54(4):2406-2414
Bumetanide, a selective Na+-K+-Cl?-co-transporter inhibitor, is widely used in clinical practice as a loop diuretic. In addition, bumetanide has been reported to attenuate ischemia-induced cerebral edema and reduce neuronal injury. This study examined whether bumetanide could influence neurogenesis and behavioral recovery in rats after experimentally induced stroke. Adult male Wistar rats were randomly assigned to four groups: sham, sham treated with bumetanide, ischemia, and ischemia treated with bumetanide. Focal cerebral ischemia was induced by injection of endothelin-1. Bumetanide (0.2 mg/kg/day) was infused into the lateral ventricle with drug administration being initiated 1 week after ischemia and continued for 3 weeks. Behavioral impairment and recovery were evaluated by tapered/ledged beam-walking test on post-stroke days 28. Then, the rats were perfused for BrdU/DCX (neuroblast marker), BrdU/NeuN (neuronal marker), BrdU/GFAP (astrocyte marker), and BrdU/Iba-1 (microglia marker) immunohistochemistry. The numbers of neuroblasts in the subventricular zone (SVZ) were significantly increased after the experimentally induced stroke. Bumetanide treatment increased migration of neuroblasts in the SVZ towards the infarct area, enhanced long-term survival of newborn neurons, and improved sensorimotor recovery, but it did not exert any effects on inflammation. In conclusion, our results demonstrated that chronic bumetanide treatment enhances neurogenesis and behavioral recovery after experimentally induced stroke in rats. 相似文献
4.
Mágada T. Schwalm Matheus Pasquali Samantha P. Miguel João Paulo A. dos Santos Francieli Vuolo Clarissa M. Comim Fabrícia Petronilho João Quevedo Daniel P. Gelain José Cláudio F. Moreira Cristiane Ritter Felipe Dal-Pizzol 《Molecular neurobiology》2014,49(1):380-385
Survivors from sepsis present long-term cognitive deficits and some of these alterations resemble the pathophysiological mechanisms of neurodegenerative diseases. For this reason, we analyzed beta-amyloid peptide (Aβ) and synaptophysin levels in the brain of rats that survived from sepsis and their relation to cognitive dysfunction and to acute brain inflammation. Sepsis was induced in rats by cecal ligation and puncture, and 30 days after surgery, the hippocampus and prefrontal cortex were isolated just after cognitive evaluation by the inhibitory avoidance test. The immunocontent of Aβ and synaptophysin were analyzed by Western blot analysis. Aβ increased and synaptophysin decreased in septic animals both in the hippocampus and prefrontal cortex concurrent with the presence of cognitive deficits. Prefrontal levels of synaptophysin correlated to the performance in the inhibitory avoidance. Two different treatments known to decrease brain inflammation and oxidative stress when administered at the acute phase of sepsis decreased Aβ levels both in the prefrontal cortex and hippocampus, increased synaptophysin levels only in the prefrontal cortex, and improved cognitive deficit in sepsis-survivor animals. In conclusion, we demonstrated that brain from sepsis-survivor animals presented an increase in Aβ content and a decrease in synaptophysin levels and cognitive impairment. These alterations can be prevented by treatments aimed to decrease acute brain inflammation and oxidative stress. 相似文献
5.
Furong Zhu Yingjun Zheng Yu-qiang Ding Yong Liu Xianghui Zhang Renrong Wu Xiaofeng Guo Jingping Zhao 《PloS one》2014,9(4)
Background
Various signs of activation of microglia have been reported in schizophrenia, and it is hypothesized that microglia activation is closely associated with the neuropathology of schizophrenia.Methods
Neonatal intrahippocampal injection of lipopolysaccharide (LPS), an activator of microglia, was performed in rats at postnatal day 7 (P7), and they were separately given saline, risperidone (0.5 mg/kg), minocycline (40 mg/kg) or a combination of both of them at P42 for consecutive 14 days. Behavioral changes (locomotion activity, social interaction, novel object recognition and prepulse inhibition) were examined and the number of microglia was assessed by using immunohistochemistry in adulthood.Results
The adult rats in LPS-injected group showed obvious behavioral alteration (e. g. deficits in social interaction, novel object recognition and prepulse inhibition) and a dramatic increase of number of activated microglial cells in the hippocampus and other brain regions such as cerebral cortex and thalamus compared to those in saline-injected group. Interestingly, application of either minocycline, risperidone or both of them significantly rescued behavioral deficits and attenuated microglia activation.Conclusion
Our results suggest that inhibition of microglia activation may be one of mechanisms underlying the antipsychotic effect of minocycline and risperidone. 相似文献6.
Lakshmikanthan Panneerselvam Kavitha Subbiah Angelin Arumugam J. Giftson Senapathy 《Biological trace element research》2013,151(1):85-91
The present study is aimed to evaluate the protective effect of ferulic acid (FA) on fluoride-induced oxidative hepatotoxicity in male Wistar rats. Fluoride (25 mg/L) was given orally to induce hepatotoxicity for 12 weeks. Hepatic damage were assessed using status of pathophysiological markers like serum marker enzymes like aspartate transaminase, alanine transaminase, alkaline phosphatase, acid phosphatase, gamma glutamyl transferase, lactate dehydrogenase, bilirubin, lipid profile, total protein content levels, and histopathological studies. Treatment with FA significantly reduced the degree of histological abberations and rescued lipid peroxidation, as observed from reduced levels of lipid hydroperoxides, nitric oxide, restored levels of enzymic and non-enzymic antioxidants, and total protein content, with a concomitant decline in the levels of marker enzymes and lipid profile in fluoride-induced rats. These results suggest that ferulic acid has the ability to protect fluoride-induced hepatic damage. 相似文献
7.
Luduvico Karina Pereira Spohr Luiza Soares Mayara Sandrielly Pereira Teixeira Fernanda Cardoso de Farias Alana Seixas Bona Natália Pontes Pedra Nathalia Stark de Oliveira Campello Felix Anelize Spanevello Roselia Maria Stefanello Francieli Moro 《Neurochemical research》2020,45(9):2032-2043
Neurochemical Research - Depression is an emotional disorder that causes mental and physical changes, and has limited pharmacotherapy. Tannic acid (TA) is a polyphenol with previously described... 相似文献
8.
常规实验操作对Wistar大鼠的影响 总被引:1,自引:1,他引:0
目的常规实验操作对Wistar大鼠的影响。方法采用Wistar大鼠,分别进行腹腔注射、肌内注射、灌胃、尾静脉切割采血、剪尾采血和固定操作,连续处理7d后,测定各组大鼠神经内分泌、免疫、血液系统主要指标及肝脏hsp72mRNA表达量,并与对照组比较,分析这些操作的影响。结果与对照组相比,腹腔注射组、肌内注射组和灌胃组的皮质酮(CORT)、γ-干扰素(IFN-γ)、γ-干扰素/白介素-4(IFN-γ/IL-4)比值极显著升高,白细胞总数(WBC)、中性粒细胞比例(WLCR)、C-反应蛋白(CRP)、β-内啡肽(β-EP)及白介素-2(IL-2)有不同程度的显著降低。与对照组相比,尾静脉切割采血组的CORT、IFN-γ、IFN-γ/IL-4比值极显著升高,WBC、β-EP有不同程度的显著降低;剪尾采血组的CORT、IFN-γ、IFN-γ/IL-4比值有不同程度的显著升高,β-EP、IL-2、CRP极显著降低;固定组的CORT、IFN-γ/IL-4比值、IL-2、CRP极显著升高,WBC、β-EP、IL-4有不同程度的显著降低。与对照组相比,所有实验操作均使热休克蛋白(HSP)hsp72mRNA表达极显著升高。此外,与对照组相比,肌内注射组的红细胞数(RBC)和血红蛋白含量(HGB)显著升高,尾静脉切割和剪尾采血组的HGB和红细胞压积(HCT)极显著降低,固定组的RBC、HGB和HCT均极显著升高。结论本研究中涉及的常规实验操作均引起了大鼠极显著的应激反应,并造成了大鼠神经内分泌系统的紊乱及免疫功能的抑制,从而对动物造成了恶性应激。同时这些操作可能会对涉及的神经内分泌及血液学指标的相关研究产生背景性干扰。 相似文献
9.
目的研究缓解-复发型EAE大鼠的基本病理改变。方法对缓解-复发型EAE大鼠进行HE染色、Weil髓鞘染色和改良的Bielschowsky染色,以免疫组化方法标记GFAP和MMP-2、MMP-9。结果组织内可见多个血管周围淋巴细胞浸润呈袖套样分布,伴有大片状脱髓鞘,部分脱失的髓鞘内有炎细胞浸润,轴索呈空泡样缺失,GFAP染色证明在旧病灶的周围部分可见星形胶质细胞增生,MMP-2、MMP-9在血管内皮细胞、细胞外基质、炎细胞及脑(脊)膜内呈阳性表达。结论①缓解-复发型EAE大鼠的组织病理学改变与临床表现一致,有活动性和非活动性病灶并存的现象。②MMP-2、MMP-9在活动性病灶内表达,参与疾病的发生。③缓解-复发型EAE病理改变与MS相似,是理想的动物模型。 相似文献
10.
Tichati Lazhari Trea Fouzia Ouali Kheireddine 《Biological trace element research》2020,194(1):228-236
Biological Trace Element Research - The present study aims to investigate the hepatoprotective effects of selenium on toxicity induced by ‘Désormone Lourd’ based on... 相似文献
11.
Rahul Chaudhary Manisha Chugh Ziauddin Darokhan Raghu Ram Katreddi Renuka Ramachandra V. Rema 《PloS one》2013,8(10)
Protein malnutrition during early development has been correlated with cognitive and learning disabilities in children, but the neuronal deficits caused by long-term protein deficiency are not well understood. We exposed rats from gestation up to adulthood to a protein-deficient (PD) diet, to emulate chronic protein malnutrition in humans. The offspring exhibited significantly impaired performance on the ‘Gap-crossing’ (GC) task after reaching maturity, a behavior that has been shown to depend on normal functioning of the somatosensory cortex. The physiological state of the somatosensory cortex was examined to determine neuronal correlates of the deficits in behavior. Extracellular multi-unit recording from layer 4 (L4) neurons that receive direct thalamocortical inputs and layers 2/3 (L2/3) neurons that are dominated by intracortical connections in the whisker-barrel cortex of PD rats exhibited significantly low spontaneous activity and depressed responses to whisker stimulation. L4 neurons were more severely affected than L2/3 neurons. The response onset was significantly delayed in L4 cells. The peak response latency of L4 and L2/3 neurons was delayed significantly. In L2/3 and L4 of the barrel cortex there was a substantial increase in GAD65 (112% over controls) and much smaller increase in NMDAR1 (12-20%), suggesting enhanced inhibition in the PD cortex. These results show that chronic protein deficiency negatively affects both thalamo-cortical and cortico-cortical transmission during somatosensory information processing. The findings support the interpretation that sustained protein deficiency interferes with features of cortical sensory processing that are likely to underlie the cognitive impairments reported in humans who have suffered from prolonged protein deficiency. 相似文献
12.
D. G. SMITH 《Journal of applied microbiology》1975,38(1):29-32
Swarming in all 27 strains of Proteus spp. tested was inhibited by the presence of 0.02% (w/v) tannic acid in the nutrient medium. Cells from colonies on this medium were nearly all short forms but were motile and piliated. The swarm-inhibition effect was not reversed by the addition of calcium chloride. The growth of other bacterial species was inhibited to varying extents by tannic acid: Gram positive cocci ( Micrococcus, Sarcina , and Staphylococcus spp.) were particularly sensitive. The relative resistance of Gram negative bacteria and the swarm-inhibition of Proteus spp. could be due to binding of tannic acid to proteins in the outer membrane of the cell wall. 相似文献
13.
The activity of IAA-oxidase increased in the leaves of Impatiensbalsamina plants receiving inductive photoperiodic cycles andin plants receiving treatments with gibberellic acid (GA3) and/ortannic acid (TA), even under non-inductive photoperiods; theactivity also increased in the stem receiving inductive photoperiodiccycles (8 h). Treatment with GA3 and TA mimics the effect ofSD cycles in the development of some isoenzymes of IAA-oxidase.Thus a new isoenzyme at Rf 0.48 developed in the leaves andone at Rf 0.82 developed in both the stem and the leaves ofall plants receiving inductive treatments photoperiodicor chemical but not in water-treated controls undernon-inductive photoperiods. Another isoenzyme at Rf 0.68 developedonly in the stems. Flowering, gibberellic acid, IAA oxidase, Impatiens, phenols, photoperiod 相似文献
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15.
SD大鼠和Wistar大鼠实验性自身免疫性脑脊髓炎发病情况比较 总被引:1,自引:0,他引:1
目的比较Wistar大鼠和Sprague-Dawley(SD)大鼠实验性自身免疫性脑脊髓炎(EAE)发病情况。方法注射以豚鼠脊髓匀浆-完全福氏佐剂制备的完全抗原,辅以百日咳疫苗加强诱导,复制Wistar大鼠和SD大鼠EAE模型,比较两组大鼠EAE的神经症状及中枢神经不同部位病理学改变。结果Wistar大鼠组发病数、潜伏期、发病达峰时间以及神经症状最高评分分别为9/12、12.33±1.37、15.17±3.19、1.33±0.41;SD大鼠组分别为11/12、15.88±0.64、18.63±1.52、3.13±1.89;两组大鼠相比,SD大鼠EAE潜伏期延长(P〈0.01),达峰时间相应推迟(P〈0.05),但神经症状较Wistar大鼠严重(P〈0.05);病理结果显示,两组大鼠CNS均以脑干病理改变最为严重,而大脑病变最轻,SD大鼠总体中枢系统炎症改变较Wistar大鼠严重(标准评分P〈0.01,血管套计数P〈0.05)。结论SD大鼠EAE与Wistar大鼠EAE比较,发病过程很相似:发病率接近,中枢炎症病理改变相仿,两者均以脑干炎症变化最严重;略有不同点是:SD大鼠EAE发病潜伏期较长(P〈0.01),神经症状较严重(P〈0.05),总体中枢炎症改变较为严重。故SD大鼠也是制备EAE模型的理想实验动物。 相似文献
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17.
Tiffany N. Eady Ludmila Belayev Larissa Khoutorova Kristal D. Atkins Changde Zhang Nicolas G. Bazan 《PloS one》2012,7(10)
Background
Docosahexaenoic acid, a major omega-3 essential fatty acid family member, improves behavioral deficit and reduces infarct volume and edema after experimental focal cerebral ischemia. We hypothesize that DHA elicits neuroprotection by inducing AKT/p70S6K phosphorylation, which in turn leads to cell survival and protects against ischemic stroke in young and aged rats.Methods and Results
Rats underwent 2 h of middle cerebral artery occlusion (MCAo). DHA, neuroprotectin D1 (NPD1) or vehicle (saline) was administered 3 h after onset of stroke. Neurological function was evaluated on days 1, 2, 3, and 7. DHA treatment improved functional recovery and reduced cortical, subcortical and total infarct volumes 7 days after stroke. DHA also reduced microglia infiltration and increased the number of astrocytes and neurons when compared to vehicle on days 1 and 7. Increases in p473 AKT and p308 AKT phosphorylation/activation were observed in animals treated with DHA 4 h after MCAo. Activation of other members of the AKT signaling pathway were also observed in DHA treated animals including increases in pS6 at 4 h and pGSK at 24 h. DHA or NPD1 remarkably reduced total and cortical infarct in aged rats. Moreover, we show that in young and aged rats DHA treatment after MCAo potentiates NPD1 biosynthesis. The phosphorylation of p308 AKT or pGSK was not different between groups in aged rats. However, pS6 expression was increased with DHA or NPD1 treatment when compared to vehicle.Conclusions
We suggest that DHA induces cell survival, modulates the neuroinflammatory response and triggers long term restoration of synaptic circuits. Both DHA and NPD1 elicited remarkable protection in aged animals. Accordingly, activation of DHA signaling might provide benefits in the management of ischemic stroke both acutely as well as long term to limit ensuing disabilities. 相似文献18.
Reddy R. Chandramouli Devaranavadagi Basavaraj Yendigeri Saeed M. Bagali Shrilaxmi Kulkarni Raghavendra V. Das Kusal K. 《Biological trace element research》2020,195(1):178-186
Biological Trace Element Research - Nickel, a widely used heavy metal is suspected as a cardiotoxic element. The aim of the present study was to assess the possible protective role of l-ascorbic... 相似文献
19.
Mohit Kwatra Ashok Jangra Murli Mishra Yogita Sharma Sahabuddin Ahmed Pinaki Ghosh Vikas Kumar Divya Vohora Razia Khanam 《Neurochemical research》2016,41(9):2352-2366
The present study was designed to investigate the neuroprotective effect of naringin (NR) alone as well as its combination with sertraline (SRT) against doxorubicin (DOX)-induced neurobehavioral and neurochemical anomalies. DOX (15 mg/kg; i.p.) administration caused behavioral alterations, oxidative stress, neuroinflammation, mitochondrial dysfunction and monoamines alteration in male Wistar rats. NR (50 and 100 mg/kg; i.p.) and SRT (5 mg/kg; i.p.) treatment significantly attenuated DOX-induced anxiety and depressive-like behavior as evident from elevated plus maze (EPM) and modified forced swimming test (mFST), respectively. NR treatment significantly attenuated DOX-induced raised plasma corticosterone (CORT), tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) levels in the hippocampus (HC). Furthermore, we found that combination of NR and SRT regimen ameliorated DOX-induced behavioral anomalies through modulation of the 5-HT level and mitochondrial complexes protection pathway along with alleviation of oxidative stress in the HC region. Therefore, NR treatment alone or in combination with SRT could be beneficial against DOX-induced neurotoxicity. 相似文献
20.
érica Maria Granjeiro Simone Saldanha Marroni Daniel Penteado Martins Dias Leni Gomes Heck Bonagamba Kauê Machado Costa Jéssica Cristina dos Santos José Ant?nio Cortes Oliveira Benedito H. Machado Norberto Garcia-Cairasco 《PloS one》2014,9(7)