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1.
以放射性配基结合分析法对正常成年小鼠大脑皮中N-甲基-D-天冬氨酸(NMDA)受体作了鉴定;观察了衰老小鼠NMDA受体、空间辨别能力、海马突触传递长时程增强的变化及补肾中药复方对这些变化的影响。结果表明:小鼠大脑皮质含有丰富的、高亲和力的NMDA受体;衰老过程中小鼠NMDA受体的最大结合容量Bmax)呈渐进性降低,空间辨别能力下降,LTP的振幅和斜率明显降低;补肾中药复方具有提高衰才小鼠NMDA受  相似文献   

2.
本实验采用放射性配基受体结合分析法,测定了猫脑外伤时大脑皮质和海马N-甲基-D-天冬氨酸受体(NMDAR)的变化。并用氨基酸自动分析仪观察了猫大脑皮质兴奋性氨基酸含量变化。结果表明,伤后2和6h两侧大脑皮质和海马NMDAR的最大结合容量明显降低,伤后2h以海马变化最大,并以伤后6h伤侧大脑皮质中降低最为显著;而大脑皮质兴奋性氨基酸含量伤后5min即显著升高,然后呈下降趋势,且以伤侧大脑皮质变化为大  相似文献   

3.
目前一般认为长时程增强效应(long-termpotentiation,LTP)和哺乳动物大脑学习记忆的机制有关。本文简述了视皮层中LTP的诱导,产生的关键期以及LTP在脑皮层功能柱的不同层中的差异。讨论了N-甲基-D-氨基丁酸(N-methyl-D-aspartate,NMDA)受体、低阈值Ga2+通道(low-thresholdCa2+channels,LTCs)在LTP诱导过程中的作用,以及视皮层LTP和海马LTP的差异。  相似文献   

4.
NAD激酶在光合作用等植物生理过程中起重要作用。NAD激酶的激活依赖于钙离子和钙调素(CalmOdulin,CaM).从植物中分离得到的一种新的CaM结合蛋白CaMBP-10(BP-10)明显抑制NAD激酶的激活活性,抑制作用可被CaM所克服.动力学研究表明,抑制效应是BP-10与CaM之间特异性相互作用的结果。实验证实BP-10对NAD激酶活性起着重要调节作用.  相似文献   

5.
NO和CO加强海马活动依赖性长时程增强效应   总被引:1,自引:0,他引:1  
NO和CO加强海马活动依赖性长时程增强效应长时程增强(long-termpotentiation,LTP)效应是突触可塑性的一种形式,突触可塑性被认为与学习记忆密切相关。海马CAl区LTP的产生需要Ca2+通过NMDA受体离子通道进入细胞内;LTP的...  相似文献   

6.
本实验采用放射性配基受体结合分析法,测定了猫脑外伤时大脑皮质和海马N─甲基─D─天冬氨酸受体(NMDAR)的变化。并用氨基酸自动分析仪观察了猫大脑皮质兴奋性氨基酸含量变化。结果表明,伤后2和6h两侧大脑皮质和海马NMDAR的最大结合容量明显降低,伤后2h以海马变化最大,并以伤后6h伤侧大脑皮质中降低最为显著;而大脑皮质兴奋性氨基酸含量伤后5min即显著升高,然后呈下降趋势,且以伤侧大脑皮质变化为大。提示:脑外伤后NMDAR的下调与兴奋性氨基酸的大量释放有关,可能在兴奋毒性脑损伤中起重要作用。  相似文献   

7.
Fyn酪氨酸激酶与酒精引起的神经元损伤有关fyn基因编码一种非受体酪氨酸激酶,可以使NMDA受体磷酸化,1992年证明该酶在突触传递的长时程增强效应(LTP)的形成以及空间学习中起重要作用。最近,日本的Niki等发现,小鼠对酒精的敏感性至少部分取决于...  相似文献   

8.
高胆固醇饲料喂养造成的动脉粥样硬化(As) 模型家兔通过静脉注射人血浆HDL 制剂, 观察HDL 对As家兔肝细胞膜LDL受体活性的影响. 结果发现, 摄取高胆固醇饲料的As 家兔, 其肝细胞膜LDL 受体 Kd 值虽无明显变化但Bmax 值显著减小( P< 0-01 , 与正常对照组比较) ; 注射HDL 制剂后, As 家兔肝细胞膜LDL受体Kd 值仍无明显改变, 但Bmax 值却显著回升( P< 0-01 , 与高脂组比较) . 表明人血浆HDL 具有增加As 家兔肝细胞膜LDL 受体活性的作用.  相似文献   

9.
CaM BP—10对NAD激酶的抑制效应   总被引:2,自引:0,他引:2  
NAD激酶在光合作用等植物生理过程中起重要作用。NAD激酶的激活依赖于钙离子和钙调素(CaM)。从植物中分离得到的一种新的CaM结合蛋白CaM BP-10(BP-10)明显抑制NAD激酶的激活活性。抑制作用可被CaM所克服。动力学研究表明,抑制效应是BP-10与CaM之间特异性相互作用的结果。实验证实BP-10对NAD激酶活性起着重要调节作用。  相似文献   

10.
对胰岛素cAMP对培养人动脉平滑肌细胞(SMC)HDL受体功能的影响进行了研究,结果发现:胰岛素使SMCHDL受体的结合容量Bmax即受体数目显著下降,而对SMCHDL受体的Kd值亲和力无影响;cAMp则SMCHDL受体亲和力增加,而对受体数目无影响。  相似文献   

11.
N-methyl-D-aspartate (NMDA) receptors are known to play an important role in learning and memory and to be involved in neuron cell death accompanying cerebral ischemia, seizures, and Alzheimer's disease. The NMDA receptor complex has been considered to consist of an L-glutamate recognition site, a strychnine-insensitive glycine modulatory site, and a voltage-dependent cation channel. In the present study, effects of age on an L-glutamate recognition site and a glycine site were examined in rat brain by quantitative in vitro autoradiography with [3H]-CPP and [3H]-glycine. Both [3H]-glycine and [3H]-CPP binding sites were most abundant in the hippocampus and cerebral cortex, and they showed a similar distribution pattern throughout the brain. [3H]-glycine binding sites were severely decreased in the telencephalic regions, including the hippocampus and cerebral cortex, in aged brain. Conversely, [3H]-CPP binding sites were well preserved in these brain areas. In the mid-brain regions and cerebellum, neither [3H]-glycine nor [3H]-CPP binding sites changed in the aged brain. Our results indicate that within the NMDA receptor complex, glycine receptors are primarily affected in the aging process.  相似文献   

12.
Zhao MG  Toyoda H  Lee YS  Wu LJ  Ko SW  Zhang XH  Jia Y  Shum F  Xu H  Li BM  Kaang BK  Zhuo M 《Neuron》2005,47(6):859-872
Cortical plasticity is thought to be important for the establishment, consolidation, and retrieval of permanent memory. Hippocampal long-term potentiation (LTP), a cellular mechanism of learning and memory, requires the activation of glutamate N-methyl-D-aspartate (NMDA) receptors. In particular, it has been suggested that NR2A-containing NMDA receptors are involved in LTP induction, whereas NR2B-containing receptors are involved in LTD induction in the hippocampus. However, LTP in the prefrontal cortex is less well characterized than in the hippocampus. Here we report that the activation of the NR2B and NR2A subunits of the NMDA receptor is critical for the induction of cingulate LTP, regardless of the induction protocol. Furthermore, pharmacological or genetic blockade of the NR2B subunit in the cingulate cortex impaired the formation of early contextual fear memory. Our results demonstrate that the NR2B subunit of the NMDA receptor in the prefrontal cortex is critically involved in both LTP and contextual memory.  相似文献   

13.
Cui Y  Jin J  Zhang X  Xu H  Yang L  Du D  Zeng Q  Tsien JZ  Yu H  Cao X 《PloS one》2011,6(5):e20312
Prefrontal cortex plays an important role in working memory, attention regulation and behavioral inhibition. Its functions are associated with NMDA receptors. However, there is little information regarding the roles of NMDA receptor NR2B subunit in prefrontal cortical synaptic plasticity and prefrontal cortex-related working memory. Whether the up-regulation of NR2B subunit influences prefrontal cortical synaptic plasticity and working memory is not yet clear. In the present study, we measured prefrontal cortical synaptic plasticity and working memory function in NR2B overexpressing transgenic mice. In vitro electrophysiological data showed that overexpression of NR2B specifically in the forebrain region resulted in enhancement of prefrontal cortical long-term potentiation (LTP) but did not alter long-term depression (LTD). The enhanced LTP was completely abolished by a NR2B subunit selective antagonist, Ro25-6981, indicating that overexpression of NR2B subunit is responsible for enhanced LTP. In addition, NR2B transgenic mice exhibited better performance in a set of working memory paradigms including delay no-match-to-place T-maze, working memory version of water maze and odor span task. Our study provides evidence that NR2B subunit of NMDA receptor in prefrontal cortex is critical for prefrontal cortex LTP and prefrontal cortex-related working memory.  相似文献   

14.
Glutathione (GSH), the major endogenous antioxidant produced by cells, can modulate the activity of N-methyl-D-aspartate receptors (NMDARs) through its reducing functions. During aging, an increase in oxidative stress leads to decreased levels of GSH in the brain. Concurrently, aging is characterized by calcium dysregulation, thought to underlie impairments in hippocampal NMDAR-dependent long-term potentiation (LTP), a form of synaptic plasticity thought to represent a cellular model for memory. Here we show that orally supplementing aged mice with N-acetylcysteine, a precursor for the formation of glutathione, reverses the L-type calcium channel-dependent LTP seen in aged animals to NMDAR-dependent LTP. In addition, introducing glutathione in the intrapipette solution during whole-cell recordings restores LTP obtained in whole-cell conditions in the aged hippocampus. We conclude that aging leads to a reduced redox potential in hippocampal neurons, triggering impairments in LTP.  相似文献   

15.
Receptors for excitatory amino acid,L-glutamate, have been classified into three subtypes named as N-methyl-D-aspartate (NMDA), quisqualate (QA) and kainate receptors. In the present study, an effect of age on binding sites of [3H]-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (3H-AMPA), a QA agonist, was studied in the rat brain through quantitative in vitro autoradiography.3H-AMPA binding sites were most concentrated in the hippocampus and cerebral cortex where glutamate receptors have been demonstrated to play a role in synaptic transmission. In aged rats,3H-AMPA binding sites in the hippocampus and cerebral cortex were not significantly changed. In our previous studies, it was noticed that strychnine-insensitive glycine receptors, which functionally coupled with NMDA receptors, showed marked age-dependent decreases in telencephalic regions. It has been shown that the glutamatergic neuronal system is involved in learning and memory. Nevertheless, it is considered that AMPA binding sites are not involved in the decline of neuronal functions, especially impairment of learning and memory, accompanying with aging process.  相似文献   

16.
We assayed N-methyl-d-aspartate (NMDA) receptors [3H]3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid ([3H]CPP) bindings) and evaluated their distribution in the brain by quantitative autoradiography in young adult and aged rats. In the young adult rats, NMDA receptors were present at relatively high concentrations in the cerebral cortex and hippocampus. In the aged rats, NMDA receptors were decreased in the nealy all areas of the brain, especially in the cerebral cortex and hippocampus. Chronic administration of bifemelane hydrochloride, a drug for sequela of cerebrovascular diseased, at a dose of 15 mg/kg/day for 14 days, markedly attenuated these decrease in NMDA receptors. Since NMDA receptors are considered to be involved in memory and learning processes, our results suggest that bifemelane hydrochloride may be applicable to the treatment of disturbed memory and learning.  相似文献   

17.
Curcumin has neuroprotective effect and could enhance memory. However, the mechanisms underlying the protection of curcumin on aging-related memory decline are not well understood. In this study, high frequency stimulation (HFS)-induced long term potentiation (LTP) was evaluated by a cellular model of memory formation. A two-input stimulation paradigm was used to record the potentiation as well as synapse input specificity. The data suggested that an N-Methyl-d-aspartate receptors (NMDAR) -dependent LTP was inducible in adult hippocampal slices with a characteristic of synapse input specificity. It also indicated that aging resulted in a reduction in LTP but more importantly a loss of synaptic input specificity. The reason behind the above conclusions is that LTP induction is more dependent on the calcium channel. This is due to a switch of the dependence of LTP induction to voltage-dependent calcium channel (VDCC) compared to NMDA receptors. Curcumin administration recovers input specificity by re-establishing NMDA receptor dependence of induction. In addition, curcumin administration ameliorated aging-related increase of brain thiobarbituric acid-reactive substances and elevated aging-related decrease of glutathione in hippocampus. It is then concluded that curcumin modulates hippocampal redox status and restores aging-related loss of synapse input specificity of HFS-induced LTP by switching VDCC calcium source into NMDA receptor-dependent one.  相似文献   

18.
Contemporary neuroscientists are paying increasing attention to subcellular, molecular and electrophysiological mechanisms underlying learning and memory processes. Recent efforts have addressed the development of transgenic mice affected at different stages of the learning process, or emulating pathological conditions involving cognition and motor-learning capabilities. However, a parallel effort is needed to develop stimulating and recording techniques suitable for use in behaving mice, in order to grasp activity-dependent neural changes taking place during the very moment of the process. These in vivo models should integrate the fragmentary information collected by different molecular and in vitro approaches. In this regard, long-term potentiation (LTP) has been proposed as the neural mechanism underlying synaptic plasticity. Moreover, N -methyl- d -aspartate (NMDA) receptors are accepted as the molecular substrate of LTP. It now seems necessary to study the relationship of both LTP and NMDA receptors with the plastic changes taking place, in selected neural structures, during actual learning. Here, we review data on the involvement of the hippocampal CA3–CA1 synapse in the acquisition of classically conditioned eyelid conditioned responses (CRs) in behaving mice. Available data show that LTP, evoked by high-frequency stimulation of Schaffer collaterals, disturbs both the acquisition of CRs and the physiological changes that occur at the CA3–CA1 synapse during learning. Moreover, the administration of NMDA-receptor antagonists is able not only to prevent LTP induction in vivo , but also to hinder the formation of both CRs and functional changes in strength of the CA3–CA1 synapse. Thus, there is experimental evidence relating activity-dependent synaptic changes taking place during actual learning with LTP mechanisms and with the role of NMDA receptors in both processes.  相似文献   

19.
As the contribution of cannabinoid (CB1) receptors in the neuroadaptations following chronic alcohol exposure is unknown, we investigated the neuroadaptations induced by chronic alcohol exposure on both NMDA and GABA(A) receptors in CB1-/- mice. Our results show that basal levels of hippocampal [(3)H]MK-801 ((1)-5-methyl-10,11-dihydro-5Hdibenzo[a,d]cyclohepten-5,10-imine) binding sites were decreased in CB1-/- mice and that these mice were also less sensitive to the locomotor effects of MK-801. Basal level of both hippocampal and cerebellar [(3)H]muscimol binding was lower and sensitivity to the hypothermic effects of diazepam and pentobarbital was increased in CB1-/- mice. GABA(A)alpha1, beta2, and gamma2 and NMDA receptor (NR) 1 and 2B subunit mRNA levels were altered in striatum of CB1-/- mice. Our results also showed that [(3)H]MK-801 binding sites were increased in cerebral cortex and hippocampus after chronic ethanol ingestion only in wild-type mice. Chronic ethanol ingestion did not modify the sensitivity to the locomotor effects of MK-801 in both genotypes. Similarly, chronic ethanol ingestion reduced the number of [(3)H]muscimol binding sites in cerebral cortex, but not in cerebellum, only in CB1+/+ mice. We conclude that lifelong deletion of CB1 receptors impairs neuroadaptations of both NMDA and GABA(A) receptors after chronic ethanol exposure and that the endocannabinoid/CB1 receptor system is involved in alcohol dependence.  相似文献   

20.
Abstract: Mice infected with the LP-BM5 murine leukemia virus (MuLV) develop an immunodeficiency syndrome (murine AIDS) and an encephalopathy characterized by impaired spatial learning and memory. Because platelet-activating factor (PAF) has been implicated in the pathogenesis of HIV-associated dementia complex, brain PAF levels were measured in LP-BM5 MuLV-infected mice. PAF levels in cerebral cortex and hippocampus were significantly increased at 6 and 12 weeks after LP-BM5 MuLV inoculation, whereas significant increases in striatal and cerebellar PAF levels were observed only at 12 weeks after inoculation. Administration of the NMDA antagonist MK-801 significantly reduced the increased PAF levels in the cerebral cortex and hippocampus of LP-BM5 MuLV-infected mice. These results indicate that the LP-BM5 MuLV-induced increases in brain PAF levels are the result of NMDA receptor activation and are consistent with the hypothesis that elevated CNS PAF levels contribute to the behavioral deficits observed in LP-BM5 MuLV-infected mice.  相似文献   

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