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Results: Among 32 tested MNs, depolarizing responses(excitatory postsynaptic potential, EPSP) were elicited by cVLF stimulation in 21 MNs, hyperpolarizing response (inhibitory postsynaptic potential, IPSP) in 1 MN, and IPSP preceded by EPSP in 4 MNs. The cVLFEPSPs were stimulus intensity-dependent, and could be abolished by low Ca(superscript 2+)/high Mg(superscript 2+) solution. compared with iVLF-EPSPs, cVLF-EPSPs showed longer latency (P.001). The cVLF-IPSP presented with membrane potential-dependent property and was eliminated by the perfusion of picrotoxin (30 μmol/L) and strychnine (1.0 μmol/L).

结果:在32个测试的MNs,观察到cVLF电刺激可在21个MNs上诱发去极化反应(即cVLF性兴奋性突触后电位,cVLF-EPSP),在1个MN上诱发超极化反应(即cVLF性抑制性突触后电位,cVLF-IPSP),在4个MNs上诱发cVLF-EPSP后复合有cVLF-IPSP的反应。cVLF-EPSP具有刺激强度依赖性、被低钙高镁溶液取消的特性,与i VLF性EPSP相比,有潜伏期较长的特点(P.001)。cVLF-IPSP呈膜电位依赖性,并被印防己毒素(30μmol/L)及士的宁(1.0μmol/L)取消。

Propofol induced Cl- currents at concentrations of 10-5 and10-4 M, which were sensitive to picrotoxin and, to a lesserextent, to strychnine. Propofol (10-6 M) enhanced -aminobutyricacidA (GABAA; 10-6 M)-induced current synergistically. Moreover,propofol (10-5 and 10-4 M) significantly increased the decaytime of evoked-inhibitory postsynaptic currents, which suggestsa postsynaptic modulation of GABAA receptors.

异丙酚在浓度10-5~10-4M 时,産生 Cl-电流,对印防己毒素敏感,在更小浓度范围内,对番木鼈碱敏感。10-6M 的异丙酚加强 GABAA 産生的电流,另外,异丙酚(10-5、10-4M )显著地增加了突触后诱发-抑制电流的衰退时间,提示了 GABAA 受体的突触后调节作用。

In the progress that presynaptic neuron was excited,which caused postsynaptic potential changing by the release of neurotransmitters,and then electrical signal was transferred,the function and form of synapses could change.

在突触前神经元兴奋,通过神经递质的释放,引起突触后电位的变化,从而完成电信号的传递过程中,突触本身的功能和形态都可能发生改变。

The in vitro effects of Gln49-PLA_2 were examined using the chick biventer cervicis nerve muscle preparation. Gln49-PLA_2 caused a dosedependent blockade of neuromuscular transmission. The time required to cause 50% blockade was about 150 min at the highest concentration 100μg/ml. This inhibition appeared to be presynaptic in origin as evidenced by the lack of effect of toxin on responses to exogenous acetylcholine in the non-stimulated BCp.

Gln49-PLA_2能够剂量依赖性地抑制颈二腹肌神经信号正常传导并影响肌肉收缩,在100μg/ml剂量下,肌肉收缩幅度在150分钟后达到50%的抑制率;同时,随着Gln49-PLA_2浓度的降低,肌肉收缩幅度的抑制效率也逐渐降低;实验证明Gln49-PLA_2对突触后膜乙酰胆碱受体敏感性无影响,对神经肌肉信号传导收缩的抑制作用位点在突触前膜。

In the presence of 500nM TTX, 70%M/T cells presented spontaneous activity. 80%M/T cells with spontaneous activity appeared excitory postsynaptic currents , which could be reverted at 20mv, 14%M/T cells appeared inhibitory postsy-naptic currents , which the reverse potential was -90mv. Few presented both EPSCs and IPSCs.

当细胞外液有1uM的河豚毒,70%的M/T细胞有自发活动,其中80%自发活动是兴奋性突触后电流、它的反转电位是20mv.14%的自发活动是抑制性突触后电流,它的反转电位是-90mv,极少数细胞同时有EPSPs和IPSPs。

Postsynaptic dense area and the close relationship between synaptic plasticity are essential for the maintenance of synaptic function properly.

突触后致密区与突触可塑性的关系十分密切,对于维持突触发挥正常功能至关重要。

RESULTS: Lidocaine inhibited both EPSP and the response foracetylcholine of the postsynaptic neuron.

结果:利多卡因同时抑制了兴奋性突触后电位和突触后神经元对乙酰胆碱的反应。

Immunoelectron microscopic examination revealed that mGluR5 was prominently located in some neuronal somata and a lot of dendrites within the superficial layers of the spinal dorsal horn. Some dendrites containing mGluR5 constituted synaptic glomeruli with the terminals exhibiting the morphological characteristics of primary afferent C fiber. The ultrastructural features indicated that mGluR5 in the dorsal horn of the spinal cord may prominently work as a postsynaptical receptor to mediate or modulate the function of glutamate in the primary sensory transmission, including the nociceptive transmission.

免疫电镜研究显示,在脊髓背角浅层内,mGluR5主要定位在部分神经元胞体和大量树突内,并常见部分含mGluR5的树突与具有一级传入C纤维终末形态特征的轴突终末构成突触小球。mGluR5在脊髓背角浅层内的超微定位特征表明,脊髓背角内的mGluR5可能主要作为突触后受体介导或调节谷氨酸传递一级感觉的功能。

We tested whether inhibitory GABAergic synaptic transmission regulates Xenopus optic tectal cell dendritic arbor development in vivo by expressing a peptide corresponding to an intracellular loop ofthe gamma2 subunit of type A GABA receptors GABA(AR, which is required to anchor GABA receptors to the postsynaptic scaffold.

我们想证明如下设想:抑制性GABA能突触传递是否能调节早蟾视顶盖细胞的树突发育。因为GABA受体的gamma2亚基有一段细胞内的跨膜端序列,这段序列对锚定GABAA受体到突触后膜是必须的,所以我们的主要方法是设计了一段特异性的争对细胞内段的序列,这样就特异性的阻断了单个细胞GABA能的突触传递。

These EDD were proved to contain calcium by X-ray microprobe analysis. The addition of 10mM/L theophylline greatly reduced the deposits in plasma membrane, mitochondria and EDD were not observed or observed rarely in subsurface cisternae.

在青蛙交感神经节突触后神经元中,包含钙离子的EDD存在于质膜、亚表面池及线粒体中;在突触前神经末梢中,突触小泡的膜上也可观察到EDD。

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