首页> 外文期刊>The European Journal of Neuroscience >Involvement of NR2A- or NR2B-containing N-methyl-D-aspartate receptors in the potentiation of cortical layer 5 pyramidal neurone inputs depends on the developmental stage.
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Involvement of NR2A- or NR2B-containing N-methyl-D-aspartate receptors in the potentiation of cortical layer 5 pyramidal neurone inputs depends on the developmental stage.

机译:皮质层5锥体神经元输入的增强中涉及NR2A或NR2B的N-甲基-D-天冬氨酸受体的参与取决于发育阶段。

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In the cortex, N-methyl-D-aspartate receptors (NMDARs) play a critical role in the control of synaptic plasticity processes. We have previously shown in rat visual cortex that the application of a high-frequency stimulation (HFS) protocol used to induce long-term potentiation in layer 2/3 leads to a parallel potentiation of excitatory and inhibitory inputs received by cortical layer 5 pyramidal neurones without changing the excitation/inhibition balance of the pyramidal neurone, indicating a homeostatic control of this parameter. We show here that the blockade of NMDARs of the neuronal network prevents the potentiation of excitatory and inhibitory inputs, and this result leaves open to question the role of the NMDAR isoform involved in the induction of long-term potentiation, which is actually being strongly debated. In postnatal day (P)18-23 rat cortical slices, the blockade of synaptic NR2B-containing NMDARs prevents the induction of the potentiation induced by the HFS protocol, whereas the blockade of NR2A-containing NMDARs reduced the potentiation itself. In P29-P32 cortical slices, the specific activation of NR2A-containing receptors fully ensures the potentiation of excitatory and inhibitory inputs. These results constitute the first report of a functional shift in subunit composition of NMDARs during the critical period (P12-P36), which explains the relative contribution of both NR2B- and NR2A-containing NMDARs in synaptic plasticity processes. These effects of the HFS protocol are mediated by the activation of synaptic NMDARs but our results also indicate that the homeostatic control of the excitation/inhibition balance is independent of NMDAR activation and is due to specialized recurrent interactions between excitatory and inhibitory networks.
机译:在皮层中,N-甲基-D-天冬氨酸受体(NMDARs)在控制突触可塑性过程中起关键作用。我们先前已经在大鼠的视皮层中显示,高频诱导(HFS)协议用于诱导第2/3层的长期增强作用的应用导致皮质第5层锥体神经元收到的兴奋性和抑制性输入平行增强而没有改变锥体神经元的激发/抑制平衡,表明该参数的稳态控制。我们在这里表明,神经元网络的NMDAR的阻断阻止了兴奋性和抑制性输入的增强,这一结果使人们质疑NMDAR同工型在诱导长期增强中所起的作用,这实际上正在激烈辩论中。 。在出生后(P)18-23天的大鼠皮层切片中,含有突触的NR2B NMDAR的阻滞阻止了HFS方案诱导的增强作用的诱导,而含有NR2A的NMDAR的阻滞降低了增强作用。在P29-P32皮质切片中,含有NR2A的受体的特异性激活充分确保了兴奋性和抑制性输入的增强。这些结果构成了关键时期(P12-P36)NMDARs亚基组成功能转变的第一份报告,这解释了含有NR2B和NR2A的NMDAR在突触可塑性过程中的相对贡献。 HFS协议的这些作用是由突触NMDAR的激活介导的,但我们的结果也表明,激发/抑制平衡的稳态控制与NMDAR激活无关,并且是由于兴奋性和抑制性网络之间的专门性反复相互作用所致。

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