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首页> 外文期刊>Journal of Neurophysiology >Cortical injury affects short-term plasticity of evoked excitatory synaptic currents.
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Cortical injury affects short-term plasticity of evoked excitatory synaptic currents.

机译：皮质损伤影响诱发的兴奋性突触电流的短期可塑性。

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摘要

The hypothesis that plastic changes in the efficacy of excitatory neurotransmission occur in areas of chronic cortical injury was tested by assessing short-term plasticity of evoked excitatory synaptic currents (EPSCs) in neurons of partially isolated neocortical islands (undercut cortex). Whole cell recordings were obtained from layer V pyramidal neurons of sensorimotor cortical slices prepared from P36-P43 control and undercut rats. AMPA/kainate receptor-mediated EPSCs elicited by stimuli delivered at 40 to 66.7 Hz exhibited more paired-pulse depression (PPD) in undercut cortex than control, the time constant of depression evoked by trains of 20- to 66.7-Hz stimuli was faster, and the steady-state amplitude of EPSCs reached after five to seven EPSCs was lower. An antagonist of the glutamate autoreceptor, group II mGluR, increased the steady-state amplitude of EPSCs from undercut but not control cortex, suggesting that activation of presynaptic receptors by released glutamate is more prominent in undercut cortex. In contrast, the GABA(B) receptor antagonist (2S)-3-[[(1S)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl](phenylmet hyl)phosphinic acid had no effect. Increasing [Ca(2+)](o) from 2 to 4 mM increased PPD, with a smaller effect in neurons of the undercut. The I-V relationship of AMPA/kainate receptor-mediated EPSCs was close to linear in both control and undercut neurons, and spermine had no significant effect on the EPSCs, suggesting that decreases in postsynaptic glutamate receptors containing the GluR2 subunit were not involved in the alterations in short-term plasticity. Results are compatible with an increase in the probability of transmitter release at excitatory synapses in undercut cortex due to functional changes in presynaptic terminals.
机译：通过评估部分分离的新皮层岛（咬边皮层）的神经元中诱发的兴奋性突触电流（EPSC）的短期可塑性，检验了在慢性皮质损伤区域中发生兴奋性神经传递功效的塑性变化的假说。从由P36-P43对照和咬边大鼠制备的感觉运动皮层切片的V层锥体神经元获得全细胞记录。在40至66.7 Hz的频率下传递的刺激引起的AMPA /海藻酸酯受体介导的EPSC在底切皮层中的成对脉冲抑制（PPD）比对照组要多，由20至66.7 Hz的频率的刺激引起的抑制的时间常数更快， 5至7个EPSC之后，EPSC达到稳态振幅。谷氨酸自身受体的拮抗剂，第II组mGluR，增加了咬合但未控制皮层的EPSC的稳态振幅，表明释放的谷氨酸对突触前受体的激活在咬合皮中更为突出。相比之下，GABA（B）受体拮抗剂（2S）-3-[[（（1S）-1-（3,4-二氯苯基）乙基]氨基-2-羟丙基]（苯基甲酰基）次膦酸没有作用。 [Ca（2 +）]（o）从2 mM增加到4 mM可增加PPD，对底切神经元的影响较小。 AMPA /海因酸酯受体介导的EPSC在对照和底切神经元中的IV关系均接近线性，并且精胺对EPSC没有显着影响，这表明含有GluR2亚基的突触后谷氨酸受体的减少不参与改变。短期可塑性。结果与底切皮层兴奋性突触释放的概率增加有关，这是由于突触前末端的功能改变所致。

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