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首页> 外文期刊>Journal of Neurophysiology >Protracted postnatal development of inhibitory synaptic transmission in rat hippocampal area CA1 neurons.
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Protracted postnatal development of inhibitory synaptic transmission in rat hippocampal area CA1 neurons.

机译：大鼠海马区CA1神经元抑制性突触传递的出生后发育延长。

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In the CNS, inhibitory synaptic function undergoes profound transformation during early postnatal development. This is due to variations in the subunit composition of subsynaptic GABA(A) receptors (GABA(A)Rs) at differing developmental stages as well as other factors. These include changes in the driving force for chloride-mediated conductances as well as the quantity and/or cleft lifetime of released neurotransmitter. The present study was undertaken to investigate the nature and time course of developmental maturation of GABAergic synaptic function in hippocampal CA1 pyramidal neurons. In neonatal [postnatal day (P) 1-7] and immature (P8-14) CA1 neurons, miniature inhibitory postsynaptic currents (mIPSCs) were significantly larger, were less frequent, and had slower kinetics compared with mIPSCs recorded in more mature neurons. Adult mIPSC kinetics were achieved by the third postnatal week in CA1 neurons. However, despite this apparent maturation of mIPSC kinetics, significant differences in modulation of mIPSCs by allosteric agonists in adolescent (P15-21) neurons were still evident. Diazepam (1-300 nM) and zolpidem (200 nM) increased the amplitude of mIPSCs in adolescent but not adult neurons. Both drugs increased mIPSC decay times equally at both ages. These differential agonist effects on mIPSC amplitude suggest that in adolescent CA1 neurons, inhibitory synapses operate differently than adult synapses and function as if subsynaptic receptors are not fully occupied by quantal release of GABA. Rapid agonist application experiments on perisomatic patches pulled from adolescent neurons provided additional support for this hypothesis. In GABA(A)R currents recorded in these patches, benzodiazepine amplitude augmentation effects were evident only when nonsaturating GABA concentrations were applied. Furthermore nonstationary noise analysis of mIPSCs in P15-21 neurons revealed that zolpidem-induced mIPSC augmentation was not due to an increase in single-channel conductance of subsynaptic GABA(A)Rs but rather to an increase in the number of open channels responding to a single GABA quantum, further supporting the hypothesis that synaptic receptors may not be saturated during synaptic function in adolescent neurons. These data demonstrate that inhibitory synaptic transmission undergoes a markedly protracted postnatal maturation in rat CA1 pyramidal neurons. In the first two postnatal weeks, mIPSCs are large in amplitude, are slow, and occur infrequently. By the third postnatal week, mIPSCs have matured kinetically but retain distinct responses to modulatory drugs, possibly reflecting continued immaturity in synaptic structure and function persisting through adolescence.
机译：在中枢神经系统中，抑制性突触功能在出生后早期发展过程中发生了深刻的转变。这是由于处于不同发育阶段的突触亚GABA（A）受体（GABA（A）Rs）亚基组成的变化以及其他因素引起的。这些包括氯化物介导的电导的驱动力的变化，以及释放的神经递质的数量和/或left裂寿命。本研究旨在研究海马CA1锥体神经元中GABA能突触功能发育成熟的性质和时间过程。与更成熟的神经元中记录的mIPSC相比，在新生儿[产后第1-7天（P）1-7]和未成熟的（P8-14）CA1神经元中，微型抑制性突触后电流（mIPSC）明显更大，频率更低且动力学更慢。出生后第三周，在CA1神经元中达到了成人mIPSC动力学。但是，尽管mIPSC动力学已经明显成熟，但在青春期（P15-21）神经元中，变构激动剂对mIPSC的调节仍存在明显差异。地西p（1-300 nM）和唑吡坦（200 nM）增加了青少年但非成人神经元中mIPSC的幅度。两种药物在两个年龄段均增加了mIPSC衰减时间。这些对mIPSC振幅的不同激动剂作用表明，在青春期CA1神经元中，抑制性突触的功能与成人突触不同，并且功能似乎好像突触下的受体并未完全被GABA的定量释放所占据。对从青春期神经元拉出的周围斑块进行的快速激动剂应用实验为这一假设提供了额外的支持。在这些斑块中记录的GABA（A）R电流中，仅当应用非饱和GABA浓度时，苯并二氮杂amplitude的幅度增强作用才明显。此外，在P15-21神经元中对mIPSC的非平稳噪声分析表明，唑吡坦诱导的mIPSC增强不是由于突触后GABA（A）Rs的单通道电导增加，而是由于响应于AABA的开放通道数量增加。单个GABA量子，进一步支持了以下假说：在青春期神经元的突触功能过程中，突触受体可能不会饱和。这些数据表明，抑制性突触传递在大鼠CA1锥体神经元中经历了明显延长的出生后成熟。在出生后的前两周，mIPSC振幅大，速度慢且不经常发生。到产后第三个星期，mIPSC在动力学上已经成熟，但对调节药物的反应却截然不同，这可能反映出突触结构和功能的不成熟持续到青春期。

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