Mechanisms controlling bursting activity induced by disinhibition in spinal cord networks
Mechanisms controlling bursting activity induced by disinhibition in spinal cord networks
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DOI：
10.1046/j.1460-9568.2002.01904.x
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发表时间：
2002-02-01
影响因子：
3.4
通讯作者：
Streit, J
中科院分区：
文献类型：
--
作者：
Darbon, P;Scicluna, L;Streit, J
去抑制可靠地诱导定期同步爆发的脊髓中间神经元网络中的文化，以及在完整的脊髓。我们结合了细胞外多位点记录使用多电极阵列与全细胞记录，探讨机制参与爆裂器官型和分离培养的胚胎大鼠脊髓。网络爆发引起单个神经元的去极化和棘波，这是通过突触传递介导的反复兴奋。当这种传输被阻断时，爆发停止。然而，紧张性尖峰持续在一些神经元。在这些神经元中，内在尖峰脉冲在爆发后被抑制，并在几秒钟后的间隔中重新出现。抑制的内在尖峰可以重现时，在快速突触传递的情况下，通过注入电流脉冲模仿突发。内源性尖峰也被轻微的超极化抑制。爆发后的后超极化被发现在大约一半的神经元。这些后超极化与兴奋性降低相结合。没有证据表明参与突触耗竭或受体脱敏的爆发被发现，因为既不率也不自发兴奋性突触后电流的大小减少后的爆发。细胞外刺激起搏脉冲串在低频率，但未能诱导脉冲串时，应用太快后，最后一个脉冲串。总之，这些结果表明，在脊髓培养的爆发主要是基于内在的尖峰在一些神经元，反复兴奋的网络和神经元兴奋性的自动调节。
Disinhibition reliably induces regular synchronous bursting in networks of spinal interneurons in culture as well as in the intact spinal cord. We have combined extracellular multisite recording using multielectrode arrays with whole cell recordings to investigate the mechanisms involved in bursting in organotypic and dissociated cultures from the spinal cords of embryonic rats. Network bursts induced depolarization and spikes in single neurons, which were mediated by recurrent excitation through glutamatergic synaptic transmission. When such transmission was blocked, bursting ceased. However, tonic spiking persisted in some of the neurons. In such neurons intrinsic spiking was suppressed following the bursts and reappeared in the intervals after several seconds. The suppression of intrinsic spiking could be reproduced when, in the absence of fast synaptic transmission, bursts were mimicked by the injection of current pulses. Intrinsic spiking was also suppressed by a slight hyperpolarization. An afterhyperpolarization following the bursts was found in roughly half of the neurons. These afterhyperpolarizations were combined with a decrease in excitability. No evidence for the involvement of synaptic depletion or receptor desensitization in bursting was found, because neither the rate nor the size of spontaneous excitatory postsynaptic currents were decreased following the bursts. Extracellular stimuli paced bursts at low frequencies, but failed to induce bursts when applied too soon after the last burst. Altogether these results suggest that bursting in spinal cultures is mainly based on intrinsic spiking in some neurons, recurrent excitation of the network and auto-regulation of neuronal excitability.