Complex intrinsic membrane properties and dopamine shape spiking activity in a motor axon.

Complex intrinsic membrane properties and dopamine shape spiking activity in a motor axon.
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DOI:
10.1523/jneurosci.0716-09.2009
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发表时间:
2009-04-22
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
通讯作者:
Bucher D
Bucher D
中科院分区:
其他
文献类型:
--
作者:
Ballo AW;Bucher D

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我们研究了美洲白鹤龙虾口胃神经节的两个幽门扩张器(PD)神经元的外周运动轴突。来自运动神经的细胞内记录显示出快速和慢速的电压和活动依赖性动态。在节律爆发期间,PD 轴突显示出尖峰幅度和持续时间的变化。药理学实验和这些现象的电压依赖性表明钠通道和 A 型钾通道的失活是造成这一现象的原因。此外,“静息”膜电位取决于持续的尖峰或爆发活动,当活动较强时,超极化值更高。神经刺激、药理学阻滞和电流钳实验表明,这是由于缓慢后超极化 (sAHP) 和通过超极化激活电流 (IH) 的内向整流之间的功能拮抗作用。在没有中枢产生的活动的情况下,多巴胺的应用导致适度的去极化和“异位”外周尖峰启动。该效应被 CsCl 和 ZD7288 阻断,与 IH 的作用一致。高频神经刺激抑制外周尖峰启动几秒钟,可能是由于 sAHP。在正常爆发活动和逆向神经刺激期间,周围神经长度上的传导延迟以复杂的方式发生变化。这表明轴突膜动力学可以对从尖峰起始位点传播到突触目标的尖峰模式的时间保真度产生重大影响,并且神经调节剂可以影响尖峰模式被修改的程度。
We studied the peripheral motor axons of the two pyloric dilator (PD) neurons of the stomatogastric ganglion in the lobster, Homarus americanus. Intracellular recordings from the motor nerve showed both fast and slow voltage- and activity-dependent dynamics. During rhythmic bursts, the PD axons displayed changes in spike amplitude and duration. Pharmacological experiments and the voltage-dependence of these phenomena suggest that inactivation of sodium and A-type potassium channels are responsible. In addition, the “resting” membrane potential was dependent on ongoing spike or burst activity, with more hyperpolarized values when activity was strong. Nerve stimulations, pharmacological block and current clamp experiments suggest that this is due to a functional antagonism between a slow after-hyperpolarization (sAHP) and inward rectification through hyperpolarization-activated current (IH). Dopamine application resulted in modest depolarization and “ectopic” peripheral spike initiation in the absence of centrally generated activity. This effect was blocked by CsCl and ZD7288, consistent with a role of IH. High frequency nerve stimulation inhibited peripheral spike initiation for several seconds, presumably due to the sAHP. Both during normal bursting activity and antidromic nerve stimulation, the conduction delay over the length of the peripheral nerve changed in a complex manner. This suggests that axonal membrane dynamics can have a substantial effect on the temporal fidelity of spike patterns propagated from a spike initiation site to a synaptic target, and that neuromodulators can influence the extent to which spike patterns are modified.