Generation of resonance-dependent oscillation by mGluR-I activation switches single spiking to bursting in mesencephalic trigeminal sensory neurons
Generation of resonance-dependent oscillation by mGluR-I activation switches single spiking to bursting in mesencephalic trigeminal sensory neurons
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DOI：
10.1111/ejn.12858
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发表时间：
2015-04-01
影响因子：
3.4
通讯作者：
Kang, Youngnam
中科院分区：
文献类型：
--
作者：
Chung, Gehoon;Saito, Mitsuru;Kang, Youngnam
提供下颌闭合肌肌梭的初级感觉神经元是独特的，因为它们在脑干的中脑三叉神经核（MTN）中具有它们的胞体，从而接收各种突触输入。MTN神经元在激活神经元能突触输入时显示爆发，同时它们忠实地传递来自外周感觉器官的相应冲动。据报道，持续性钠电流（I-NaP）负责脉冲串的产生和脉冲的中继。我们解决了I-NaP是如何控制触发突发或中继各自的脉冲作为单个尖峰在MTN神经元。蛋白激酶C（PKC）激活增强I-NaP仅在低电压。在比静息电位更去极化的膜电位下，PKC激活促进了棘波的产生。通过注入斜坡电流脉冲，从去极化的膜电位触发尖峰脉冲串，而其瞬时尖峰频率几乎保持恒定，尽管斜坡增加电流强度超过阈值。在斜坡脉冲之前的谷氨酸的抽吸应用降低了斜坡脉冲引起爆发的阈值，而白屈菜红碱消除了谷氨酸的这种作用。二羟基苯甘氨酸，mGluR1/5的激动剂，也引起了类似的效果，并增加了膜共振的频率和阻抗。免疫组织化学显示，mGluR1/5和Nav1.6共同定位于干轴突上的神经元突触。两者合计，到干轴突上的神经元能突触输入可能能够将中继切换到爆发模式。
The primary sensory neurons supplying muscle spindles of jaw-closing muscles are unique in that they have their somata in the mesencephalic trigeminal nucleus (MTN) in the brainstem, thereby receiving various synaptic inputs. MTN neurons display bursting upon activation of glutamatergic synaptic inputs while they faithfully relay respective impulses arising from peripheral sensory organs. The persistent sodium current (I-NaP) is reported to be responsible for both the generation of bursts and the relay of impulses. We addressed how I-NaP is controlled either to trigger bursts or to relay respective impulses as single spikes in MTN neurons. Protein kinase C (PKC) activation enhanced I-NaP only at low voltages. Spike generation was facilitated by PKC activation at membrane potentials more depolarized than the resting potential. By injection of a ramp current pulse, a burst of spikes was triggered from a depolarized membrane potential whereas its instantaneous spike frequency remained almost constant despite the ramp increases in the current intensity beyond the threshold. A puff application of glutamate preceding the ramp pulse lowered the threshold for evoking bursts by ramp pulses while chelerythrine abolished such effects of glutamate. Dihydroxyphenylglycine, an agonist of mGluR1/5, also caused similar effects, and increased both the frequency and impedance of membrane resonance. Immunohistochemistry revealed that glutamatergic synapses are made onto the stem axons, and that mGluR1/5 and Nav1.6 are co-localized in the stem axon. Taken together, glutamatergic synaptic inputs onto the stem axon may be able to switch the relaying to the bursting mode.