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1 Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka, 565-0871, Japan; The Research Institute of Personalized Health Science, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido, Japan
2 Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Suita, Osaka, Japan
3 Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Suita, Osaka, Japan; United States
4 Division for Interdisciplinary Dentistry, Osaka University Dental Hospital, Suita, Osaka, Japan
5 The Research Institute of Personalized Health Science, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido, Japan
6 Department of Oral Anatomy, School of Dentistry, Kyungpook National University, Daegu, Korea, Republic of
* To whom correspondence should be addressed. E-mail: kang{at}dent.osaka-u.ac.jp.
It has recently been shown that the persistent Na+ current (INaP) is generated in the proximal axon in response to somatic depolarization in neocortical pyramidal neurons, while the involvement of INaP in spike-initiation is still unclear. Here we show a potential role of INaP in spike-initiation of primary sensory neurons in the mesencephalic trigeminal nucleus (MTN) that display a backpropagation of the spike initiated in the stem axon toward the soma in response to soma depolarization. Riluzole (10 µM) and tetrodotoxin (10 nM) caused an activation delay or a stepwise increase in the threshold for evoking soma spikes (S-spikes) without affecting the spike itself. Simultaneous patch-clamp recordings from the soma and axon hillock (AH) revealed that bath application of 50 nM tetrodotoxin increased the delay in spike activation in response to soma depolarization, leaving the spike-backpropagation time from the AH to soma unchanged. This indicates that the increase in activation delay occurred in the stem axon. Furthermore, under a decreasing intracellular concentration gradient of QX-314 from the soma to AH created by QX-314-containing and QX-314-free patch pipettes, the amplitude and maximum rate of rise (MRR) of AH-spikes decreased with an increase in the activation delay following repetition of current pulse injections, while S-spikes displayed much less decreases in amplitude and MRR. This suggests that comparing to S-spikes, AH-spikes more accurately reflect the attenuation of axonal-spike by QX-314, consistent with the spike-backpropagation nature. These observations strongly suggest that low-voltage-activated INaP is involved in spike-initiation in the stem axon of MTN neurons.
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