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This Article Full Text Full Text (PDF) All Versions of this Article: 97/3/2385    most recent 01191.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Kang, Y. Articles by Bae, Y.-C. Search for Related Content PubMed PubMed Citation Articles by Kang, Y. Articles by Bae, Y.-C.

Involvement of Persistent Na⁺ Current in Spike Initiation in Primary Sensory Neurons of the Rat Mesencephalic Trigeminal Nucleus

¹Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry; ²Division for Interdisciplinary Dentistry, Osaka University Dental Hospital, Osaka; ³The Research Institute of Personalized Health Science, Health Sciences University of Hokkaido, Hokkaido, Japan; and ⁴Department of Oral Anatomy, School of Dentistry, Kyungpook National University, Daegu, South Korea

Submitted 9 November 2006; accepted in final form 16 January 2007

It was recently shown that the persistent Na⁺ current (I_NaP) is generated in the proximal axon in response to somatic depolarization in neocortical pyramidal neurons, although the involvement of I_NaP in spike initiation is still unclear. Here we show a potential role of I_NaP 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 (TTX, 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 TTX 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, whereas S-spikes displayed decreases of considerably lesser degree in amplitude and MRR. This suggests that compared to S-spikes, AH-spikes more accurately reflect the attenuation of axonal spike by QX-314, consistent with the nature of spike backpropagation. These observations strongly suggest that low-voltage–activated I_NaP is involved in spike initiation in the stem axon of MTN neurons.

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