2004 Fiscal Year Final Research Report Summary
Regulatory Mechanisms of Excitability in the Mesencephalic Trigeminal Neurons
| Project/Area Number |
14370597
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Osaka University |
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Principal Investigator |
KANG Youngnam Osaka University, Graduate School of Dentistry, Professor, 大学院・歯学研究科, 教授 (50177755)
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Masayuki Osaka University, Graduate School of Dentistry, Lecture, 大学院・歯学研究科, 講師 (00300830)
SAITO Mitsuru Osaka University, Graduate School of Dentistry, Instructor, 大学院・歯学研究科, 助手 (50347770)
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| Project Period (FY) |
2002 – 2004
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| Keywords | mesencephalic trigeminal neuron / primary sensory neuron / masticatory movement / h-channel / Na^+-K^+ pump / A-like current / voltage-dependent Na^+ channel / gap junction channel |
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| Research Abstract |
(1)Bidirectional interactions between h-channels and Na^+-K^+ pumps in MTN neurons
Activation of h-current (I-h) leads to the generation of two types of ouabain-sensitive Na^+-K^+ pump current (I-p) with temporal profiles similar to those of instantaneous and slow components of I-h, presumably reflecting Na^+-transients in a restricted cellular space. Moreover, the I-p activated by instantaneous I-h can facilitate the subsequent activation of slow I-h. These observations indicate that the interactions are bidirectional and mediated by Na^+ ions. Also following substitution of extracellular Na^+ with Li^+, the tail I-h was markedly reduced in spite of an enhancement of I-h itself, due to a negative shift of the reversal potential for I-h presumably caused by intracellular accumulation of Li^+ ions. This suggests the presence of Na^+-microdomain where the interactions can take place. Consistent with these findings, HCN1/2 subunits and the Na^+-K^+ pump α3 isoform were colocalized in plasm
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a membrane of mesencephalic trigeminal neurons having numerous spines.
(2)Impulse trafficking in primary sensory neurons of MTN
Simultaneous patch-clamp recordings from the soma and axon hillock(AH) revealed a spike-backpropagation in response to somatic depolarization, and disclosed the spike-initiation site in the stem axon. Repetition of current pulse injection, under the condition of decreasing intracellular concentration gradient of QX-314 from the soma to AH created by QX-314-containing and QX-314-free patch pipettes, unexpectedly attenuated the AH-spike, leaving the soma-spike(S-spike) almost unchanged. When S- or AH-spikes were evoked alternately by injection of current pulses into the soma or AH and by stimulation of the stem axon, bath application of 50 nM TTX first rendered the axonal stimulation ineffective in evoking all-or-nothing axonal spikes, leaving the S- or AH-spikes to be evoked by injection of current pulses with a stepwise increased intensity. Under this condition, spike-backpropagation was no longer seen in the S- or AH-spikes. These observations suggest the presence of low-voltage-activated and highly QX-314- and TTX-sensitive Na^+ channels across the AH and stem axon, which are responsible for both spike-backpropagation and spike-invasion. Furthermore, depending on whether S-spikes were backpropagated or invaded, A-like current was involved in differentially shaping S-spikes, thereby regulating the pattern of S-spike trains in a manner dependent on the origin of spikes. It is likely that somatic inputs or peripherally arising impulses whichever trigger spikes in the stem axon first is forwarded to the central axon, which should be reflected by differentially shaped S-spikes in the soma. Less
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Research Products
(11 results)
