Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Persistent Sodium and Calcium Currents in Rat Hypoglossal Motoneurons

Persistent Sodium and Calcium Currents in Rat Hypoglossal Motoneurons Abstract Voltage-dependent persistent inward currents are thought to make an important contribution to the input–output properties of α−motoneurons, influencing both the transfer of synaptic current to the soma and the effects of that current on repetitive discharge. Recent studies have paid particular attention to the contribution of L-type calcium channels, which are thought to be widely distributed on both the somatic and the dendritic membrane. However, the relative contribution of different channel subtypes as well as their somatodendritic distribution may vary among motoneurons of different species, developmental stages, and motoneuron pools. In this study, we have characterized persistent inward currents in juvenile (10- to 24-day-old) rat hypoglossal (HG) motoneurons. Whole-cell, voltage-clamp recordings were made from the somata of visualized rat HG motoneurons in 300-μm brain stem slices. Slow (10 s), triangular voltage-clamp commands from a holding potential of −70 to 0 mV and back elicited whole-cell currents that were dominated by outward, potassium currents, but often showed a region of negative slope resistance on the rising phase of the command. In the presence of potassium channel blockers (internal cesium and external 4-aminopyridine and tetraethylammonium), net inward currents were present on both the rising and falling phases of the voltage-clamp command. A portion of the inward current present on the ascending phase of the command was mediated by TTX-sensitive sodium channels, whereas calcium channels mediated the remainder of the current. We found roughly the same relative contributions of P-, N-, and L-type channels to the calcium currents recorded at the soma that had previously been found in neonatal rat HG motoneurons. In most cells, the somatic voltage thresholds for calcium current onset and offset were similar and the peak current was largest on the ascending phase of the clamp command. However, about one-third of the cells exhibited a substantial clockwise current hysteresis, i.e., inward currents were present at lower voltages on the descending phase of the clamp command. In the same cells, 1-s depolarizing voltage-clamp commands were followed by prolonged tail currents, consistent with a prominent contribution from dendritic channels. In contrast to previous reports on turtle and mouse motoneurons, blocking L-type calcium channels did not eliminate these presumed dendritic currents. Footnotes Address for reprint requests: R. K. Powers, Department of Physiology and Biophysics, University of Washington, School of Medicine, Box 357290, Seattle, Washington 98195 (E-mail: rkpowers@u.washington.edu ). Copyright © 2003 The American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurophysiology The American Physiological Society

Persistent Sodium and Calcium Currents in Rat Hypoglossal Motoneurons

Journal of Neurophysiology , Volume 89 (1): 615 – Jan 1, 2003

Loading next page...
 
/lp/the-american-physiological-society/persistent-sodium-and-calcium-currents-in-rat-hypoglossal-motoneurons-rXkrgJpG0U

References

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0022-3077
eISSN
1522-1598
DOI
10.1152/jn.00241.2002
pmid
12522206
Publisher site
See Article on Publisher Site

Abstract

Abstract Voltage-dependent persistent inward currents are thought to make an important contribution to the input–output properties of α−motoneurons, influencing both the transfer of synaptic current to the soma and the effects of that current on repetitive discharge. Recent studies have paid particular attention to the contribution of L-type calcium channels, which are thought to be widely distributed on both the somatic and the dendritic membrane. However, the relative contribution of different channel subtypes as well as their somatodendritic distribution may vary among motoneurons of different species, developmental stages, and motoneuron pools. In this study, we have characterized persistent inward currents in juvenile (10- to 24-day-old) rat hypoglossal (HG) motoneurons. Whole-cell, voltage-clamp recordings were made from the somata of visualized rat HG motoneurons in 300-μm brain stem slices. Slow (10 s), triangular voltage-clamp commands from a holding potential of −70 to 0 mV and back elicited whole-cell currents that were dominated by outward, potassium currents, but often showed a region of negative slope resistance on the rising phase of the command. In the presence of potassium channel blockers (internal cesium and external 4-aminopyridine and tetraethylammonium), net inward currents were present on both the rising and falling phases of the voltage-clamp command. A portion of the inward current present on the ascending phase of the command was mediated by TTX-sensitive sodium channels, whereas calcium channels mediated the remainder of the current. We found roughly the same relative contributions of P-, N-, and L-type channels to the calcium currents recorded at the soma that had previously been found in neonatal rat HG motoneurons. In most cells, the somatic voltage thresholds for calcium current onset and offset were similar and the peak current was largest on the ascending phase of the clamp command. However, about one-third of the cells exhibited a substantial clockwise current hysteresis, i.e., inward currents were present at lower voltages on the descending phase of the clamp command. In the same cells, 1-s depolarizing voltage-clamp commands were followed by prolonged tail currents, consistent with a prominent contribution from dendritic channels. In contrast to previous reports on turtle and mouse motoneurons, blocking L-type calcium channels did not eliminate these presumed dendritic currents. Footnotes Address for reprint requests: R. K. Powers, Department of Physiology and Biophysics, University of Washington, School of Medicine, Box 357290, Seattle, Washington 98195 (E-mail: rkpowers@u.washington.edu ). Copyright © 2003 The American Physiological Society

Journal

Journal of NeurophysiologyThe American Physiological Society

Published: Jan 1, 2003

There are no references for this article.