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J Neurophysiol 88: 2242-2250, 2002; doi:10.1152/jn.00081.2002
0022-3077/02 $5.00
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J Neurophysiol (November 1, 2002). 10.1152/jn.00081.2002
Submitted on 6 February 2002
Accepted on 22 July 2002

Persistent Sodium Current, Membrane Properties and Bursting Behavior of Pre-Bötzinger Complex Inspiratory Neurons In Vitro

Christopher A. Del Negro,1,* Naohiro Koshiya,1,2,* Robert J. Butera Jr.,3 and Jeffrey C. Smith1

 1Cellular and Systems Neurobiology Section, Laboratory of Neural Control, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-4455;  2Blanchette Rockefeller Neurosciences Institute, Rockville, Maryland 20850-3332; and  3Laboratory for Neuroengineering, Institute for Bioengineering and Biosciences, Georgia Institute of Technology, Atlanta, Georgia 30332

Del Negro, Christopher A., Naohiro Koshiya, Robert J. Butera Jr., and Jeffrey C. Smith. Persistent Sodium Current, Membrane Properties and Bursting Behavior of Pre-Bötzinger Complex Inspiratory Neurons In Vitro. J. Neurophysiol. 88: 2242-2250, 2002. We measured persistent Na+ current and membrane properties of bursting-pacemaker and nonbursting inspiratory neurons of the neonatal rat pre-Bötzinger complex (pre-BötC) in brain stem slice preparations with a rhythmically active respiratory network in vitro. In whole-cell recordings, slow voltage ramps (<= 100 mV/s) inactivated the fast, spike-generating Na+ current and yielded N-shaped current-voltage relationships with nonmonotonic, negative-slope regions between -60 and -35 mV when the voltage-sensitive component was isolated. The underlying current was a TTX-sensitive persistent Na+ current (INaP) since the inward current was present at slow voltage ramp speeds (3.3-100 mV/s) and the current was blocked by 1 µM TTX. We measured the biophysical properties of INaP after subtracting the voltage-insensitive "leak" current (ILeak) in the presence of Cd2+ and in some cases tetraethylammonium (TEA). Peak INaP ranged from -50 to -200 pA at a membrane potential of -30 mV. Decreasing the speed of the voltage ramp caused time-dependent INaP inactivation, but this current was present at ramp speeds as low as 3.3 mV/s. INaP activated at -60 mV and obtained half-maximal activation near -40 mV. The subthreshold voltage dependence and slow inactivation kinetics of INaP, which closely resemble those of INaP mathematically modeled as a burst-generation mechanism in pacemaker neurons of the pre-BötC, suggest that INaP predominantly influences bursting dynamics of pre-BötC inspiratory pacemaker neurons in vitro. We also found that the ratio of persistent Na+ conductance to leak conductance (gNaP/gLeak) can distinguish the phenotypic subpopulations of bursting pacemaker and nonbursting inspiratory neurons: pacemaker neurons showed gNaP/gLeak > gNaP/gLeak in nonpacemaker cells (P < 0.0002). We conclude that INaP is ubiquitously expressed by pre-BötC inspiratory neurons and that bursting pacemaker behavior within the heterogeneous population of inspiratory neurons is achieved with specific ratios of these two conductances, gNaP and gLeak.

* C. A. Del Negro and N. Koshiya contributed equally to this study.




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