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This Article Full Text Full Text (PDF) All Versions of this Article: 586/7/1921    most recent jphysiol.2008.150946v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Hayes, J. A. Articles by Del Negro, C. A. PubMed PubMed Citation Articles by Hayes, J. A. Articles by Del Negro, C. A. Related Collections Neuroscience

¹ Department of Applied Science, McGlothlin-Street Hall, Room 318, The College of William and Mary, Williamsburg, VA 23187-8795, USA

We measured a low-threshold, inactivating K⁺ current, i.e. A-current (I_A), in respiratory neurons of the preBötzinger complex (preBötC) in rhythmically active slice preparations from neonatal C57BL/6 mice. The majority of inspiratory neurons (21/34 = 61.8%), but not expiratory neurons (1/8 = 12.5%), expressed I_A. In whole-cell and somatic outside-out patches I_A activated at –60 mV (half-activation voltage measured –16.3 mV) and only fully inactivated above –40 mV (half-inactivation voltage measured –85.6 mV), indicating that I_A can influence membrane trajectory at baseline voltages during respiratory rhythm generation in vitro. 4-Aminopyridine (4-AP, 2 mM) attenuated I_A in both whole-cell and somatic outside-out patches. In the context of rhythmic network activity, 4-AP caused irregular respiratory-related motor output on XII nerves and disrupted rhythmogenesis as detected with whole-cell and field recordings in the preBötC. Whole-cell current-clamp recordings showed that 4-AP changed the envelope of depolarization underlying inspiratory bursts (i.e. inspiratory drive potentials) from an incrementing pattern to a decrementing pattern during rhythm generation and abolished current pulse-induced delayed excitation. These data suggest that I_A opposes excitatory synaptic depolarizations at baseline voltages of approximately –60 mV and influences the inspiratory burst pattern. We propose that I_A promotes orderly recruitment of constituent rhythmogenic neurons by minimizing the activity of these neurons until they receive massive coincident synaptic input, which reduces the periodic fluctuations of inspiratory activity.

(Received 10 January 2008; accepted after revision 5 February 2008; first published online 7 February 2008)
Corresponding author C. A. Del Negro: Department of Applied Science, McGlothlin-Street Hall, Room 318, The College of William and Mary, Williamsburg, VA 23187-8795, USA.  Email: cadeln{at}wm.edu