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This Article Full Text Full Text (PDF) All Versions of this Article: 586/18/4531    most recent jphysiol.2008.154765v1 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 Morgado-Valle, C. Articles by Feldman, J. L. PubMed PubMed Citation Articles by Morgado-Valle, C. Articles by Feldman, J. L. Related Collections Respiratory

¹ Systems Neurobiology Laboratory, Department of Neurobiology, David Geffen School of Medicine at UCLA, University of California Los Angeles, Box 951763, Los Angeles, CA 90095-1763, USA
² Division of Head and Neck Surgery, David Geffen School of Medicine at UCLA, University of California Los Angeles, Los Angeles, CA 90095-1794, USA
³ Department of Physiology, David Geffen School of Medicine at UCLA, University of California Los Angeles, Los Angeles, CA 90095-1751, USA

PreBötzinger Complex (preBötC) neurons are postulated to underlie respiratory rhythm generation. The inspiratory phase of the respiratory cycle in vitro results from preBötC neurons firing synchronous bursts of action potentials (APs) on top of 10–20 mV, 0.3–0.8 s inspiratory drive potentials. Is the inspiratory drive in individual neurons simply the result of the passive integration of inspiratory-modulated synaptic currents or do active processes modulate these currents? As somatic Ca²⁺ is known to increase during inspiration, we hypothesized that it affects inspiratory drive. We combined whole cell recording in an in vitro slice preparation with Ca²⁺ microfluorometry to detect single inspiratory neuron somatic Ca²⁺ transients with high temporal resolution (µs). In neurons loaded with either Fluo-4 or Oregon Green BAPTA 5 N, we observed Ca²⁺ transients associated with each AP. During inspiration, significant somatic Ca²⁺ influx was a direct consequence of activation of voltage-gated Ca²⁺ channels by APs. However, when we isolated the inspiratory drive potential in active preBötC neurons (by blocking APs with intracellular QX-314 or by hyperpolarization), we did not detect somatic Ca²⁺ transients; yet, the parameters of inspiratory drive were the same with or without APs. We conclude that, in the absence of APs, somatic Ca²⁺ transients do not shape the somatic inspiratory drive potential. This suggests that in preBötC neurons, substantial and widespread somatic Ca²⁺ influx is a consequence of APs during the inspiratory phase and does not contribute substantively to the inspiratory drive potential. Given evidence that the Ca²⁺ buffer BAPTA can significantly reduce inspiratory drive, we hypothesize that dendritic Ca²⁺ transients amplify inspiratory-modulated synaptic currents.

(Received 3 April 2008; accepted after revision 14 July 2008; first published online 17 July 2008)
Corresponding author C. Morgado-Valle: Department of Neurobiology, David Geffen School of Medicine at UCLA, Box 951763, Los Angeles, CA 90095-1763, USA. Email: cmorgado{at}mednet.ucla.edu