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Articles in PresS, published online ahead of print September 18, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00346.2002
Submitted on July 25, 2002
Accepted on September 10, 2002
1 Physiology and Biophysics, Wright State University, Dayton, OH, USA
* To whom correspondence should be addressed. E-mail: robert.putnam{at}wright.edu.
We studied chemosensitive signaling in LC neurons using both perforated and whole cell patch techniques. Upon inhibition of fast Na+ spikes by TTX, hypercapnic acidosis (HA-15% CO2, pHo 6.8) induced small, slow spikes. These spikes were inhibited by Co2+ or nifedipine and were attributed to activation of L-type Ca2+ channels by HA. Upon inhibition of both Na+ and Ca2+ spikes, HA resulted in a membrane depolarization of 3.52±0.61 mV (n=17), that was reduced by TEA (1.49±0.70 mV, n=7; P<0.05) and absent (-0.97±0.73 mV, n=7; P<0.001) upon exposure to isohydric hypercapnia (IH-15% CO2, 77 mM HCO3-, pHo 7.45). Either HA or IH, but not 50 mM Na-propionate, activated Ca2+ channels. Inhibition of L-type Ca2+ channels by nifedipine reduced HA-induced increased firing rate and eliminated IH-induced increased firing rate. We conclude that chemosensitive signals (e.g. HA or IH) have multiple targets in LC neurons, including TEA-sensitive K+ channels and TASK channels. Further, HA and IH activate L-type Ca2+ channels and this activation is part of chemosensitive signaling in LC neurons.
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