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Am J Physiol Cell Physiol 284: C145-C155, 2003. First published September 18, 2002; doi:10.1152/ajpcell.00346.2002
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Vol. 284, Issue 1, C145-C155, January 2003

Multiple targets of chemosensitive signaling in locus coeruleus neurons: role of K+ and Ca2+ channels

Jessica A. Filosa and Robert W. Putnam

Department of Physiology and Biophysics, Wright State University School of Medicine, Dayton, Ohio 45435

We studied chemosensitive signaling in locus coeruleus (LC) neurons using both perforated and whole cell patch techniques. Upon inhibition of fast Na+ spikes by tetrodotoxin (TTX), hypercapnic acidosis [HA; 15% CO2, extracellular pH (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 tetraethylammonium (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 HCO<UP><SUB>3</SUB><SUP>−</SUP></UP>, 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 TWIK-related acid-sensitive K+ (TASK) channels. Furthermore, HA and IH activate L-type Ca2+ channels, and this activation is part of chemosensitive signaling in LC neurons.

acidosis; membrane potential; perforated patch clamp; respiration; whole cell patch clamp


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