Somatic vs. dendritic responses to hypercapnia in chemosensitive locus coeruleus neurons from neonatal rats

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Abstract
Cardiorespiratory control is mediated in part by central chemosensitive neurons that respond to increased CO2 (hypercapnia). Activation of these neurons is thought to involve hypercapnia-induced decreases in intracellular pH (pHi). All previous measurements of hypercapnia-induced pHi changes in chemosensitive neurons have been obtained from the soma, but chemosensitive signaling could be initiated in the dendrites of these neurons. In this study, membrane potential ( Vm) and pHi were measured simultaneously in chemosensitive locus coeruleus (LC) neurons from neonatal rat brain stem slices using whole cell pipettes and the pH-sensitive fluorescent dye pyranine. We measured pHi from the soma as well as from primary dendrites to a distance 160 μm from the edge of the soma. Hypercapnia [15% CO2, external pH (pHo) 7.00; control, 5% CO2, pHo 7.45] resulted in an acidification of similar magnitude in dendrites and soma (∼0.26 pH unit), but acidification was faster in the more distal regions of the dendrites. Neither the dendrites nor the soma exhibited pHi recovery during hypercapnia-induced acidification; but both regions contained pH-regulating transporters, because they exhibited pHi recovery from an NH4Cl prepulse-induced acidification (at constant pHo 7.45). Exposure of a portion of the dendrites to hypercapnic solution did not increase the firing rate, but exposing the soma to hypercapnic solution resulted in a near-maximal increase in firing rate. These data show that while the pHi response to hypercapnia is similar in the dendrites and soma, somatic exposure to hypercapnia plays a major role in the activation of chemosensitive LC neurons from neonatal rats.