CO₂ decreases membrane conductance and depolarizes neurons in the nucleus tractus solitarii

Summary

To identify central sites of potential CO₂/H⁺-chemoreceptive neurons, and the mechanism responsible for neuronal chemosensitivity, intracellular recordings were made in rat tissue slices in two cardiopulmonary-related regions (i.e., nucleus tractus solitarii, NTS; nucleus ambiguus, AMBc) during exposure to high CO₂. When the NTS was explored slices were bisected and the ventral half discarded. Utilizing such “dorsal” medullary slices removed any impinging synaptic input from putative chemoreceptors in the ventrolateral medulla. In the NTS, CO₂-induced changes in firing rate were associated with membrane depolarizations ranging from 2–25 mV (n = 15). In some cases increased e.p.s.p. activity was observed during CO₂ exposure. The CO₂-induced depolarization occurred concomitantly with an increased input resistance ranging from 19–23 MΩ (n = 5). The lower membrane conductance during hypercapnia suggests that CO₂-induced depolarization is due to a decreased outward potassium conductance. Unlike neurons in the NTS, AMBc neurons were not spontaneously active and were rarely depolarized by hypercapnia. Eleven of 12 cells tested were either hyperpolarized by or insensitive to CO₂. Only 1 neuron in the AMBc was depolarized and it also showed an increased input resistance during CO₂ exposure. Our findings suggest that CO₂/H⁺-related stimuli decrease potassium conductance which depolarizes the cell and increases firing rate. Although our in vitro studies cannot guarantee the specific function of these cells, we believe they may be involved with brain pH homeostasis and cardiopulmonary regulation.