Erlichman, JS; Leiter, JC*

American Zoologist [AM. ZOOL.], vol. 37, no. 1, pp. 54-64, Jan 1997

Gas exchange in pulmonate snails of the family Helicidae occurs through a highly vascularized diffusion lung known as the mantle. The extent of ventilation of the mantle depends upon the duration and size of opening of an occlusible pore known as the pneumostome. In Helix aspersa and Helix pomatia, pneumostomal size and frequency of opening are exquisitely sensitive to CO sub(2). Respiratory CO sub(2) chemosensitivity resides in a discrete region of the subesophageal ganglia. The discharge pattern of many neurons in the chemoreceptor area changes during stimulation with CO sub(2). However, the electrophysiological response to CO sub(2) stimulation alone does not discriminate between CO sub(2) chemoreceptor cells and CO sub(2)-insensitive neurons active in the pneumostomal response to CO sub(2). We identified a subset of CO sub(2)-sensitive neurons from the larger population of neurons active during CO sub(2) stimulation. The action potential discharge frequency of CO sub(2) chemosensory neurons increased in response to CO sub(2) stimulation. An increased discharge frequency of CO sub(2)-sensitive neurons was associated with increased pneumostomal opening, and both the size and the frequency of pneumostomal opening increased during CO sub(2) stimulation. Injecting depolarizing current into individual chemosensory neurons elicited opening of the pneumostome in the absence of CO sub(2). Action potential generation in response to CO sub(2) was independent of synaptic transmission. Removal of individual CO sub(2)-sensitive cells or inhibition of action potential generation in CO sub(2)-sensitive cells reduced or eliminated pneumostomal responses to CO sub(2). CO sub(2) sensitivity in chemoreceptor cells required extracellular calcium, but not sodium. Substituting barium for calcium supported chemoreceptor activity. In summary, we have identified respiratory related, chemosensory neurons that are CO sub(2) sensitive in the absence of synaptic input.